«Covid» redirects here. Not to be confused with corvid.
| Coronavirus disease 2019 (COVID-19) |
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| Other names | COVID, (the) coronavirus |
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Transmission and life-cycle of SARS-CoV-2 causing COVID-19 |
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| Pronunciation |
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| Specialty | Infectious disease |
| Symptoms | Fever, cough, fatigue, shortness of breath, vomiting, loss of taste or smell; some cases asymptomatic[2][3] |
| Complications | Pneumonia, viral sepsis, acute respiratory distress syndrome, kidney failure, cytokine release syndrome, respiratory failure, pulmonary fibrosis, paediatric multisystem inflammatory syndrome, long COVID |
| Usual onset | 2–14 days (typically 5) from infection |
| Duration | 5 days to chronic |
| Causes | Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) |
| Diagnostic method | rRT‑PCR testing, CT scan, Rapid antigen test |
| Prevention | Vaccination,[4] face coverings, quarantine, physical/social distancing, ventilation, hand washing[5] |
| Treatment | Symptomatic and supportive |
| Frequency | 664,338,243[6] confirmed cases |
| Deaths | 6,707,311[6] |
Coronavirus disease 2019 (COVID-19) is a contagious disease caused by a virus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first known case was identified in Wuhan, China, in December 2019.[7] The disease quickly spread worldwide, resulting in the COVID-19 pandemic.
The symptoms of COVID‑19 are variable but often include fever,[8] cough, headache,[9] fatigue, breathing difficulties, loss of smell, and loss of taste.[10][11][12] Symptoms may begin one to fourteen days after exposure to the virus. At least a third of people who are infected do not develop noticeable symptoms.[13] Of those who develop symptoms noticeable enough to be classified as patients, most (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging), and 5% develop critical symptoms (respiratory failure, shock, or multiorgan dysfunction).[14] Older people are at a higher risk of developing severe symptoms. Some people continue to experience a range of effects (long COVID) for months after recovery, and damage to organs has been observed.[15] Multi-year studies are underway to further investigate the long-term effects of the disease.[15]
COVID‑19 transmits when people breathe air contaminated by droplets and small airborne particles containing the virus. The risk of breathing these is highest when people are in close proximity, but they can be inhaled over longer distances, particularly indoors. Transmission can also occur if contaminated fluids are splashed or sprayed in the eyes, nose, or mouth, or, more rarely, via contaminated surfaces. People remain contagious for up to 20 days and can spread the virus even if they do not develop symptoms.[16][17]
Testing methods for COVID-19 to detect the virus’s nucleic acid include real-time reverse transcription polymerase chain reaction (rRT‑PCR),[18][19] transcription-mediated amplification,[18][19][20] and reverse transcription loop-mediated isothermal amplification (RT‑LAMP)[18][19] from a nasopharyngeal swab.[21]
Several COVID-19 vaccines have been approved and distributed in various countries, which have initiated mass vaccination campaigns. Other preventive measures include physical or social distancing, quarantining, ventilation of indoor spaces, use of face masks or coverings in public, covering coughs and sneezes, hand washing, and keeping unwashed hands away from the face. While work is underway to develop drugs that inhibit the virus, the primary treatment is symptomatic. Management involves the treatment of symptoms through supportive care, isolation, and experimental measures.
Nomenclature
During the initial outbreak in Wuhan, the virus and disease were commonly referred to as «coronavirus» and «Wuhan coronavirus»,[22][23][24] with the disease sometimes called «Wuhan pneumonia».[25][26] In the past, many diseases have been named after geographical locations, such as the Spanish flu,[27] Middle East respiratory syndrome, and Zika virus.[28] In January 2020, the World Health Organization (WHO) recommended 2019-nCoV[29] and 2019-nCoV acute respiratory disease[30] as interim names for the virus and disease per 2015 guidance and international guidelines against using geographical locations or groups of people in disease and virus names to prevent social stigma.[31][32][33] The official names COVID‑19 and SARS-CoV-2 were issued by the WHO on 11 February 2020 with COVID-19 being shorthand for «coronavirus disease 2019».[34][35] The WHO additionally uses «the COVID‑19 virus» and «the virus responsible for COVID‑19» in public communications.[34][36]
Signs and symptoms
The symptoms of COVID-19 are variable depending on the type of variant contracted, ranging from mild symptoms to a potentially fatal illness.[37][38] Common symptoms include coughing, fever, loss of smell (anosmia) and taste (ageusia), with less common ones including headaches, nasal congestion and runny nose, muscle pain, sore throat, diarrhea, eye irritation,[39] and toes swelling or turning purple,[40] and in moderate to severe cases, breathing difficulties.[41] People with the COVID-19 infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; and a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea.[41] In people without prior ear, nose, or throat disorders, loss of taste combined with loss of smell is associated with COVID-19 and is reported in as many as 88% of symptomatic cases.[42][43][44]
Of people who show symptoms, 81% develop only mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) that require hospitalization, and 5% of patients develop critical symptoms (respiratory failure, septic shock, or multiorgan dysfunction) requiring ICU admission.[45] At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time.[46][47] These asymptomatic carriers tend not to get tested and can still spread the disease.[47][48][49][50] Other infected people will develop symptoms later (called «pre-symptomatic») or have very mild symptoms and can also spread the virus.[50]
As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days[51] possibly being infectious on 1-4 of those days.[52] Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.[51][53]
Most people recover from the acute phase of the disease. However, some people—over half of a cohort of home-isolated young adults identified in June, 2021[54][55] continued to experience a range of effects, such as fatigue, for months even after recovery. This is the result of a condition called long COVID, which can be described as a range of persistent symptoms that continue for weeks and/or months at a time.[56] Long-term damage to organs has also been observed after the onset of COVID-19. Multi-year studies are underway to further investigate the potential long-term effects of the disease.[57]
The Omicron variant became dominant in the U.S. in December 2021. Symptoms with the Omicron variant are less severe than they are with other variants.[58]
Cause
COVID‑19 is caused by infection with a strain of coronavirus known as ‘Severe Acute Respiratory Syndrome coronavirus 2’ (SARS-CoV-2).[59]
Transmission
| Transmission of COVID-19 | |
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| Other names | Mode of spread of COVID-19 |
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| Specialty | Infection prevention and control |
| Types | Respiratory droplet, airborne transmission, fomites |
| Prevention | Face coverings, quarantine, physical/social distancing, ventilation, hand washing, vaccination |
COVID-19 is mainly transmitted when people breathe in air contaminated by droplets/aerosols and small airborne particles containing the virus. Infected people exhale those particles as they breathe, talk, cough, sneeze, or sing.[60][61][62][63] Transmission is more likely the more physically close people are. However, infection can occur over longer distances, particularly indoors.[60][64]
Infectivity can begin four to five days before the onset of symptoms,[65] although contact tracing typically begins only two to three days before symptom onset.[66] Infected people can spread the disease even if they are pre-symptomatic or asymptomatic.[66] Most commonly, the peak viral load in upper respiratory tract samples occurs close to the time of symptom onset and declines after the first week after symptoms begin.[66] Current evidence suggests a duration of viral shedding and the period of infectiousness of up to ten days following symptom onset for people with mild to moderate COVID-19, and up to 20 days for persons with severe COVID-19, including immunocompromised people.[67][66]
Infectious particles range in size from aerosols that remain suspended in the air for long periods of time to larger droplets that remain airborne briefly or fall to the ground.[68][69][70][71] Additionally, COVID-19 research has redefined the traditional understanding of how respiratory viruses are transmitted.[71][72] The largest droplets of respiratory fluid do not travel far, but can be inhaled or land on mucous membranes on the eyes, nose, or mouth to infect.[70] Aerosols are highest in concentration when people are in close proximity, which leads to easier viral transmission when people are physically close,[70][71][72] but airborne transmission can occur at longer distances, mainly in locations that are poorly ventilated;[70] in those conditions small particles can remain suspended in the air for minutes to hours.[70]
The number of people generally infected by one infected person varies,[73] but it is estimated that the R0 («R nought» or «R zero») number is around 2.5.[74] The disease often spreads in clusters, where infections can be traced back to an index case or geographical location.[75] Often in these instances, superspreading events occur, where many people are infected by one person.[73]
Virology
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel severe acute respiratory syndrome coronavirus. It was first isolated from three people with pneumonia connected to the cluster of acute respiratory illness cases in Wuhan.[76] All structural features of the novel SARS-CoV-2 virus particle occur in related coronaviruses in nature.[77]
Outside the human body, the virus is destroyed by household soap, which bursts its protective bubble.[78]
SARS-CoV-2 is closely related to the original SARS-CoV.[79] It is thought to have an animal (zoonotic) origin. Genetic analysis has revealed that the coronavirus genetically clusters with the genus Betacoronavirus, in subgenus Sarbecovirus (lineage B) together with two bat-derived strains. It is 96% identical at the whole genome level to other bat coronavirus samples (BatCov RaTG13).[80][81][82] The structural proteins of SARS-CoV-2 include membrane glycoprotein (M), envelope protein (E), nucleocapsid protein (N), and the spike protein (S). The M protein of SARS-CoV-2 is about 98% similar to the M protein of bat SARS-CoV, maintains around 98% homology with pangolin SARS-CoV, and has 90% homology with the M protein of SARS-CoV; whereas, the similarity is only around 38% with the M protein of MERS-CoV.[83]
SARS-CoV-2 variants
The many thousands of SARS-CoV-2 variants are grouped into either clades or lineages.[84][85] The WHO, in collaboration with partners, expert networks, national authorities, institutions and researchers, have established nomenclature systems for naming and tracking SARS-CoV-2 genetic lineages by GISAID, Nextstrain and Pango. The expert group convened by the WHO recommended the labelling of variants using letters of the Greek alphabet, for example, Alpha, Beta, Delta, and Gamma, giving the justification that they «will be easier and more practical to discussed by non-scientific audiences.»[86] Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR).[87] The Pango tool groups variants into lineages, with many circulating lineages being classed under the B.1 lineage.[85][88]
Several notable variants of SARS-CoV-2 emerged throughout 2020.[89][90] Cluster 5 emerged among minks and mink farmers in Denmark.[91] After strict quarantines and a mink euthanasia campaign, the cluster was assessed to no longer be circulating among humans in Denmark as of 1 February 2021.[92]
As of December 2021, there are five dominant variants of SARS-CoV-2 spreading among global populations: the Alpha variant (B.1.1.7, formerly called the UK variant), first found in London and Kent, the Beta variant (B.1.351, formerly called the South Africa variant), the Gamma variant (P.1, formerly called the Brazil variant), the Delta variant (B.1.617.2, formerly called the India variant),[93] and the Omicron variant (B.1.1.529), which had spread to 57 countries as of 7 December.[94][95]
Pathophysiology
The SARS-CoV-2 virus can infect a wide range of cells and systems of the body. COVID‑19 is most known for affecting the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs).[96] The lungs are the organs most affected by COVID‑19 because the virus accesses host cells via the receptor for the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant on the surface of type II alveolar cells of the lungs.[97] The virus uses a special surface glycoprotein called a «spike» to connect to the ACE2 receptor and enter the host cell.[98]
Respiratory tract
Following viral entry, COVID‑19 infects the ciliated epithelium of the nasopharynx and upper airways.[99]
Nervous system
One common symptom, loss of smell, results from infection of the support cells of the olfactory epithelium, with subsequent damage to the olfactory neurons.[100] The involvement of both the central and peripheral nervous system in COVID‑19 has been reported in many medical publications.[101] It is clear that many people with COVID-19 exhibit neurological or mental health issues. The virus is not detected in the central nervous system (CNS) of the majority of COVID-19 patients with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID‑19, but these results need to be confirmed.[102] While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain.[103][104][105] The virus may also enter the bloodstream from the lungs and cross the blood–brain barrier to gain access to the CNS, possibly within an infected white blood cell.[102]
Research conducted when Alpha was the dominant variant has suggested COVID-19 may cause brain damage. It is unknown if such damage is temporary or permanent, and whether Omicron has similar effects.[106][107] Observed individuals infected with COVID-19 (most with mild cases) experienced an additional 0.2% to 2% of brain tissue lost in regions of the brain connected to the sense of smell compared with uninfected individuals, and the overall effect on the brain was equivalent on average to at least one extra year of normal ageing; infected individuals also scored lower on several cognitive tests. All effects were more pronounced among older ages.[108]
Gastrointestinal tract
The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium[109] as well as endothelial cells and enterocytes of the small intestine.[110]
Cardiovascular system
The virus can cause acute myocardial injury and chronic damage to the cardiovascular system.[111][112] An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China,[113] and is more frequent in severe disease.[114] Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart.[112] ACE2 receptors are highly expressed in the heart and are involved in heart function.[112][115]
