Etiology

Virology

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a previously unknown betacoronavirus that was discovered in bronchoalveolar lavage samples taken from clusters of patients who presented with pneumonia of unknown cause in Wuhan City, Hubei Province, China, in December 2019.[44]

  • Coronaviruses are a large family of enveloped RNA viruses, some of which cause illness in people (e.g., common cold, severe acute respiratory syndrome [SARS], Middle East respiratory syndrome [MERS]), and others that circulate among mammals and birds. Rarely, animal coronaviruses can spread to humans and subsequently spread between people, as was the case with SARS and MERS.

  • SARS-CoV-2 belongs to the Sarbecovirus subgenus of the Coronaviridae family, and is the seventh coronavirus known to infect humans. The virus has been found to be similar to SARS-like coronaviruses from bats, but it is distinct from SARS-CoV and MERS-CoV.[45][46] 

  • See the Classification section for information on SARS-CoV-2 variants.

[Figure caption and citation for the preceding image starts]: Illustration revealing ultrastructural morphology exhibited by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) when viewed with electron microscopicallyCenters for Disease Control and Prevention [Citation ends].com.bmj.content.model.Caption@6a692cdc

Origin of virus

  • A majority of patients in the initial stages of this outbreak reported a link