A high incidence of thrombosis and venous thromboembolism occurs in people transferred to intensive care units with COVID‑19 infections, and may be related to poor prognosis.[116] Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) may have a significant role in mortality, incidences[spelling?] of clots leading to pulmonary embolisms, and ischaemic events within the brain found as complications leading to death in people infected with COVID‑19.[117] Infection may initiate a chain of vasoconstrictive responses within the body, including pulmonary vasoconstriction – a possible mechanism in which oxygenation decreases during pneumonia.[117] Furthermore, damage of arterioles and capillaries was found in brain tissue samples of people who died from COVID‑19.[118][119]
COVID‑19 may also cause substantial structural changes to blood cells, sometimes persisting for months after hospital discharge.[120] A low level of blood lymphocytes may result from the virus acting through ACE2-related entry into lymphocytes.[121]
Other organs
Another common cause of death is complications related to the kidneys.[117] Early reports show that up to 30% of hospitalised patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.[122]
Autopsies of people who died of COVID‑19 have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung.[123]
Immunopathology
Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, people with severe COVID‑19 have symptoms of systemic hyperinflammation. Clinical laboratory findings of elevated IL‑2, IL‑7, IL‑6, granulocyte-macrophage colony-stimulating factor (GM‑CSF), interferon gamma-induced protein 10 (IP‑10), monocyte chemoattractant protein 1 (MCP1), macrophage inflammatory protein 1‑alpha (MIP‑1‑alpha), and tumour necrosis factor (TNF‑α) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology.[113]
Interferon alpha plays a complex, Janus-faced role in the pathogenesis of COVID-19. Although it promotes the elimination of virus-infected cells, it also upregulates the expression of ACE-2, thereby facilitating the SARS-Cov2 virus to enter cells and to replicate.[124][125] A competition of negative feedback loops (via protective effects of interferon alpha) and positive feedback loops (via upregulation of ACE-2) is assumed to determine the fate of patients suffering from COVID-19.[126]
Additionally, people with COVID‑19 and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin.[127]
Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in people with COVID‑19.[128] Lymphocytic infiltrates have also been reported at autopsy.[123]
Viral and host factors
Virus proteins
Multiple viral and host factors affect the pathogenesis of the virus. The S-protein, otherwise known as the spike protein, is the viral component that attaches to the host receptor via the ACE2 receptors. It includes two subunits: S1 and S2. S1 determines the virus-host range and cellular tropism via the receptor-binding domain. S2 mediates the membrane fusion of the virus to its potential cell host via the H1 and HR2, which are heptad repeat regions. Studies have shown that S1 domain induced IgG and IgA antibody levels at a much higher capacity. It is the focus spike proteins expression that are involved in many effective COVID‑19 vaccines.[129]
The M protein is the viral protein responsible for the transmembrane transport of nutrients. It is the cause of the bud release and the formation of the viral envelope.[130] The N and E protein are accessory proteins that interfere with the host’s immune response.[130]
Host factors
Human angiotensin converting enzyme 2 (hACE2) is the host factor that SARS-CoV-2 virus targets causing COVID‑19. Theoretically, the usage of angiotensin receptor blockers (ARB) and ACE inhibitors upregulating ACE2 expression might increase morbidity with COVID‑19, though animal data suggest some potential protective effect of ARB; however no clinical studies have proven susceptibility or outcomes. Until further data is available, guidelines and recommendations for hypertensive patients remain.[131]
The effect of the virus on ACE2 cell surfaces leads to leukocytic infiltration, increased blood vessel permeability, alveolar wall permeability, as well as decreased secretion of lung surfactants. These effects cause the majority of the respiratory symptoms. However, the aggravation of local inflammation causes a cytokine storm eventually leading to a systemic inflammatory response syndrome.[132]
Among healthy adults not exposed to SARS-CoV-2, about 35% have CD4+ T cells that recognise the SARS-CoV-2 S protein (particularly the S2 subunit) and about 50% react to other proteins of the virus, suggesting cross-reactivity from previous common colds caused by other coronaviruses.[133]
It is unknown whether different persons use similar antibody genes in response to COVID‑19.[134]
Host cytokine response
The severity of the inflammation can be attributed to the severity of what is known as the cytokine storm.[135] Levels of interleukin 1B, interferon-gamma, interferon-inducible protein 10, and monocyte chemoattractant protein 1 were all associated with COVID‑19 disease severity. Treatment has been proposed to combat the cytokine storm as it remains to be one of the leading causes of morbidity and mortality in COVID‑19 disease.[136]
A cytokine storm is due to an acute hyperinflammatory response that is responsible for clinical illness in an array of diseases but in COVID‑19, it is related to worse prognosis and increased fatality. The storm causes acute respiratory distress syndrome, blood clotting events such as strokes, myocardial infarction, encephalitis, acute kidney injury, and vasculitis. The production of IL-1, IL-2, IL-6, TNF-alpha, and interferon-gamma, all crucial components of normal immune responses, inadvertently become the causes of a cytokine storm. The cells of the central nervous system, the microglia, neurons, and astrocytes, are also involved in the release of pro-inflammatory cytokines affecting the nervous system, and effects of cytokine storms toward the CNS are not uncommon.[137]
Pregnancy response
There are many unknowns for pregnant women during the COVID-19 pandemic. Given that they are prone to have complications and severe disease infection with other types of coronaviruses, they have been identified as a vulnerable group and advised to take supplementary preventive measures.[138]
Physiological responses to pregnancy can include:
- Immunological: The immunological response to COVID-19, like other viruses, depends on a working immune system. It adapts during pregnancy to allow the development of the foetus whose genetic load is only partially shared with their mother, leading to a different immunological reaction to infections during the course of pregnancy.[138]
- Respiratory: Many factors can make pregnant women more vulnerable to hard respiratory infections. One of them is the total reduction of the lungs’ capacity and inability to clear secretions.[138]
- Coagulation: During pregnancy, there are higher levels of circulating coagulation factors, and the pathogenesis of SARS-CoV-2 infection can be implicated. The thromboembolic events with associated mortality are a risk for pregnant women.[138]
However, from the evidence base, it is difficult to conclude whether pregnant women are at increased risk of grave consequences of this virus.[138]
In addition to the above, other clinical studies have proved that SARS-CoV-2 can affect the period of pregnancy in different ways. On the one hand, there is little evidence of its impact up to 12 weeks gestation. On the other hand, COVID-19 infection may cause increased rates of unfavourable outcomes in the course of the pregnancy. Some examples of these could be foetal growth restriction, preterm birth, and perinatal mortality, which refers to the foetal death past 22 or 28 completed weeks of pregnancy as well as the death among live-born children up to seven completed days of life.[138]
Unvaccinated women in later stages of pregnancy with COVID-19 are more likely than other patients to need very intensive care. Babies born to mothers with COVID-19 are more likely to have breathing problems. Pregnant women are strongly encouraged to get vaccinated.[139]
Diagnosis
COVID‑19 can provisionally be diagnosed on the basis of symptoms and confirmed using reverse transcription polymerase chain reaction (RT-PCR) or other nucleic acid testing of infected secretions.[21][140] Along with laboratory testing, chest CT scans may be helpful to diagnose COVID‑19 in individuals with a high clinical suspicion of infection.[141] Detection of a past infection is possible with serological tests, which detect antibodies produced by the body in response to the infection.[21]
Viral testing
The standard methods of testing for presence of SARS-CoV-2 are nucleic acid tests,[21][142] which detects the presence of viral RNA fragments.[143] As these tests detect RNA but not infectious virus, its «ability to determine duration of infectivity of patients is limited.»[144] The test is typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab or sputum sample may also be used.[145][146] Results are generally available within hours.[21] The WHO has published several testing protocols for the disease.[147]
Several laboratories and companies have developed serological tests, which detect antibodies produced by the body in response to infection. Several have been evaluated by Public Health England and approved for use in the UK.[148]
The University of Oxford’s CEBM has pointed to mounting evidence[149][150] that «a good proportion of ‘new’ mild cases and people re-testing positives after quarantine or discharge from hospital are not infectious, but are simply clearing harmless virus particles which their immune system has efficiently dealt with» and have called for «an international effort to standardize and periodically calibrate testing»[151] In September 2020, the UK government issued «guidance for procedures to be implemented in laboratories to provide assurance of positive SARS-CoV-2 RNA results during periods of low prevalence, when there is a reduction in the predictive value of positive test results».[152]
Imaging
A CT scan of a person with COVID-19 shows lesions (bright regions) in the lungs
CT scan of rapid progression stage of COVID-19
Chest X-ray showing COVID‑19 pneumonia
Chest CT scans may be helpful to diagnose COVID‑19 in individuals with a high clinical suspicion of infection but are not recommended for routine screening.[141][153] Bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and posterior distribution are common in early infection.[141][154] Subpleural dominance, crazy paving (lobular septal thickening with variable alveolar filling), and consolidation may appear as the disease progresses.[141][155] Characteristic imaging features on chest radiographs and computed tomography (CT) of people who are symptomatic include asymmetric peripheral ground-glass opacities without pleural effusions.[156]
Many groups have created COVID‑19 datasets that include imagery such as the Italian Radiological Society which has compiled an international online database of imaging findings for confirmed cases.[157] Due to overlap with other infections such as adenovirus, imaging without confirmation by rRT-PCR is of limited specificity in identifying COVID‑19.[156] A large study in China compared chest CT results to PCR and demonstrated that though imaging is less specific for the infection, it is faster and more sensitive.[140]
Coding
In late 2019, the WHO assigned emergency ICD-10 disease codes U07.1 for deaths from lab-confirmed SARS-CoV-2 infection and U07.2 for deaths from clinically or epidemiologically diagnosed COVID‑19 without lab-confirmed SARS-CoV-2 infection.[158]
Pathology
The main pathological findings at autopsy are:
- Macroscopy: pericarditis, lung consolidation and pulmonary oedema[123]
- Lung findings:
- minor serous exudation, minor fibrin exudation[123]
- pulmonary oedema, pneumocyte hyperplasia, large atypical pneumocytes, interstitial inflammation with lymphocytic infiltration and multinucleated giant cell formation[123]
- diffuse alveolar damage (DAD) with diffuse alveolar exudates. DAD is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxaemia.[123]
- organisation of exudates in alveolar cavities and pulmonary interstitial fibrosis[123]
- plasmocytosis in BAL[159]
- Blood and vessels: disseminated intravascular coagulation (DIC);[160] leukoerythroblastic reaction,[161] endotheliitis,[162] hemophagocytosis[162]
- Heart: cardiac muscle cell necrosis[162]
- Liver: microvesicular steatosis[123]
- Nose: shedding of olfactory epithelium[100]
- Brain: infarction[162]
- Kidneys: acute tubular damage.[162]
- Spleen: white pulp depletion.[162]
Prevention
Without pandemic containment measures – such as social distancing, vaccination, and face masks – pathogens can spread exponentially.[163] This graphic shows how early adoption of containment measures tends to protect wider swaths of the population.
Preventive measures to reduce the chances of infection include getting vaccinated, staying at home, wearing a mask in public, avoiding crowded places, keeping distance from others, ventilating indoor spaces, managing potential exposure durations,[164] washing hands with soap and water often and for at least twenty seconds, practising good respiratory hygiene, and avoiding touching the eyes, nose, or mouth with unwashed hands.[165][166]
Those diagnosed with COVID‑19 or who believe they may be infected are advised by the CDC to stay home except to get medical care, call ahead before visiting a healthcare provider, wear a face mask before entering the healthcare provider’s office and when in any room or vehicle with another person, cover coughs and sneezes with a tissue, regularly wash hands with soap and water and avoid sharing personal household items.[167][168]
The first COVID‑19 vaccine was granted regulatory approval on 2 December 2020 by the UK medicines regulator MHRA.[169] It was evaluated for emergency use authorization (EUA) status by the US FDA, and in several other countries.[170] Initially, the US National Institutes of Health guidelines do not recommend any medication for prevention of COVID‑19, before or after exposure to the SARS-CoV-2 virus, outside the setting of a clinical trial.[171][172] Without a vaccine, other prophylactic measures, or effective treatments, a key part of managing COVID‑19 is trying to decrease and delay the epidemic peak, known as «flattening the curve».[173] This is done by slowing the infection rate to decrease the risk of health services being overwhelmed, allowing for better treatment of active cases, and delaying additional cases until effective treatments or a vaccine become available.[173][174]
Vaccine
Different vaccine candidate types in development for SARS-CoV-2
A COVID‑19 vaccine is a vaccine intended to provide acquired immunity against severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2), the virus that causes coronavirus disease 2019 (COVID‑19).
Prior to the COVID‑19 pandemic, an established body of knowledge existed about the structure and function of coronaviruses causing diseases like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). This knowledge accelerated the development of various vaccine platforms during early 2020.[175] The initial focus of SARS-CoV-2 vaccines was on preventing symptomatic, often severe illness.[176] In January 2020, the SARS-CoV-2 genetic sequence data was shared through GISAID, and by March 2020, the global pharmaceutical industry announced a major commitment to address COVID‑19.[177] In 2020, the first COVID‑19 vaccines were developed and made available to the public through emergency authorizations[178] and conditional approvals.[179][180] Initially, most COVID‑19 vaccines were two-dose vaccines, with the sole exception being the single-dose Janssen COVID-19 vaccine.[178] However, immunity from the vaccines has been found to wane over time, requiring people to get booster doses of the vaccine to maintain protection against COVID‑19.[178]
Face masks and respiratory hygiene
Masks with an exhalation valve. The valves are a weak point that can transmit the viruses outwards.
The WHO and the US CDC recommend individuals wear non-medical face coverings in public settings where there is an increased risk of transmission and where social distancing measures are difficult to maintain.[181][182] This recommendation is meant to reduce the spread of the disease by asymptomatic and pre-symptomatic individuals and is complementary to established preventive measures such as social distancing.[182][183] Face coverings limit the volume and travel distance of expiratory droplets dispersed when talking, breathing, and coughing.[182][183] A face covering without vents or holes will also filter out particles containing the virus from inhaled and exhaled air, reducing the chances of infection.[184] However, if the mask includes an exhalation valve, a wearer that is infected (and possibly asymptomatic) may transmit the virus through the valve. Many countries and local jurisdictions encourage or mandate the use of face masks or cloth face coverings by members of the public to limit the spread of the virus.[185]
Masks are also strongly recommended for those who may have been infected and those taking care of someone who may have the disease.[186] When not wearing a mask, the CDC recommends covering the mouth and nose with a tissue when coughing or sneezing and recommends using the inside of the elbow if no tissue is available. Proper hand hygiene after any cough or sneeze is encouraged. Healthcare professionals interacting directly with people who have COVID‑19 are advised to use respirators at least as protective as NIOSH-certified N95 or equivalent, in addition to other personal protective equipment.[187]
Indoor ventilation and avoiding crowded indoor spaces
The CDC recommends that crowded indoor spaces should be avoided.[188] When indoors, increasing the rate of air change, decreasing recirculation of air and increasing the use of outdoor air can reduce transmission.[188][189] The WHO recommends ventilation and air filtration in public spaces to help clear out infectious aerosols.[190][191][192]
Exhaled respiratory particles can build-up within enclosed spaces with inadequate ventilation. The risk of COVID‑19 infection increases especially in spaces where people engage in physical exertion or raise their voice (e.g., exercising, shouting, singing) as this increases exhalation of respiratory droplets. Prolonged exposure to these conditions, typically more than 15 minutes, leads to higher risk of infection.[188]
Displacement ventilation with large natural inlets can move stale air directly to the exhaust in laminar flow while significantly reducing the concentration of droplets and particles. Passive ventilation reduces energy consumption and maintenance costs but may lack controllability and heat recovery. Displacement ventilation can also be achieved mechanically with higher energy and maintenance costs. The use of large ducts and openings helps to prevent mixing in closed environments. Recirculation and mixing should be avoided because recirculation prevents dilution of harmful particles and redistributes possibly contaminated air, and mixing increases the concentration and range of infectious particles and keeps larger particles in the air.[193]
Hand-washing and hygiene
Thorough hand hygiene after any cough or sneeze is required.[194] The WHO also recommends that individuals wash hands often with soap and water for at least twenty seconds, especially after going to the toilet or when hands are visibly dirty, before eating and after blowing one’s nose.[195] When soap and water are not available, the CDC recommends using an alcohol-based hand sanitiser with at least 60% alcohol.[196] For areas where commercial hand sanitisers are not readily available, the WHO provides two formulations for local production. In these formulations, the antimicrobial activity arises from ethanol or isopropanol. Hydrogen peroxide is used to help eliminate bacterial spores in the alcohol; it is «not an active substance for hand antisepsis.» Glycerol is added as a humectant.[197]
Social distancing (also known as physical distancing) includes infection control actions intended to slow the spread of the disease by minimising close contact between individuals. Methods include quarantines; travel restrictions; and the closing of schools, workplaces, stadiums, theatres, or shopping centres. Individuals may apply social distancing methods by staying at home, limiting travel, avoiding crowded areas, using no-contact greetings, and physically distancing themselves from others.[198] Many governments are mandating or recommending social distancing in regions affected by the outbreak.[199]
Outbreaks have occurred in prisons due to crowding and an inability to enforce adequate social distancing.[200][201] In the United States, the prisoner population is ageing and many of them are at high risk for poor outcomes from COVID‑19 due to high rates of coexisting heart and lung disease, and poor access to high-quality healthcare.[200]
Surface cleaning
After being expelled from the body, coronaviruses can survive on surfaces for hours to days. If a person touches the dirty surface, they may deposit the virus at the eyes, nose, or mouth where it can enter the body and cause infection.[202] Evidence indicates that contact with infected surfaces is not the main driver of COVID‑19,[203][204][205] leading to recommendations for optimised disinfection procedures to avoid issues such as the increase of antimicrobial resistance through the use of inappropriate cleaning products and processes.[206][207] Deep cleaning and other surface sanitation has been criticised as hygiene theatre, giving a false sense of security against something primarily spread through the air.[208][209]
The amount of time that the virus can survive depends significantly on the type of surface, the temperature, and the humidity.[210] Coronaviruses die very quickly when exposed to the UV light in sunlight.[210] Like other enveloped viruses, SARS-CoV-2 survives longest when the temperature is at room temperature or lower, and when the relative humidity is low (<50%).[210]
On many surfaces, including glass, some types of plastic, stainless steel, and skin, the virus can remain infective for several days indoors at room temperature, or even about a week under ideal conditions.[210][211] On some surfaces, including cotton fabric and copper, the virus usually dies after a few hours.[210] The virus dies faster on porous surfaces than on non-porous surfaces due to capillary action within pores and faster aerosol droplet evaporation.[212][205][210] However, of the many surfaces tested, two with the longest survival times are N95 respirator masks and surgical masks, both of which are considered porous surfaces.[210]
The CDC says that in most situations, cleaning surfaces with soap or detergent, not disinfecting, is enough to reduce risk of transmission.[213][214] The CDC recommends that if a COVID‑19 case is suspected or confirmed at a facility such as an office or day care, all areas such as offices, bathrooms, common areas, shared electronic equipment like tablets, touch screens, keyboards, remote controls, and ATMs used by the ill persons should be disinfected.[215] Surfaces may be decontaminated with 62–71 per cent ethanol, 50–100 per cent isopropanol, 0.1 per cent sodium hypochlorite, 0.5 per cent hydrogen peroxide, 0.2–7.5 per cent povidone-iodine, or 50–200 ppm hypochlorous acid. Other solutions, such as benzalkonium chloride and chlorhexidine gluconate, are less effective. Ultraviolet germicidal irradiation may also be used,[190] although popular devices require 5–10 min exposure and may deteriorate some materials over time.[216] A datasheet comprising the authorised substances to disinfection in the food industry (including suspension or surface tested, kind of surface, use dilution, disinfectant and inocuylum volumes) can be seen in the supplementary material of.[206]
Self-isolation
Self-isolation at home has been recommended for those diagnosed with COVID‑19 and those who suspect they have been infected. Health agencies have issued detailed instructions for proper self-isolation.[217] Many governments have mandated or recommended self-quarantine for entire populations. The strongest self-quarantine instructions have been issued to those in high-risk groups.[218] Those who may have been exposed to someone with COVID‑19 and those who have recently travelled to a country or region with the widespread transmission have been advised to self-quarantine for 14 days from the time of last possible exposure.[219]
A 2021 Cochrane rapid review found that based upon low-certainty evidence, international travel-related control measures such as restricting cross-border travel may help to contain the spread of COVID‑19.[220] Additionally, symptom/exposure-based screening measures at borders may miss many positive cases.[220] While test-based border screening measures may be more effective, it could also miss many positive cases if only conducted upon arrival without follow-up. The review concluded that a minimum 10-day quarantine may be beneficial in preventing the spread of COVID‑19 and may be more effective if combined with an additional control measure like border screening.[220]
Treatment
An overview of COVID-19 therapeutics and drugs
Although several medications have been approved in different countries as of April 2022, not all countries have these medications. Patients with mild to moderate symptoms who are in the risk groups can take nirmatrelvir/ritonavir (marketed as Paxlovid) or remdesivir, either of which reduces the risk of serious illness or hospitalization.[221] In the US, the Biden Administration COVID-19 action plan includes the Test to Treat initiative, where people can go to a pharmacy, take a COVID test, and immediately receive free Paxlovid if they test positive.[222]
Highly effective vaccines have reduced mortality related to SARS-CoV-2; however, for those awaiting vaccination, as well as for the estimated millions of immunocompromised persons who are unlikely to respond robustly to vaccination, treatment remains important.[223] The cornerstone of management of COVID-19 has been supportive care, which includes treatment to relieve symptoms, fluid therapy, oxygen support and prone positioning as needed, and medications or devices to support other affected vital organs.[224][225][226]
Most cases of COVID-19 are mild. In these, supportive care includes medication such as paracetamol or NSAIDs to relieve symptoms (fever, body aches, cough), proper intake of fluids, rest, and nasal breathing.[227][228][229][230] Good personal hygiene and a healthy diet are also recommended.[231] As of April 2020 the U.S. Centers for Disease Control and Prevention (CDC) recommended that those who suspect they are carrying the virus isolate themselves at home and wear a face mask.[232]
As of November 2020 use of the glucocorticoid dexamethasone had been strongly recommended in those severe cases treated in hospital with low oxygen levels, to reduce the risk of death.[233][234][235] Noninvasive ventilation and, ultimately, admission to an intensive care unit for mechanical ventilation may be required to support breathing.[236] Extracorporeal membrane oxygenation (ECMO) has been used to address respiratory failure, but its benefits are still under consideration.[237][238] Some of the cases of severe disease course are caused by systemic hyper-inflammation, the so-called cytokine storm.[239]
Prognosis and risk factors
The severity of COVID‑19 varies. The disease may take a mild course with few or no symptoms, resembling other common upper respiratory diseases such as the common cold. In 3–4% of cases (7.4% for those over age 65) symptoms are severe enough to cause hospitalisation.[240] Mild cases typically recover within two weeks, while those with severe or critical diseases may take three to six weeks to recover. Among those who have died, the time from symptom onset to death has ranged from two to eight weeks.[80] The Italian Istituto Superiore di Sanità reported that the median time between the onset of symptoms and death was twelve days, with seven being hospitalised. However, people transferred to an ICU had a median time of ten days between hospitalisation and death.[241] Abnormal sodium levels during hospitalization with COVID-19 are associated with poor prognoses: high sodium with a greater risk of death, and low sodium with an increased chance of needing ventilator support.[242][243] Prolonged prothrombin time and elevated C-reactive protein levels on admission to the hospital are associated with severe course of COVID‑19 and with a transfer to ICU.[244][245]
Some early studies suggest 10% to 20% of people with COVID‑19 will experience symptoms lasting longer than a month.[246][247] A majority of those who were admitted to hospital with severe disease report long-term problems including fatigue and shortness of breath.[248] On 30 October 2020, WHO chief Tedros Adhanom warned that «to a significant number of people, the COVID virus poses a range of serious long-term effects.» He has described the vast spectrum of COVID‑19 symptoms that fluctuate over time as «really concerning». They range from fatigue, a cough and shortness of breath, to inflammation and injury of major organs – including the lungs and heart, and also neurological and psychologic effects. Symptoms often overlap and can affect any system in the body. Infected people have reported cyclical bouts of fatigue, headaches, months of complete exhaustion, mood swings, and other symptoms. Tedros therefore concluded that a strategy of achieving herd immunity by infection, rather than vaccination, is «morally unconscionable and unfeasible».[249]
In terms of hospital readmissions about 9% of 106,000 individuals had to return for hospital treatment within two months of discharge. The average to readmit was eight days since first hospital visit. There are several risk factors that have been identified as being a cause of multiple admissions to a hospital facility. Among these are advanced age (above 65 years of age) and presence of a chronic condition such as diabetes, COPD, heart failure or chronic kidney disease.[250][251]
According to scientific reviews smokers are more likely to require intensive care or die compared to non-smokers.[252][253] Acting on the same ACE2 pulmonary receptors affected by smoking, air pollution has been correlated with the disease.[253] Short term[254] and chronic[255] exposure to air pollution seems to enhance morbidity and mortality from COVID‑19.[256][257][258] Pre-existing heart and lung diseases[259] and also obesity, especially in conjunction with fatty liver disease, contributes to an increased health risk of COVID‑19.[253][260][261][262]
It is also assumed that those that are immunocompromised are at higher risk of getting severely sick from SARS-CoV-2.[263] One research study that looked into the COVID‑19 infections in hospitalised kidney transplant recipients found a mortality rate of 11%.[264]
Men with untreated hypogonadism were 2.4 times more likely than men with eugonadism to be hospitalized if they contracted COVID-19; Hypogonad men treated with testosterone were less likely to be hospitalized for COVID-19 than men who were not treated for hypogonadism.[265]
Genetic risk factors
Genetics plays an important role in the ability to fight off Covid.[266] For instance, those that do not produce detectable type I interferons or produce auto-antibodies against these may get much sicker from COVID‑19.[267][268] Genetic screening is able to detect interferon effector genes.[269] Some genetic variants are risk factors in specific populations. For instance, and allele of the DOCK2 gene (dedicator of cytokinesis 2 gene) is a common risk factor in Asian populations but much less common in Europe. The mutation leads to lower expression of DOCK2 especially in younger patients with severe Covid.[270] In fact, many other genes and genetic variants have been found that determine the outcome of SARS-CoV-2 infections.[271]
Children
While very young children have experienced lower rates of infection, older children have a rate of infection that is similar to the population as a whole.[272][273] Children are likely to have milder symptoms and are at lower risk of severe disease than adults.[274] The CDC reports that in the US roughly a third of hospitalised children were admitted to the ICU,[275] while a European multinational study of hospitalised children from June 2020, found that about 8% of children admitted to a hospital needed intensive care.[276] Four of the 582 children (0.7%) in the European study died, but the actual mortality rate may be «substantially lower» since milder cases that did not seek medical help were not included in the study.[277][278]
Complications
Complications may include pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, septic shock, and death.[279][280][281][282] Cardiovascular complications may include heart failure, arrhythmias (including atrial fibrillation), heart inflammation, and thrombosis, particularly venous thromboembolism.[283][284][285][286][287][288] Approximately 20–30% of people who present with COVID‑19 have elevated liver enzymes, reflecting liver injury.[289][172]
Neurologic manifestations include seizure, stroke, encephalitis, and Guillain–Barré syndrome (which includes loss of motor functions).[290][291] Following the infection, children may develop paediatric multisystem inflammatory syndrome, which has symptoms similar to Kawasaki disease, which can be fatal.[292][293] In very rare cases, acute encephalopathy can occur, and it can be considered in those who have been diagnosed with COVID‑19 and have an altered mental status.[294]
In the case of pregnant women, it is important to note that, according to the US Centers for Disease Control and Prevention, pregnant women are at increased risk of becoming seriously ill from COVID‑19.[295] This is because pregnant women with COVID‑19 appear to be more likely to develop respiratory and obstetric complications that can lead to miscarriage, premature delivery and intrauterine growth restriction.[295]
Fungal infections such as aspergillosis, candidiasis, cryptococcosis and mucormycosis have been recorded in patients recovering from COVID‑19.[296][297]
Longer-term effects
Some early studies suggest that 10–20% of people with COVID‑19 will experience symptoms lasting longer than a month.[298][247] A majority of those who were admitted to hospital with severe disease report long-term problems, including fatigue and shortness of breath.[299] About 5–10% of patients admitted to hospital progress to severe or critical disease, including pneumonia and acute respiratory failure.[300]
By a variety of mechanisms, the lungs are the organs most affected in COVID‑19.[301] In people requiring hospital admission, up to 98% of CT scans performed show lung abnormalities after 28 days of illness even if they had clinically improved.[302]
People with advanced age, severe disease, prolonged ICU stays, or who smoke are more likely to have long-lasting effects, including pulmonary fibrosis.[303] Overall, approximately one-third of those investigated after four weeks will have findings of pulmonary fibrosis or reduced lung function as measured by DLCO, even in asymptomatic people, but with the suggestion of continuing improvement with the passing of more time.[301] After severe disease, lung function can take anywhere from three months to a year or more to return to previous levels.[304]
The risks of cognitive deficit, dementia, psychotic disorders, and epilepsy or seizures persists at an increased level two years after infection.[305]
Immunity
The immune response by humans to SARS-CoV-2 virus occurs as a combination of the cell-mediated immunity and antibody production,[306] just as with most other infections.[307] B cells interact with T cells and begin dividing before selection into the plasma cell, partly on the basis of their affinity for antigen.[308] Since SARS-CoV-2 has been in the human population only since December 2019, it remains unknown if the immunity is long-lasting in people who recover from the disease.[309] The presence of neutralising antibodies in blood strongly correlates with protection from infection, but the level of neutralising antibody declines with time. Those with asymptomatic or mild disease had undetectable levels of neutralising antibody two months after infection. In another study, the level of neutralising antibodies fell four-fold one to four months after the onset of symptoms. However, the lack of antibodies in the blood does not mean antibodies will not be rapidly produced upon reexposure to SARS-CoV-2. Memory B cells specific for the spike and nucleocapsid proteins of SARS-CoV-2 last for at least six months after the appearance of symptoms.[309]
As of August 2021, reinfection with COVID‑19 was possible but uncommon. The first case of reinfection was documented in August 2020.[310] A systematic review found 17 cases of confirmed reinfection in medical literature as of May 2021.[310] With the Omicron variant, as of 2022, reinfections have become common, albeit it is unclear how common.[311] COVID-19 reinfections are thought to likely be less severe than primary infections, especially if one was previously infected by the same variant.[311][additional citation(s) needed]
Mortality
Several measures are commonly used to quantify mortality.[312] These numbers vary by region and over time and are influenced by the volume of testing, healthcare system quality, treatment options, time since the initial outbreak, and population characteristics such as age, sex, and overall health.[313]
The mortality rate reflects the number of deaths within a specific demographic group divided by the population of that demographic group. Consequently, the mortality rate reflects the prevalence as well as the severity of the disease within a given population. Mortality rates are highly correlated to age, with relatively low rates for young people and relatively high rates among the elderly.[314][315][316] In fact, one relevant factor of mortality rates is the age structure of the countries’ populations. For example, the case fatality rate for COVID‑19 is lower in India than in the US since India’s younger population represents a larger percentage than in the US.[317]
Case fatality rate
The case fatality rate (CFR) reflects the number of deaths divided by the number of diagnosed cases within a given time interval. Based on Johns Hopkins University statistics, the global death-to-case ratio is 1.01% (6,707,311/664,338,243) as of 9 January 2023.[6] The number varies by region.[318][319]
-
Total confirmed cases over time
-
Total confirmed cases of COVID‑19 per million people[320]
-
Total deaths over time
-
Total confirmed deaths due to COVID‑19 per million people[321]
![Total confirmed cases of COVID‑19 per million people[320]](https://upload.wikimedia.org/wikipedia/commons/thumb/7/75/World_map_of_total_confirmed_COVID-19_cases_per_million_people.svg/255px-World_map_of_total_confirmed_COVID-19_cases_per_million_people.svg.png)
![Total confirmed deaths due to COVID‑19 per million people[321]](https://upload.wikimedia.org/wikipedia/commons/thumb/3/3a/World_map_of_total_confirmed_COVID-19_deaths_per_million_people_by_country.svg/255px-World_map_of_total_confirmed_COVID-19_deaths_per_million_people_by_country.svg.png)
Infection fatality rate
A key metric in gauging the severity of COVID‑19 is the infection fatality rate (IFR), also referred to as the infection fatality ratio or infection fatality risk.[322][323][324] This metric is calculated by dividing the total number of deaths from the disease by the total number of infected individuals; hence, in contrast to the CFR, the IFR incorporates asymptomatic and undiagnosed infections as well as reported cases.[325]
Estimates
The red line shows the estimate of infection fatality rate (IFR), in percentage terms, as a function of age. The shaded region depicts the 95% confidence interval for that estimate. Markers denotes specific observations used in the meta-analysis.[326]
The same relationship plotted on a log scale
A December 2020 systematic review and meta-analysis estimated that population IFR during the first wave of the pandemic was about 0.5% to 1% in many locations (including France, Netherlands, New Zealand, and Portugal), 1% to 2% in other locations (Australia, England, Lithuania, and Spain), and exceeded 2% in Italy.[326] That study also found that most of these differences in IFR reflected corresponding differences in the age composition of the population and age-specific infection rates; in particular, the metaregression estimate of IFR is very low for children and younger adults (e.g., 0.002% at age 10 and 0.01% at age 25) but increases progressively to 0.4% at age 55, 1.4% at age 65, 4.6% at age 75, and 15% at age 85.[326] These results were also highlighted in a December 2020 report issued by the WHO.[327]
| Age group | IFR |
|---|---|
| 0–34 | 0.004% |
| 35–44 | 0.068% |
| 45–54 | 0.23% |
| 55–64 | 0.75% |
| 65–74 | 2.5% |
| 75–84 | 8.5% |
| 85 + | 28.3% |
An analysis of those IFR rates indicates that COVID‑19 is hazardous not only for the elderly but also for middle-aged adults, for whom the infection fatality rate of COVID-19 is two orders of magnitude greater than the annualised risk of a fatal automobile accident and far more dangerous than seasonal influenza.[326]
Earlier estimates of IFR
At an early stage of the pandemic, the World Health Organization reported estimates of IFR between 0.3% and 1%.[328][329] On 2 July, The WHO’s chief scientist reported that the average IFR estimate presented at a two-day WHO expert forum was about 0.6%.[330][331] In August, the WHO found that studies incorporating data from broad serology testing in Europe showed IFR estimates converging at approximately 0.5–1%.[332] Firm lower limits of IFRs have been established in a number of locations such as New York City and Bergamo in Italy since the IFR cannot be less than the population fatality rate. (After sufficient time however, people can get reinfected).[333] As of 10 July, in New York City, with a population of 8.4 million, 23,377 individuals (18,758 confirmed and 4,619 probable) have died with COVID‑19 (0.3% of the population).[334] Antibody testing in New York City suggested an IFR of ≈0.9%,[335] and ≈1.4%.[336] In Bergamo province, 0.6% of the population has died.[337] In September 2020, the U.S. Centers for Disease Control and Prevention (CDC) reported preliminary estimates of age-specific IFRs for public health planning purposes.[338]
Sex differences
| Percentage of infected people who are hospitalised | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| 0–19 | 20–29 | 30–39 | 40–49 | 50–59 | 60–69 | 70–79 | 80+ | Total | |
| Female | 0.1 (0.07–0.2) |
0.5 (0.3–0.8) |
0.9 (0.5–1.5) |
1.3 (0.7–2.1) |
2.6 (1.5–4.2) |
5.1 (2.9–8.3) |
7.8 (4.4–12.8) |
19.3 (10.9–31.6) |
2.6 (1.5–4.3) |
| Male | 0.2 (0.08–0.2) |
0.6 (0.3–0.9) |
1.2 (0.7–1.9) |
1.6 (0.9–2.6) |
3.2 (1.8–5.2) |
6.7 (3.7–10.9) |
11.0 (6.2–17.9) |
37.6 (21.1–61.3) |
3.3 (1.8–5.3) |
| Total | 0.1 (0.08–0.2) |
0.5 (0.3–0.8) |
1.1 (0.6–1.7) |
1.4 (0.8–2.3) |
2.9 (1.6–4.7) |
5.8 (3.3–9.5) |
9.3 (5.2–15.1) |
26.2 (14.8–42.7) |
2.9 (1.7–4.8) |
| Percentage of hospitalised people who go to Intensive Care Unit | |||||||||
| 0–19 | 20–29 | 30–39 | 40–49 | 50–59 | 60–69 | 70–79 | 80+ | Total | |
| Female | 16.7 (14.3–19.3) |
8.7 (7.5–9.9) |
11.9 (10.9–13.0) |
16.6 (15.6–17.7) |
20.7 (19.8–21.6) |
23.1 (22.2–24.0) |
18.7 (18.0–19.5) |
4.2 (4.0–4.5) |
14.3 (13.9–14.7) |
| Male | 26.9 (23.1–31.1) |
14.0 (12.2–16.0) |
19.2 (17.6–20.9) |
26.9 (25.4–28.4) |
33.4 (32.0–34.8) |
37.3 (36.0–38.6) |
30.2 (29.1–31.3) |
6.8 (6.5–7.2) |
23.1 (22.6–23.6) |
| Total | 22.2 (19.1–25.7) |
11.6 (10.1–13.2) |
15.9 (14.5–17.3) |
22.2 (21.0–23.5) |
27.6 (26.5–28.7) |
30.8 (29.8–31.8) |
24.9 (24.1–25.8) |
5.6 (5.3–5.9) |
19.0 (18.7–19.44) |
| Percent of hospitalised people who die | |||||||||
| 0–19 | 20–29 | 30–39 | 40–49 | 50–59 | 60–69 | 70–79 | 80+ | Total | |
| Female | 0.5 (0.2–1.0) |
0.9 (0.5–1.3) |
1.5 (1.2–1.9) |
2.6 (2.3–3.0) |
5.2 (4.8–5.6) |
10.1 (9.5–10.6) |
16.7 (16.0–17.4) |
25.2 (24.4–26.0) |
14.4 (14.0–14.8) |
| Male | 0.7 (0.3–1.5) |
1.3 (0.8–1.9) |
2.2 (1.7–2.7) |
3.8 (3.3–4.4) |
7.6 (7.0–8.2) |
14.8 (14.1–15.6) |
24.6 (23.7–25.6) |
37.1 (36.1–38.2) |
21.2 (20.8–21.7) |
| Total | 0.6 (0.2–1.3) |
1.1 (0.7–1.6) |
1.9 (1.5–2.3) |
3.3 (2.9–3.8) |
6.5 (6.0–7.0) |
12.6 (12.0–13.2) |
21.0 (20.3–21.7) |
31.6 (30.9–32.4) |
18.1 (17.8–18.4) |
| Percent of infected people who die – infection fatality rate (IFR) | |||||||||
| 0–19 | 20–29 | 30–39 | 40–49 | 50–59 | 60–69 | 70–79 | 80+ | Total | |
| Female | 0.001 (<0.001–0.002) |
0.004 (0.002–0.007) |
0.01 (0.007–0.02) |
0.03 (0.02–0.06) |
0.1 (0.08–0.2) |
0.5 (0.3–0.8) |
1.3 (0.7–2.1) |
4.9 (2.7–8.0) |
0.4 (0.2–0.6) |
| Male | 0.001 (<0.001–0.003) |
0.007 (0.003–0.01) |
0.03 (0.02–0.05) |
0.06 (0.03–0.1) |
0.2 (0.1–0.4) |
1.0 (0.6–1.6) |
2.7 (1.5–1.4) |
14.0 (7.9–22.7) |
0.7 (0.4–1.1) |
| Total | 0.001 (<0.001–0.002) |
0.005 (0.003–0.01) |
0.02 (0.01–0.03) |
0.05 (0.03–0.08) |
0.2 (0.1–0.3) |
0.7 (0.4–1.2) |
1.9 (1.1–3.2) |
8.3 (4.7–13.5) |
0.5 (0.3–0.9) |
| Numbers in parentheses are 95% credible intervals for the estimates. |
COVID‑19 case fatality rates are higher among men than women in most countries. However, in a few countries like India, Nepal, Vietnam, and Slovenia the fatality cases are higher in women than men.[317] Globally, men are more likely to be admitted to the ICU and more likely to die.[340][341] One meta-analysis found that globally, men were more likely to get COVID‑19 than women; there were approximately 55 men and 45 women per 100 infections (CI: 51.43–56.58).[342]
The Chinese Center for Disease Control and Prevention reported the death rate was 2.8% for men and 1.7% for women.[343] Later reviews in June 2020 indicated that there is no significant difference in susceptibility or in CFR between genders.[344][345] One review acknowledges the different mortality rates in Chinese men, suggesting that it may be attributable to lifestyle choices such as smoking and drinking alcohol rather than genetic factors.[346] Smoking, which in some countries like China is mainly a male activity, is a habit that contributes to increasing significantly the case fatality rates among men.[317] Sex-based immunological differences, lesser prevalence of smoking in women and men developing co-morbid conditions such as hypertension at a younger age than women could have contributed to the higher mortality in men.[347] In Europe as of February 2020, 57% of the infected people were men and 72% of those died with COVID‑19 were men.[348] As of April 2020, the US government is not tracking sex-related data of COVID‑19 infections.[349] Research has shown that viral illnesses like Ebola, HIV, influenza and SARS affect men and women differently.[349]
Ethnic differences
In the US, a greater proportion of deaths due to COVID‑19 have occurred among African Americans and other minority groups.[350] Structural factors that prevent them from practising social distancing include their concentration in crowded substandard housing and in «essential» occupations such as retail grocery workers, public transit employees, health-care workers and custodial staff. Greater prevalence of lacking health insurance and care of underlying conditions such as diabetes,[351] hypertension, and heart disease also increase their risk of death.[352] Similar issues affect Native American and Latino communities.[350] On the one hand, in the Dominican Republic there is a clear example of both gender and ethnic inequality. In this Latin American territory, there is great inequality and precariousness that especially affects Dominican women, with greater emphasis on those of Haitian descent.[353] According to a US health policy non-profit, 34% of American Indian and Alaska Native People (AIAN) non-elderly adults are at risk of serious illness compared to 21% of white non-elderly adults.[354] The source attributes it to disproportionately high rates of many health conditions that may put them at higher risk as well as living conditions like lack of access to clean water.[355]
Leaders have called for efforts to research and address the disparities.[356] In the UK, a greater proportion of deaths due to COVID‑19 have occurred in those of a Black, Asian, and other ethnic minority background.[357][358][359] More severe impacts upon patients including the relative incidence of the necessity of hospitalisation requirements, and vulnerability to the disease has been associated via DNA analysis to be expressed in genetic variants at chromosomal region 3, features that are associated with European Neanderthal heritage. That structure imposes greater risks that those affected will develop a more severe form of the disease.[360] The findings are from Professor Svante Pääbo and researchers he leads at the Max Planck Institute for Evolutionary Anthropology and the Karolinska Institutet.[360] This admixture of modern human and Neanderthal genes is estimated to have occurred roughly between 50,000 and 60,000 years ago in Southern Europe.[360]
Comorbidities
Biological factors (immune response) and the general behaviour (habits) can strongly determine the consequences of COVID‑19.[317] Most of those who die of COVID‑19 have pre-existing (underlying) conditions, including hypertension, diabetes mellitus,[351] and cardiovascular disease.[361] According to March data from the United States, 89% of those hospitalised had preexisting conditions.[362] The Italian Istituto Superiore di Sanità reported that out of 8.8% of deaths where medical charts were available, 96.1% of people had at least one comorbidity with the average person having 3.4 diseases.[241] According to this report the most common comorbidities are hypertension (66% of deaths), type 2 diabetes (29.8% of deaths), ischaemic heart disease (27.6% of deaths), atrial fibrillation (23.1% of deaths) and chronic renal failure (20.2% of deaths).
Most critical respiratory comorbidities according to the US Centers for Disease Control and Prevention (CDC), are: moderate or severe asthma, pre-existing COPD, pulmonary fibrosis, cystic fibrosis.[363] Evidence stemming from meta-analysis of several smaller research papers also suggests that smoking can be associated with worse outcomes.[364][365] When someone with existing respiratory problems is infected with COVID‑19, they might be at greater risk for severe symptoms.[366] COVID‑19 also poses a greater risk to people who misuse opioids and amphetamines, insofar as their drug use may have caused lung damage.[367]
In August 2020, the CDC issued a caution that tuberculosis (TB) infections could increase the risk of severe illness or death. The WHO recommended that people with respiratory symptoms be screened for both diseases, as testing positive for COVID‑19 could not rule out co-infections. Some projections have estimated that reduced TB detection due to the pandemic could result in 6.3 million additional TB cases and 1.4 million TB-related deaths by 2025.[368]
History
The virus is thought to be of natural animal origin, most likely through spillover infection.[77][369][370] A joint-study conducted in early 2021 by the People’s Republic of China and the World Health Organization indicated that the virus descended from a coronavirus that infects wild bats, and likely spread to humans through an intermediary wildlife host.[371] There are several theories about where the index case originated and investigations into the origin of the pandemic are ongoing.[372] According to articles published in July 2022 in Science, virus transmission into humans occurred through two spillover events in November 2019 and was likely due to live wildlife trade on the Huanan wet market in the city of Wuhan (Hubei, China).[373][374][375] Doubts about the conclusions have mostly centred on the precise site of spillover.[376] Earlier phylogenetics estimated that SARS-CoV-2 arose in October or November 2019.[377][378][379] A phylogenetic algorithm analysis suggested that the virus may have been circulating in Guangdong before Wuhan.[380] U.S intelligence agencies and other scientists have found that the virus may have been unintentionally leaked from a laboratory such as the Wuhan Institute of Virology, but that it was not developed as a biological weapon and is unlikely to have been genetically engineered.[381][382][383][384]
The first confirmed human infections were in Wuhan. A study of the first 41 cases of confirmed COVID‑19, published in January 2020 in The Lancet, reported the earliest date of onset of symptoms as 1 December 2019.[385][386][387] Official publications from the WHO reported the earliest onset of symptoms as 8 December 2019.[388] Human-to-human transmission was confirmed by the WHO and Chinese authorities by 20 January 2020.[389][390] According to official Chinese sources, these were mostly linked to the Huanan Seafood Wholesale Market, which also sold live animals.[391] In May 2020, George Gao, the director of the CDC, said animal samples collected from the seafood market had tested negative for the virus, indicating that the market was the site of an early superspreading event, but that it was not the site of the initial outbreak.[392] Traces of the virus have been found in wastewater samples that were collected in Milan and Turin, Italy, on 18 December 2019.[393]
By December 2019, the spread of infection was almost entirely driven by human-to-human transmission.[343][394] The number of COVID-19 cases in Hubei gradually increased, reaching sixty by 20 December,[395] and at least 266 by 31 December.[396] On 24 December, Wuhan Central Hospital sent a bronchoalveolar lavage fluid (BAL) sample from an unresolved clinical case to sequencing company Vision Medicals. On 27 and 28 December, Vision Medicals informed the Wuhan Central Hospital and the Chinese CDC of the results of the test, showing a new coronavirus.[397] A pneumonia cluster of unknown cause was observed on 26 December and treated by the doctor Zhang Jixian in Hubei Provincial Hospital, who informed the Wuhan Jianghan CDC on 27 December.[398] On 30 December, a test report addressed to Wuhan Central Hospital, from company CapitalBio Medlab, stated an erroneous positive result for SARS, causing a group of doctors at Wuhan Central Hospital to alert their colleagues and relevant hospital authorities of the result. The Wuhan Municipal Health Commission issued a notice to various medical institutions on «the treatment of pneumonia of unknown cause» that same evening.[399] Eight of these doctors, including Li Wenliang (punished on 3 January),[400] were later admonished by the police for spreading false rumours and another, Ai Fen, was reprimanded by her superiors for raising the alarm.[401]
The Wuhan Municipal Health Commission made the first public announcement of a pneumonia outbreak of unknown cause on 31 December, confirming 27 cases[402][403][404] – enough to trigger an investigation.[405]
During the early stages of the outbreak, the number of cases doubled approximately every seven and a half days.[406] In early and mid-January 2020, the virus spread to other Chinese provinces, helped by the Chinese New Year migration and Wuhan being a transport hub and major rail interchange.[80] On 20 January, China reported nearly 140 new cases in one day, including two people in Beijing and one in Shenzhen.[407] Later official data shows 6,174 people had already developed symptoms by then,[343] and more may have been infected.[408] A report in The Lancet on 24 January indicated human transmission, strongly recommended personal protective equipment for health workers, and said testing for the virus was essential due to its «pandemic potential».[113][409] On 30 January, the WHO declared COVID-19 a Public Health Emergency of International Concern.[408] By this time, the outbreak spread by a factor of 100 to 200 times.[410]
Italy had its first confirmed cases on 31 January 2020, two tourists from China.[411] Italy overtook China as the country with the most deaths on 19 March 2020.[412] By 26 March the United States had overtaken China and Italy with the highest number of confirmed cases in the world.[413] Research on coronavirus genomes indicates the majority of COVID-19 cases in New York came from European travellers, rather than directly from China or any other Asian country.[414] Retesting of prior samples found a person in France who had the virus on 27 December 2019,[415][416] and a person in the United States who died from the disease on 6 February 2020.[417]
RT-PCR testing of untreated wastewater samples from Brazil and Italy have suggested detection of SARS-CoV-2 as early as November and December 2019, respectively, but the methods of such sewage studies have not been optimised, many have not been peer-reviewed, details are often missing, and there is a risk of false positives due to contamination or if only one gene target is detected.[418] A September 2020 review journal article said, «The possibility that the COVID‑19 infection had already spread to Europe at the end of last year is now indicated by abundant, even if partially circumstantial, evidence,» including pneumonia case numbers and radiology in France and Italy in November and December.[419]
As of 1 October 2021, Reuters reported that it had estimated the worldwide total number of deaths due to COVID‑19 to have exceeded five million.[420]
Misinformation
After the initial outbreak of COVID‑19, misinformation and disinformation regarding the origin, scale, prevention, treatment, and other aspects of the disease rapidly spread online.[421][422][423]
In September 2020, the US Centers for Disease Control and Prevention (CDC) published preliminary estimates of the risk of death by age groups in the United States, but those estimates were widely misreported and misunderstood.[424][425]
Other species
Humans appear to be capable of spreading the virus to some other animals, a type of disease transmission referred to as zooanthroponosis.
Some pets, especially cats and ferrets, can catch this virus from infected humans.[426][427] Symptoms in cats include respiratory (such as a cough) and digestive symptoms.[426] Cats can spread the virus to other cats, and may be able to spread the virus to humans, but cat-to-human transmission of SARS-CoV-2 has not been proven.[426][428] Compared to cats, dogs are less susceptible to this infection.[428] Behaviours which increase the risk of transmission include kissing, licking, and petting the animal.[428]
The virus does not appear to be able to infect pigs, ducks, or chickens at all.[426] Mice, rats, and rabbits, if they can be infected at all, are unlikely to be involved in spreading the virus.[428]
Tigers and lions in zoos have become infected as a result of contact with infected humans.[428] As expected, monkeys and great ape species such as orangutans can also be infected with the COVID‑19 virus.[428]
Minks, which are in the same family as ferrets, have been infected.[428] Minks may be asymptomatic, and can also spread the virus to humans.[428] Multiple countries have identified infected animals in mink farms.[429] Denmark, a major producer of mink pelts, ordered the slaughter of all minks over fears of viral mutations,[429] following an outbreak referred to as Cluster 5. A vaccine for mink and other animals is being researched.[429]
Research
International research on vaccines and medicines in COVID‑19 is underway by government organisations, academic groups, and industry researchers.[430][431] The CDC has classified it to require a BSL3 grade laboratory.[432] There has been a great deal of COVID‑19 research, involving accelerated research processes and publishing shortcuts to meet the global demand.[433]
As of December 2020, hundreds of clinical trials have been undertaken, with research happening on every continent except Antarctica.[434] As of November 2020, more than 200 possible treatments have been studied in humans.[435]
Transmission and prevention research
Modelling research has been conducted with several objectives, including predictions of the dynamics of transmission,[436] diagnosis and prognosis of infection,[437] estimation of the impact of interventions,[438][439] or allocation of resources.[440] Modelling studies are mostly based on compartmental models in epidemiology,[441] estimating the number of infected people over time under given conditions. Several other types of models have been developed and used during the COVID‑19 including computational fluid dynamics models to study the flow physics of COVID‑19,[442] retrofits of crowd movement models to study occupant exposure,[443] mobility-data based models to investigate transmission,[444] or the use of macroeconomic models to assess the economic impact of the pandemic.[445] Further, conceptual frameworks from crisis management research have been applied to better understand the effects of COVID‑19 on organisations worldwide.[446][447]
Seven possible drug targets in viral replication process and drugs
Repurposed antiviral drugs make up most of the research into COVID‑19 treatments.[448][449] Other candidates in trials include vasodilators, corticosteroids, immune therapies, lipoic acid, bevacizumab, and recombinant angiotensin-converting enzyme 2.[449]
In March 2020, the World Health Organization (WHO) initiated the Solidarity trial to assess the treatment effects of some promising drugs: an experimental drug called remdesivir; anti-malarial drugs chloroquine and hydroxychloroquine; two anti-HIV drugs, lopinavir/ritonavir; and interferon-beta.[450][451] More than 300 active clinical trials are underway as of April 2020.[172]
Research on the antimalarial drugs hydroxychloroquine and chloroquine showed that they were ineffective at best,[452][453] and that they may reduce the antiviral activity of remdesivir.[454] By May 2020, France, Italy, and Belgium had banned the use of hydroxychloroquine as a COVID‑19 treatment.[455]
In June, initial results from the randomised RECOVERY Trial in the United Kingdom showed that dexamethasone reduced mortality by one third for people who are critically ill on ventilators and one fifth for those receiving supplemental oxygen.[456] Because this is a well-tested and widely available treatment, it was welcomed by the WHO, which is in the process of updating treatment guidelines to include dexamethasone and other steroids.[457][458] Based on those preliminary results, dexamethasone treatment has been recommended by the NIH for patients with COVID‑19 who are mechanically ventilated or who require supplemental oxygen but not in patients with COVID‑19 who do not require supplemental oxygen.[459]
In September 2020, the WHO released updated guidance on using corticosteroids for COVID‑19.[460][461] The WHO recommends systemic corticosteroids rather than no systemic corticosteroids for the treatment of people with severe and critical COVID‑19 (strong recommendation, based on moderate certainty evidence).[460] The WHO suggests not to use corticosteroids in the treatment of people with non-severe COVID‑19 (conditional recommendation, based on low certainty evidence).[460] The updated guidance was based on a meta-analysis of clinical trials of critically ill COVID‑19 patients.[462][463]
In September 2020, the European Medicines Agency (EMA) endorsed the use of dexamethasone in adults and adolescents from twelve years of age and weighing at least 40 kilograms (88 lb) who require supplemental oxygen therapy.[464][465] Dexamethasone can be taken by mouth or given as an injection or infusion (drip) into a vein.[464]
In November 2020, the US Food and Drug Administration (FDA) issued an emergency use authorization for the investigational monoclonal antibody therapy bamlanivimab for the treatment of mild-to-moderate COVID‑19.[466] Bamlanivimab is authorised for people with positive results of direct SARS-CoV-2 viral testing who are twelve years of age and older weighing at least 40 kilograms (88 lb), and who are at high risk for progressing to severe COVID‑19 or hospitalisation.[466] This includes those who are 65 years of age or older, or who have chronic medical conditions.[466]
In February 2021, the FDA issued an emergency use authorization (EUA) for bamlanivimab and etesevimab administered together for the treatment of mild to moderate COVID‑19 in people twelve years of age or older weighing at least 40 kilograms (88 lb) who test positive for SARS‑CoV‑2 and who are at high risk for progressing to severe COVID‑19. The authorised use includes treatment for those who are 65 years of age or older or who have certain chronic medical conditions.[467]
In April 2021, the FDA revoked the emergency use authorization (EUA) that allowed for the investigational monoclonal antibody therapy bamlanivimab, when administered alone, to be used for the treatment of mild-to-moderate COVID‑19 in adults and certain paediatric patients.[468]
Cytokine storm
Various therapeutic strategies for targeting cytokine storm
A cytokine storm can be a complication in the later stages of severe COVID‑19. A cytokine storm is a potentially deadly immune reaction where a large amount of pro-inflammatory cytokines and chemokines are released too quickly. A cytokine storm can lead to ARDS and multiple organ failure.[469] Data collected from Jin Yin-tan Hospital in Wuhan, China indicates that patients who had more severe responses to COVID‑19 had greater amounts of pro-inflammatory cytokines and chemokines in their system than patients who had milder responses. These high levels of pro-inflammatory cytokines and chemokines indicate presence of a cytokine storm.[470]
Tocilizumab has been included in treatment guidelines by China’s National Health Commission after a small study was completed.[471][472] It is undergoing a Phase II non-randomised trial at the national level in Italy after showing positive results in people with severe disease.[473][474] Combined with a serum ferritin blood test to identify a cytokine storm (also called cytokine storm syndrome, not to be confused with cytokine release syndrome), it is meant to counter such developments, which are thought to be the cause of death in some affected people.[475] The interleukin-6 receptor (IL-6R) antagonist was approved by the FDA to undergo a Phase III clinical trial assessing its effectiveness on COVID‑19 based on retrospective case studies for the treatment of steroid-refractory cytokine release syndrome induced by a different cause, CAR T cell therapy, in 2017.[476] There is no randomised, controlled evidence that tocilizumab is an efficacious treatment for CRS. Prophylactic tocilizumab has been shown to increase serum IL-6 levels by saturating the IL-6R, driving IL-6 across the blood–brain barrier, and exacerbating neurotoxicity while having no effect on the incidence of CRS.[477]
Lenzilumab, an anti-GM-CSF monoclonal antibody, is protective in murine models for CAR T cell-induced CRS and neurotoxicity and is a viable therapeutic option due to the observed increase of pathogenic GM-CSF secreting T cells in hospitalised patients with COVID‑19.[478]
Passive antibodies
Transferring purified and concentrated antibodies produced by the immune systems of those who have recovered from COVID‑19 to people who need them is being investigated as a non-vaccine method of passive immunisation.[479][480] Viral neutralisation is the anticipated mechanism of action by which passive antibody therapy can mediate defence against SARS-CoV-2. The spike protein of SARS-CoV-2 is the primary target for neutralising antibodies.[481] As of 8 August 2020, eight neutralising antibodies targeting the spike protein of SARS-CoV-2 have entered clinical studies.[482] It has been proposed that selection of broad-neutralising antibodies against SARS-CoV-2 and SARS-CoV might be useful for treating not only COVID‑19 but also future SARS-related CoV infections.[481] Other mechanisms, however, such as antibody-dependant cellular cytotoxicity or phagocytosis, may be possible.[479] Other forms of passive antibody therapy, for example, using manufactured monoclonal antibodies, are in development.[479]
The use of passive antibodies to treat people with active COVID‑19 is also being studied. This involves the production of convalescent serum, which consists of the liquid portion of the blood from people who recovered from the infection and contains antibodies specific to this virus, which is then administered to active patients.[479] This strategy was tried for SARS with inconclusive results.[479] An updated Cochrane review in May 2021 found high certainty evidence that, for the treatment of people with moderate to severe COVID‑19, convalescent plasma did not reduce mortality or bring about symptom improvement.[480] There continues to be uncertainty about the safety of convalescent plasma administration to people with COVID‑19 and differing outcomes measured in different studies limits their use in determining efficacy.[480]
Bioethics
Since the outbreak of the COVID‑19 pandemic, scholars have explored the bioethics, normative economics, and political theories of healthcare policies related to the public health crisis.[483] Academics have pointed to the moral distress of healthcare workers, ethics of distributing scarce healthcare resources such as ventilators,[484] and the global justice of vaccine diplomacies.[citation needed] The socio-economic inequalities between genders,[485] races,[486] groups with disabilities,[487] communities,[488] regions, countries,[489] and continents have also drawn attention in academia and the general public.
Effects on other diseases
The use of social distancing and the wearing of surgical masks and similar precautions against COVID‑19 may have caused a drop in the spread of the common cold and the flu.[490][491]
See also
- Coronavirus diseases, a group of closely related syndromes
- Disease X, a WHO term
- Law of declining virulence – Disproved hypothesis of epidemiologist Theobald Smith
- Theory of virulence – Theory by biologist Paul W. Ewald
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Text was copied from this source, which is available under a Creative Commons Attribution 4.0 International License.
This article incorporates text from this source, which is in the public domain: «Hydroxychloroquine does not benefit adults hospitalized with COVID-19». National Institutes of Health (NIH) (Press release). 9 November 2020Further reading
- Erola Pairo-Castineira; Sara Clohisey; Lucija Klarić; et al. (11 December 2020). «Genetic mechanisms of critical illness in Covid-19». Nature. doi:10.1038/S41586-020-03065-Y. ISSN 1476-4687. PMID 33307546. Wikidata Q104287299. Scholia Q104287299.
- «Progress report on the coronavirus pandemic». Nature. 584 (7821): 325. 1 August 2020. doi:10.1038/D41586-020-02414-1. ISSN 1476-4687. PMID 32814893. Wikidata Q98568681.
- COVID-19 infection prevention and control measures for primary care, including general practitioner practices, dental clinics and pharmacy settings: first update. European Centre for Disease Prevention and Control (ECDC) (Report). October 2020.
External links
Health agencies
- Coronavirus disease (COVID‑19) Facts by the World Health Organization (WHO)
- Coronavirus 2019 (COVID-19) by the US Centers for Disease Control and Prevention (CDC)
- Coronavirus (COVID‑19) by the UK National Health Service (NHS)
Directories
- Coronavirus Resource Center at the Center for Inquiry
- COVID-19 at Curlie
- COVID‑19 Resource Directory on OpenMD
- COVID‑19 Information on FireMountain.net Archived 13 January 2022 at the Wayback Machine
Medical journals
- Coronavirus Disease 2019 (COVID‑19) by JAMA
- BMJ’s Coronavirus (covid‑19) Hub by the BMJ
- Novel Coronavirus Information Center by Elsevier
- COVID‑19 Resource Centre by The Lancet
- Coronavirus (COVID‑19) Research Highlights by Springer Nature
- Coronavirus (Covid‑19) by The New England Journal of Medicine
- Covid‑19: Novel Coronavirus Archived 24 September 2020 at the Wayback Machine by Wiley Publishing
Treatment guidelines
- «JHMI Clinical Recommendations for Available Pharmacologic Therapies for COVID-19» (PDF). Johns Hopkins Medicine.
- «Bouncing Back From COVID-19: Your Guide to Restoring Movement» (PDF). Johns Hopkins Medicine.
- «Guidelines on the Treatment and Management of Patients with COVID-19». Infectious Diseases Society of America.
- «Coronavirus Disease 2019 (COVID-19) Treatment Guidelines» (PDF). National Institutes of Health.
- World Health Organization (2022). Therapeutics and COVID-19: living guideline, 14 January 2022 (Report). hdl:10665/351006. WHO/2019-nCoV/therapeutics/2022.1.
- NHS England and NHS Improvement. National Guidance for post-COVID syndrome assessment clinics (Report).
На основании Вашего запроса эти примеры могут содержать грубую лексику.
На основании Вашего запроса эти примеры могут содержать разговорную лексику.
Перевод «ковид» на английский
У всех здесь отрицательный тест на ковид, как и у тебя.
Everybody in here has been tested negative for COVID, just like you.
Вы знаете, что у меня был ковид?
Did you know that I had COVID?
Кто-то прислал мне статью про тройную противовирусную терапию для ковид положительных.
Someone sent me an article about triple antiviral therapy for Covid patients.
Пациент поступил для респираторной поддержки четыре дня назад, после положительного теста на ковид.
Patient was admitted for respiratory support four days ago, after a positive Covid test.
Сначала вы взяли Огги, потом этот ковид.
I mean, taking in Auggie and then, now COVID.
Я пришла сделать вам тест на Ковид.
It’s Dr. Helm. I’m here to do your COVID test.
Слушай, у многих сейчас КОВИД.
Look, a few hundred people have COVID.
Но мы не сообщили, что у неё КОВИД.
But we’re not telling people she has COVID.
Ковид это просто лотерея.
Или это у Алекс КОВИД?
Or does Alex have COVID?
Все восточное крыло отведено под ковид.
The entire east wing is now a Covid ward.
У обоих отрицательный тест на ковид.
При поступлении взяли тест на ковид, положительный.
потому что ковид просто захватил это место.
Сначала ковид поборол, а теперь это?
обеспечить достаточное количество тестов на ковид для всего персонала.
to secure enough Covid tests for the entire staff.
Ковид быстро прогрессирует, и потом мы уже ничем не можем помочь…
COVID comes on so fast, we can’t get ahead of it…
А для чего нужен тест на КОВИД?
Экспресс-тест на ковид отрицательный.
Тест на ковид еще не пришел.
Результатов: 25. Точных совпадений: 25. Затраченное время: 22 мс
Documents
Корпоративные решения
Спряжение
Синонимы
Корректор
Справка и о нас
Индекс слова: 1-300, 301-600, 601-900
Индекс выражения: 1-400, 401-800, 801-1200
Индекс фразы: 1-400, 401-800, 801-1200
Название коронавируса официально внесли в оксфордский словарь английского языка. COVID-19 получил определение как вызванное коронавирусом острое респираторное заболевание, особенно опасное для пожилых и людей с сопутствующими заболеваниями. Лингвисты в беседе с сайтом «Невские новости» рассказали, русифицировалось ли новое слово и можно ли его склонять.
Лексикографы помимо COVID-19 внесли и неологизмы, такие, как «самоизоляция», «социальная дистанция» и аббревиатура WFH (work from home — «работа из дома»).
Илья Мищенко, переводчик, лингвист Топонимической комиссии Санкт-Петербурга, сообщил, что на данный момент стоит придерживаться латинского написания болезни. Если использовать аббревиатуру на русском языке, то она изменится, так как ее будет необходимо перевести.
Эксперт сомневается, что болезнь можно будет называть «ковидом».
Сергей Кузнецов, советский и российский лингвист-русист, специалист в области семантики, морфологии, теории и практики лексикографии, основатель и глава Центра коммуникативных компетенций Центра экспертиз СПбГУ, наоборот же считает, что слово уже прошло стадию русификации, и писать его кириллицей допустимо. Речь идет именно об аббревиатуре — КОВИД-19.
Портал «Текст.ру» считает, что COVID-19 правильнее писать латиницей.
Аббревиатура COVID-19 расшифровывается как CoronaVirus Disease 2019, что в переводе с английского на русский означает «коронавирусное заболевание 2019 года».
Этим термином официально назвали вирус, обнаруженный в китайском городе Ухань 31 декабря 2019 года и вызвавший самую опасную эпидемию XXI века. К концу мая 2020 года количество жертв COVID-19 в мире превысило 370 тысяч человек, большую часть из которых составляют преклонные старики. В большинстве языков аббревиатура COVID произносится как «ковид», и от неё уже успели понаделать модных слов, таких как COVIDiot, например.
- serega
- 2017-02-28 19:55:05
- 1-4
- Английский язык
- 5+3 б
девятнадцать по-английски как написать?
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- snowzilla
- Мегамозг
- 2017-02-28 19:55:05
19 на английском языке пишется вот так: nineteen.
Ответ: 19 по-английски — nineteen
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Правило
Слово «ковид» пишут с буквой «д» на конце. Написание этого слова важно запомнить, так как его невозможно проверить.
Русский вариант повторяет аббревиатуру COVID, которую можно расшифровать как COronaVIrus Disease. Полное название практически не употребляется, а вот аббревиатура часто используется в разговорной речи для определения вирусной инфекции.
Значение слова
«Ковид» — коронавирусная инфекция, которая провоцирует заболевания легких и может быть причиной пневмонии.
Примеры употребления слова в предложениях
- Диагностировать Ковид-19 можно только путем проведения специального тестирования.
- Распространение Ковид-19 было признано пандемией, что вызвало закрытие стран на карантин.
- Пока нет точных сведений, какой процент людей способен переносить инфекцию Ковид-19 бессимптомно.
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На разных ТВ-каналах дикторы, похоже, не могут договориться и произносят COVID-19 кто с ударением на первый, а кто — на второй слог. То же самое наблюдалось и до сих пор наблюдается с произношением африканского вируса Эбола, а также итальянского города Бергамо. Скорее всего, ответ на этот вопрос про кОвид/ковИд мы получим чуть позже, когда одна из форм закрепится как наиболее употребимая и словари начнут её давать в качестве нормы. система выбрала этот ответ лучшим
COVID-19 (название нового коронавируса) — это Произносят название в разных странах по-разному. Где-то перечисляют буквы в соответствии с правилами английского языка, а американцы чаще просто говорят: «ковид найнтин». Прослушать варианты произнесения названия различными людьми из США, Великобритании, Испании и других стран можно здесь.
Рождённый в С С С Р более года назад Моя младшая сестра как-то в разговоре заметила, что с ударением на И говорят обыватели: ковИд. А практически все знакомые медицинские работники или люди, каким-то боком к врачеванию относящиеся — все говорят: кОвид. Наверное, не просто так. Наверное, им так на всяких учёбах-конференциях произносят название этого вируса поганого.
Алекс98 более года назад В период распространения новой коронавирусной инфекции никто особенно не вдается в подробности произношения названия COVID-19. А вопрос довольно-таки интересный. Насколько мне известно, в большинстве случаев разные люди произносят по-разному. В большинстве случаев, ударение ставится на вторую гласную букву (английскую «I»). Из телевизионных новостных источников информации ударение такое же. Считаю правильным говорить именно: «КовИд» с ударением на «И». Хотя я бы предпочел проще называть — коронавирус, хоть Ковид это и сокращенно и быстрее говорится, лично мне это слово как-то не нравится, не по душе.
линза более года назад Думаю, что произнесение данной аббревиатуры «COVID-19», так же, как и других служебных аббревиатур, может делиться на разговорный, общепринятый вариант, так и на специфический, профессиональный. Привожу примеры:
Так и в случае с этим проклятым Ковидом, лучше бы никогда не знать и не произносить это слово. Медики говорят кОвид, учителя говорят ковИд, а простые люди, вообще называют «наказанием за грехи», и «чёртовой заразой»… Так что поверьте, в данное время, в отношении пандемии во всём мире, не так важны ударения в слове, которым назвали вирусную беду.
Joel Miller более года назад SARS-CoV-2 — РНК-вирус, из-за которого сейчас эпидемия идет. При чем это — международное название вируса. Есть еще синоним — 2019-nCoV. Болезнь, которую вызывает этот вирус — COVID-19, сокращенно от COronaVIrusDisease-2019. В простонародье, да и в медицинских кругах болезнь просто называют «Ковид», или «Корона», в официальных источниках — новая коронавирусная инфекция — сокращенно НКВИ.
Пучеглазик 2 года назад Многие интересуются, как правильно произносится название «Ковид-19» («Covid-19»). Немногие знают, что оно означает не название вируса (коронавируса), а название болезни, которую вызывает эта вирусная инфекция. Covid-19 означает «атипичная инфекционная пневмония», а число «19» означает год, когда она была обнаружена. Касательно ударения в этом слове нет особого правила, поэтому можно произносить как «кОвид», так и «ковИд», значения не имеет.
Точно в цель более года назад COVID-19 — это болезнь, которую вызывает коронавирусная инфекция, простым словом. Сама аббревиатура произошла от COrona Virus Dease 2019 — COVID-19. Так как слово относительное новое, то определенных правил произношения еще не сформировалось. Кто-то произносит его как ковИд (ударение на «И») а кто-то как кОвид (ударение на букву «О»). Оба варианта правильные.
владсандрович более года назад В этом страшно живучем вирусе, который уже явно многих испугал собой и надоел думаю уж точно практически всем, ударение люди из области медицины, делают на первый слог то есть его название COVID-19, правильно произносить как кОвид-19.
alexm12 2 года назад Правильно COVID-19 произносится как «Си О Ви Ай Ди Найнтин» или «Цэ О Вэ И Дэ девятнадцать». Если вам эту аббревиатуру хочется произносить, как ввели м моду американцы, одним словом, то говорите «ковид».
Павел Ппп более года назад Правильно писать «короновирус» или «КОВИБ». КОроноВИрусная Болезнь. Знаете ответ? |
Official nomenclature and journalistic practice
A recent item by Elisabeth Ribbans, «COVID or Covid? The comfort of pedantry at a time of national crisis,» in The Guardian (April 19, 2020), asserts that initial-capping acronyms (abbreviations pronounced phonetically as approximately the sum of their letter sounds, rather than as as a series of names of the constituent alphabet letters) is the prevailing style at «most British newspapers»:
I fell into happy correspondence the weekend before last with a medical specialist who wanted to know why the media was “incorrectly” spelling COVID-19 as Covid-19. I explained that, like most British newspapers, the Guardian’s style is to use uppercase for abbreviations that are written and spoken as a collection of letters, such as BBC, IMF and NHS, whereas acronyms pronounced as words go upper and lower, eg Nasa, Unicef and, now, Covid-19. The reader was remarkably understanding given that her query turned out to be more than passing curiosity: she was busily correcting scientific articles by authors who’d adopted the media’s style. We each apologised for having caused the other work and moved on better informed about our respective fields.
The International Committee on Taxonomy of Viruses has an interesting undated news item titled, «Naming the 2019 Coronavirus,» about the naming of the coronavirus responsible for COVID-19, which it calls «severe acute respiratory syndrome coronavirus 2,» shortened to «SARS-CoV-2.» Note that «SARS,» like «COVID» is generally pronounced as an acronym, not as an initialism, and yet the ICTV renders it in all caps but renders the «CoV» part of the virus name (which is short for «coronavirus») as mixed uppercase and lowercase. The ICTV item then continues as follows:
The disease name (which in many cases is different from the virus name) has been designated as COVID-19 by the WHO. The ’19’ in COVID-19 stands for the year, 2019, that the virus was first seen. The number ’19’ has nothing whatsoever to do with virus strains, genotypes, or anything else related to the virus’ genetics. The virus name was announced by the World Health Organization on February 11, 2020. See the February 11 World Health Organization Situation Report. This clearly states that «WHO has named the disease COVID-19, short for ‘coronavirus disease 2019’.”
So the World Health Organization and the ICTV appear to be aligned on the formatting of the disease name as all-caps. This explains why the medical specialist was at odds with The Guardian writer/editor over the treatment of the acronym COVID-19.
Newspaper guidelines for formatting of ‘COVID-19’/’Covid-19’
It’s tempting to view preference for spelling acronyms as all-lowercase or initial-capped-only words as peculiar to British journalism. Certainly, the New York Times (for example) doesn’t follow The Guardian in spelling NASA as Nasa—but its style for dealing with acronyms is far from consistent, as these consecutive entries in The New York Times Manual of Style and Usage, revised edition (1999) make clear:
NASA for the National Aeronautics and Space Administration.
Nascar for the National Association for Stock Car Auto Racing.
In fact, NYT also endorses (on the one hand) Nasdaq, Unesco, Unicef, and Waves, and (on the other) NATO, OPEC, OSHA, PATH, RICO, and WAC. It shows similar inconsistency in formatting some initialisms (such as N.A.A.C.P., N.C.A.A., N.L.R.B., N.Y.U., and P.S.A.T.) with periods, and others (such as NOAA, NPR, PTA, SAT, and SUNY) without.
As it turns out, there is actually a slender thread of logic behind the split in the NYT treatment of, for example, NATO and Unesco:
acronyms. An acronym is a word formed from the first letter (or letters) of each word in a series: NATO from North Atlantic Treaty Organization; radar from radio detection and ranging. (Unless pronounced as a word, an abbreviation is not an acronym.) When an acronym serves as a proper name and exceeds four letters, capitalize only the first letter: Unesco, Unicef.
COVID is more than four letters long, so NYT style for acronyms would dictate spelling the disease name as as Covid-19—just as The Guardian does, albeit for a different reason—and that is in fact what it does.
The style guideline for acronyms in The Associated Press Stylebook (2007) is very similar to the one in New York Times, with one critical difference in detail:
Use only an initial cap and then lowercase for acronyms of more than six letters, unless listed otherwise in this stylebook or Webster’s New World College Dictionary.
Because COVID is five letters long, it triggers the Covid spelling according to NYT style but the COVID spelling in AP style. My local newspaper, which follows AP style, thus uses the form COVID-19.
The ever-whimsical stylists at The New Yorker, take a third way, setting COVID-19 in small caps (COVID-19)—a practice that the magazine follows with all acronyms (as opposed to initialisms), regardless of their length.
Book style manual guidance for formatting acronyms
Moving now to book style guidelines for acronyms, I find far less inclination to adopt a length-based difference in formatting. The Oxford Guide to Style (2002), for example, has this comment about differential treatment of acronyms by length:
Any all-capital proper-name acronym is, in some house styles, fashioned with a single initial capital if it exceeds four letters (Basic, Unesco, Unicef). Editors should avoid this rule, useful though it is, where the result runs against the common practice of a discipline (CARPE, SSHRCC, WYSIWYG), or where similar terms would be treated dissimilarly based on length alone.
The Chicago Manual of Style, sixteenth edition (2010) seems even less inclined than Oxford to endorse length-based all-caps versus initial-cap-only decisions:
10.6 Capitals versus lowercase for acronyms and initialisms. Initialisms tend to appear in all capital letters, even when they are not derived from proper names (HIV, VP, LCD). With frequent use, however, acronyms—especially those of five or more letters—will sometimes become lowercase (scuba); those that are derived from proper nouns retain an initial capital. Chicago generally prefers the all-capital form, unless the term is listed otherwise in Webster’s.
[Example:] NAFTA (not Nafta)
This view puts Chicago squarely in the COVID-19 camp, whereas Oxford‘s position is harder to anticipate and may be determined by situational considerations—for example, if a book mentions AIDS, Oxford might be more inclined to render the novel coronavirus disease as COVID-19 for consistency, despite the purported usefulness of the five-letters-or-more rule.A quick check of Merriam-Webster’s Eleventh Collegiate Dictionary (2003) reveals that NASCAR, UNESCO, and UNICEF all receive all-caps formatting in their entries; the Eleventh Collegiate and MW Online don’t have a separate entry for Nasdaq, but most references to the acronym in the online dictionary initial-cap the term.
Webster’s Standard American Style Manual (1985) confirms that MW has no interest in length-based rules for handling acronyms:
Most abbreviations that are pronounced as words, rather than as a series of letters, are capitalized. If they have been assimilated into the language as words in their own right, however, they are most often lowercased.
[All-cap examples:] OPEC; NATO; MIRV; NOW account
[All-lowercase examples:] quasar; laser; sonar; scuba
Webster’s includes no examples of acronyms that it would render in initial-cap-but-otherwise-lowercase format. So even if MW weren’t inclined to accept the WHO’s preferred all-cap formatting of COVID-19 (which I think it would be), there is no reason to suppose that it would endorse the form Covid-19.
In the course of a fairly lengthy discussion of acronym and initialisms, Bryan Garner, Garner’s Modern American Usage (2003) has this to say about capitalization:
[C]apitalization raises various questions. In AmE there is a tendency to print initialisms in all capitals (e.g., FMLA, NJDEP) and acronyms in small capitals )e.g., GAAP, MADD, NASA). Some publications , however, use all capitals for both kinds. But in BrE the tendency is to uppercase only the first letter, as with Ifor and Isa for Implementation Force and individual savings account. An influential British commentator once suggested (with little success on his side of the Atlantic) that the lowercasing be avoided: «From the full name to the simplified label three stages can be detected. For instance, the Society {for Checking the Abuse of Public Advertising} … becomes first S.C.A.P.A., then SCAPA, and finally Scapa. In the interests of clarity this last stage might well be discouraged, since thereby the reference is made unnecessarily cryptic.» Simeon Potter, Our Language 177 (rev. ed. 1966). American writers have generally agreed with this view.
Like Merriam-Webster, Garner doesn’t acknowledge the length-based differential treatment of acronyms cited in such guidebooks as AP, the New York Times, Oxford, and Chicago.
Conclusions
The reason you are likely to see different formatting choices for COVID-19 is that different publishers base their formatting choice on different rules. Publishers that opt for COVID-19 may simply be using the form preferred by the World Health Organization in, for example, Situation Report — 22 (February 11, 2020):
Following WHO best practices for naming of new human infectious diseases, which were developed in consultation and collaboration with the World Organisation for Animal Health (OIE) and the Food and Agriculture Organization of the United Nations (FAO), WHO has named the disease COVID-19, short for “coronavirus disease 2019.”
Others that favor COVID-19 may be following the standard US book publishing style of using all caps for acronyms of any length, or Associated Press Stylebook style, which calls for all-capping acronyms of six letters or less.
Those that favor Covid-19 may be following the Guardian style preference for initial-capping any acronym, the New York Times preference for initial-capping acronyms of five letters or longer, or general advice to the same effect from (for example) Oxford University Press.
And those that favor COVID-19 may be enforcing an older U.S. book style preference or be responsible for editorial choices at The New Yorker.
The option of using CoViD-19 may appeal to publishers that want to indicate where the word breaks in the original phrase fall—but in choosing this mix of capitals and lowercase letters, they don’t appear to be on the strongest ground, technically speaking, since coronavirus is generally spelled as a single word. (Although Merriam-Webster dates the term to 1968, coronavirus didn’t debut in an edition of the Collegiate Dictionary until the Eleventh Edition (2003)—and it did so then as a single word.) It follows that only the C (for coronavirus) and the D (for disease) are markers of separate words. A publisher attempting to be true to the source words of the acronym might therefore do better to adopt the form Co’vi’D-19 (a form that, as far as I know, no one uses, perhaps because it looks ridiculous).
Official nomenclature and journalistic practice
A recent item by Elisabeth Ribbans, «COVID or Covid? The comfort of pedantry at a time of national crisis,» in The Guardian (April 19, 2020), asserts that initial-capping acronyms (abbreviations pronounced phonetically as approximately the sum of their letter sounds, rather than as as a series of names of the constituent alphabet letters) is the prevailing style at «most British newspapers»:
I fell into happy correspondence the weekend before last with a medical specialist who wanted to know why the media was “incorrectly” spelling COVID-19 as Covid-19. I explained that, like most British newspapers, the Guardian’s style is to use uppercase for abbreviations that are written and spoken as a collection of letters, such as BBC, IMF and NHS, whereas acronyms pronounced as words go upper and lower, eg Nasa, Unicef and, now, Covid-19. The reader was remarkably understanding given that her query turned out to be more than passing curiosity: she was busily correcting scientific articles by authors who’d adopted the media’s style. We each apologised for having caused the other work and moved on better informed about our respective fields.
The International Committee on Taxonomy of Viruses has an interesting undated news item titled, «Naming the 2019 Coronavirus,» about the naming of the coronavirus responsible for COVID-19, which it calls «severe acute respiratory syndrome coronavirus 2,» shortened to «SARS-CoV-2.» Note that «SARS,» like «COVID» is generally pronounced as an acronym, not as an initialism, and yet the ICTV renders it in all caps but renders the «CoV» part of the virus name (which is short for «coronavirus») as mixed uppercase and lowercase. The ICTV item then continues as follows:
The disease name (which in many cases is different from the virus name) has been designated as COVID-19 by the WHO. The ’19’ in COVID-19 stands for the year, 2019, that the virus was first seen. The number ’19’ has nothing whatsoever to do with virus strains, genotypes, or anything else related to the virus’ genetics. The virus name was announced by the World Health Organization on February 11, 2020. See the February 11 World Health Organization Situation Report. This clearly states that «WHO has named the disease COVID-19, short for ‘coronavirus disease 2019’.”
So the World Health Organization and the ICTV appear to be aligned on the formatting of the disease name as all-caps. This explains why the medical specialist was at odds with The Guardian writer/editor over the treatment of the acronym COVID-19.
Newspaper guidelines for formatting of ‘COVID-19’/’Covid-19’
It’s tempting to view preference for spelling acronyms as all-lowercase or initial-capped-only words as peculiar to British journalism. Certainly, the New York Times (for example) doesn’t follow The Guardian in spelling NASA as Nasa—but its style for dealing with acronyms is far from consistent, as these consecutive entries in The New York Times Manual of Style and Usage, revised edition (1999) make clear:
NASA for the National Aeronautics and Space Administration.
Nascar for the National Association for Stock Car Auto Racing.
In fact, NYT also endorses (on the one hand) Nasdaq, Unesco, Unicef, and Waves, and (on the other) NATO, OPEC, OSHA, PATH, RICO, and WAC. It shows similar inconsistency in formatting some initialisms (such as N.A.A.C.P., N.C.A.A., N.L.R.B., N.Y.U., and P.S.A.T.) with periods, and others (such as NOAA, NPR, PTA, SAT, and SUNY) without.
As it turns out, there is actually a slender thread of logic behind the split in the NYT treatment of, for example, NATO and Unesco:
acronyms. An acronym is a word formed from the first letter (or letters) of each word in a series: NATO from North Atlantic Treaty Organization; radar from radio detection and ranging. (Unless pronounced as a word, an abbreviation is not an acronym.) When an acronym serves as a proper name and exceeds four letters, capitalize only the first letter: Unesco, Unicef.
COVID is more than four letters long, so NYT style for acronyms would dictate spelling the disease name as as Covid-19—just as The Guardian does, albeit for a different reason—and that is in fact what it does.
The style guideline for acronyms in The Associated Press Stylebook (2007) is very similar to the one in New York Times, with one critical difference in detail:
Use only an initial cap and then lowercase for acronyms of more than six letters, unless listed otherwise in this stylebook or Webster’s New World College Dictionary.
Because COVID is five letters long, it triggers the Covid spelling according to NYT style but the COVID spelling in AP style. My local newspaper, which follows AP style, thus uses the form COVID-19.
The ever-whimsical stylists at The New Yorker, take a third way, setting COVID-19 in small caps (COVID-19)—a practice that the magazine follows with all acronyms (as opposed to initialisms), regardless of their length.
Book style manual guidance for formatting acronyms
Moving now to book style guidelines for acronyms, I find far less inclination to adopt a length-based difference in formatting. The Oxford Guide to Style (2002), for example, has this comment about differential treatment of acronyms by length:
Any all-capital proper-name acronym is, in some house styles, fashioned with a single initial capital if it exceeds four letters (Basic, Unesco, Unicef). Editors should avoid this rule, useful though it is, where the result runs against the common practice of a discipline (CARPE, SSHRCC, WYSIWYG), or where similar terms would be treated dissimilarly based on length alone.
The Chicago Manual of Style, sixteenth edition (2010) seems even less inclined than Oxford to endorse length-based all-caps versus initial-cap-only decisions:
10.6 Capitals versus lowercase for acronyms and initialisms. Initialisms tend to appear in all capital letters, even when they are not derived from proper names (HIV, VP, LCD). With frequent use, however, acronyms—especially those of five or more letters—will sometimes become lowercase (scuba); those that are derived from proper nouns retain an initial capital. Chicago generally prefers the all-capital form, unless the term is listed otherwise in Webster’s.
[Example:] NAFTA (not Nafta)
This view puts Chicago squarely in the COVID-19 camp, whereas Oxford‘s position is harder to anticipate and may be determined by situational considerations—for example, if a book mentions AIDS, Oxford might be more inclined to render the novel coronavirus disease as COVID-19 for consistency, despite the purported usefulness of the five-letters-or-more rule.A quick check of Merriam-Webster’s Eleventh Collegiate Dictionary (2003) reveals that NASCAR, UNESCO, and UNICEF all receive all-caps formatting in their entries; the Eleventh Collegiate and MW Online don’t have a separate entry for Nasdaq, but most references to the acronym in the online dictionary initial-cap the term.
Webster’s Standard American Style Manual (1985) confirms that MW has no interest in length-based rules for handling acronyms:
Most abbreviations that are pronounced as words, rather than as a series of letters, are capitalized. If they have been assimilated into the language as words in their own right, however, they are most often lowercased.
[All-cap examples:] OPEC; NATO; MIRV; NOW account
[All-lowercase examples:] quasar; laser; sonar; scuba
Webster’s includes no examples of acronyms that it would render in initial-cap-but-otherwise-lowercase format. So even if MW weren’t inclined to accept the WHO’s preferred all-cap formatting of COVID-19 (which I think it would be), there is no reason to suppose that it would endorse the form Covid-19.
In the course of a fairly lengthy discussion of acronym and initialisms, Bryan Garner, Garner’s Modern American Usage (2003) has this to say about capitalization:
[C]apitalization raises various questions. In AmE there is a tendency to print initialisms in all capitals (e.g., FMLA, NJDEP) and acronyms in small capitals )e.g., GAAP, MADD, NASA). Some publications , however, use all capitals for both kinds. But in BrE the tendency is to uppercase only the first letter, as with Ifor and Isa for Implementation Force and individual savings account. An influential British commentator once suggested (with little success on his side of the Atlantic) that the lowercasing be avoided: «From the full name to the simplified label three stages can be detected. For instance, the Society {for Checking the Abuse of Public Advertising} … becomes first S.C.A.P.A., then SCAPA, and finally Scapa. In the interests of clarity this last stage might well be discouraged, since thereby the reference is made unnecessarily cryptic.» Simeon Potter, Our Language 177 (rev. ed. 1966). American writers have generally agreed with this view.
Like Merriam-Webster, Garner doesn’t acknowledge the length-based differential treatment of acronyms cited in such guidebooks as AP, the New York Times, Oxford, and Chicago.
Conclusions
The reason you are likely to see different formatting choices for COVID-19 is that different publishers base their formatting choice on different rules. Publishers that opt for COVID-19 may simply be using the form preferred by the World Health Organization in, for example, Situation Report — 22 (February 11, 2020):
Following WHO best practices for naming of new human infectious diseases, which were developed in consultation and collaboration with the World Organisation for Animal Health (OIE) and the Food and Agriculture Organization of the United Nations (FAO), WHO has named the disease COVID-19, short for “coronavirus disease 2019.”
Others that favor COVID-19 may be following the standard US book publishing style of using all caps for acronyms of any length, or Associated Press Stylebook style, which calls for all-capping acronyms of six letters or less.
Those that favor Covid-19 may be following the Guardian style preference for initial-capping any acronym, the New York Times preference for initial-capping acronyms of five letters or longer, or general advice to the same effect from (for example) Oxford University Press.
And those that favor COVID-19 may be enforcing an older U.S. book style preference or be responsible for editorial choices at The New Yorker.
The option of using CoViD-19 may appeal to publishers that want to indicate where the word breaks in the original phrase fall—but in choosing this mix of capitals and lowercase letters, they don’t appear to be on the strongest ground, technically speaking, since coronavirus is generally spelled as a single word. (Although Merriam-Webster dates the term to 1968, coronavirus didn’t debut in an edition of the Collegiate Dictionary until the Eleventh Edition (2003)—and it did so then as a single word.) It follows that only the C (for coronavirus) and the D (for disease) are markers of separate words. A publisher attempting to be true to the source words of the acronym might therefore do better to adopt the form Co’vi’D-19 (a form that, as far as I know, no one uses, perhaps because it looks ridiculous).
С конца 2019 года, в связи с масштабом нового заболевания, окутавшего весь мир, русский язык значительно пополнился неологизмами, добавив привычным словам, новые оттенки.
Согласно данным петербургских лингвистов, подсчет выявил около тысячи новых словоформ, что в скором времени поспособствует появлению русского ковидного словаря. И не смотря на то, что в отличие от других стран, где пандемийные слова заняли лидирующие позиции, в российском конкурсе «Слово года-2020» почетное место заняло слово «обнуление», не стоит игнорировать последующие призовые места, на которых расположились «самоизоляция», «коронавирус», «локдаун» и другие.
Впоследствие внедрения слов, появилось множество синонимов коронавирусной болезни, и в частности латинская аббревиатура «COVID» вошла в русский язык, как «ковид», написанная строчными русскими буквами. Отсюда и появилось множество вопросов о правильности написания и произношения слова, например, как правильно: «кови́д» или «ко́вид»?
Происхождение слова «ковид»
Как мы уже выяснили «ковид» — это русский вариант написания исходной аббревиатуры СOVID, которое появилось путем сокращения от английского словосочетания «coronavirus disease». Официальное название было присвоено новой болезни 11.02.2020 года Всемирной Организацией Здравоохранения. И укоренившись в повседневной речи, словоформа «ковид» стала жить по всем законам русского языка, подвергаясь склонению по числам (ковид, ковиды), падежам (ковида, ковидом) и образовывая новые слова:
- Прилагательное «ковидный»;
- «Ковидник» — больной на короновирусную инфекцию;
- «Ковидиот» — термин, состоящий из двух слов, которым называют тех, кто недооценивают опасность болезни;
- «Ковидиворс» (англ. Covidivorce) – термин, означающий разрыв отношений по причине, что пара не может находится вместе в одном замкнутом пространстве;
- «Противоковидный», «антиковидный» и так далее.
Как правильно «кОвид» или «ковИд»?
К сожалению, со времён советской эпохи, скорость реакции российской лексикографии осталась очень низкой, и потому орфоэпические словари давно не пополнялись новыми словами и их формами.
Для того чтобы новую словоформу можно было включить в большой толковый словарь, должно было пройти не менее пяти лет. Однако есть надежда, что в эпоху развития интернета и социальных сетей, которые значительно влияют на распространение новых слов, на примере виртуальных толковых словарей английского языка — Оксфордского и Весберта, в которых фиксация неологизмов происходит значительно быстрее, российские лингвисты наберут обороты и не уступят западу в скорости наполнения своих словарей.
Поэтому говорить об исконно верном произношении слова «ковид» пока не приходится. Ещё больше придает сомнений то, что «Covid» в разных странах произносится с разными ударениями.
Однако, по словам филологов Государственного института русского языка им. Пушкина, уже сейчас можно выделить правильность ударения в слове «ковид», которое в последствии и закрепится в более достоверных источниках. Исходя из слов профессора данного института Михаила Осадчего, в орфоэпические словари чаще всего входит наиболее частый вариант произношения, присущий более грамотным гражданам, имеющим высшее образование.
В таком случае, с учетом более частого использования варианта с ударением на вторую гласную, верно говорить «кови́д» с ударением на «и»
Еще один способ убедиться в том, что ударение падает на вторую гласную — это обратиться к истоку формирования самой аббревиатуры, которая образовалась путем выделения некоторых букв в исходном словосочетании «CoronaVirus Disease». Как видим, «o» в отличие от «i» не попадает под ударение, тем самым подтверждая, что правильно говорить «кови́д».
Примеры в предложениях
Определившись с более правильной расстановкой акцентов, предлагаем ознакомиться со словоформой в разных ее вариациях на примере в предложениях.
- В связи со сложившейся ситуацией в городе, были приняты все противокови́дные меры в школах и на предприятиях.
- В большинстве крупных городов мира прошли митинги против антикови́дных ограничений.
- В связи с высокой скоростью распространения кови́д-19, работать вы продолжите удалённо.
Наши авторы и редакторы практически каждый день пишут о COVID-19. Многие из них уже очень давно начали спрашивать: зачем переключать регистр и раскладку, когда есть простое «ковид» и производные от него? Поэтому мы решили спросить лингвиста Максима Кронгауза, стало ли слово «ковид» частью языка, и можно ли его использовать за пределами разговорной речи.
Для начала стоит напомнить, как возникло это слово. Исходно COVID-19 — английская аббревиатура от английского выражения «coronavirus disease». Это официальное название, которое было присвоено новой коронавирусной инфекции решением ВОЗ 11 февраля 2020 года. До этого использовалось название 2019-nCoV. Теперь в русской повседневной речи эта аббревиатура превратилась в слово «ковид», которое живет уже по всем законам русского языка, оно склоняется, от него образуются новые слова («ковидный», «ковидарий»).
Примеров таких превращений в русском языке множество. Например, советская аббревиатура БОМЖ («без определенного места жительства», обычно в сочетании типа «лица БОМЖ» в документах правоохранителей) превратилась в обычную лексему «бомж». В качестве примера такого же превращения англоязычной аббревиатуры можно привести слово «пиар», которое возникло из PR («public relations») и положило начало целому гнезду новых слов — пиарить, пиаровский и тому подобных.
Но возникает вопрос: в какой момент такое новое слово можно считать частью литературного языка? Лингвисты в этой ситуации не могут предписывать, какие слова в какой ситуации употреблять. Их задача — зафиксировать его для всех, чтобы каждый сомневающийся мог открыть словарь и убедиться, что у слова нет стилистических помет, проверить правописание этого слова, выяснить, куда ставить ударение.
К сожалению, скорость реакции советской, а теперь российской лексикографии традиционно очень низка. В советское время регулярно выходили словари новых слов и выражений. Слово должно было просуществовать в языке еще лет пять-десять и только потом могло быть включено в «серьезный», большой толковый словарь.
Но сейчас ситуация кардинально изменилась: появление интернета и соцсетей значительно усилило значимость повседневной речи, теперь новые слова распространяются намного быстрее, и западная лексикография научилась очень быстро на эти изменения реагировать. Например, в интернет-версии Оксфордского словаря английского языка новые слова фиксируются чрезвычайно быстро, и в этом смысле российская лексикографическая традиция очень сильно отстает от английской.
В России нет универсального интернет-словаря, который бы оперативно и регулярно обновлялся, и вряд ли можно рассчитывать, что он скоро появится. Более того, у нас хотят, чтобы словарь (и орфографические правила) утверждались правительственным решением, а это заведомо дело небыстрое. Если бы был универсальный большой словарь русского языка в интернете, то имело бы смысл говорить о критериях включения новых слов.
Поэтому, сейчас отвечая на вопрос «вошло ли слово „ковид“ в язык»?, мы не можем положиться на авторитетный источник. В качестве эрзаца можно использовать «Викисловарь», где слово «ковид» уже присутствует, но этот словарь вряд ли можно назвать авторитетным источником.
Однако если посмотреть, как часто и в каких ситуациях употребляется это слово, то не останется сомнений, что слово действительно вошло в язык. Оно десятки и сотни раз в день употребляется в сообщениях СМИ. Наверное можно сказать, что этого достаточно. Но какая должна быть планка отсечения? Есть промежуточные случаи, когда в данных Гугла или в Яндекса встречается 100 употреблений за пять лет, здесь лингвистам нужно думать. Но слово «ковид» употребляется значительно чаще, причем чаще формально верной аббревиатуры.
Слово употребляется всеми и повсюду. Да, иногда употребляется с прописными буквами, иногда его могут писать латиницей, но массово все же употребляется в СМИ кириллицей, строчными буквами и прекрасно склоняется.
По моим ощущениям, неспециалисты использовали слово «коронавирус» во время первой волны, в первую очередь, в качестве названия болезни. А во время второй волны инфекции «ковид» стал употребляться в роли обозначения заболевания и вытеснил «коронавирус» из этой ячейки, новое слово оказалось более «удобным».
Консервативный лексикограф может сказать: давайте подождем, пусть пройдет еще пять лет. Но представьте, что пандемия закончится совсем скоро, и слово «ковид» хотя и не исчезнет совсем, но станет чрезвычайно редким, и скорее, не словом обыденного языка, а медицинским термином. В этом случае лексикографы уже вроде бы справедливо откажутся включать его в словари, оно не пройдет «временной ценз». Потерять это слово будет жаль, ведь оно сыграло большую роль, пусть и в течении небольшого времени. В идеальном интернет-словаре такое слово присутствовало бы совершенно законно, пусть и с пометой, указывающей на время его активного использования.
От редакции
В России пока нет большого, оперативного и авторитетного онлайн-словаря, на который можно опереться, решая дилемму «ковид / COVID-19», поэтому нам остается руководствоваться узусом, то есть словоупотреблением. С этого момента мы будем использовать слово «ковид» там, где речь идет о новой коронавирусной инфекции.
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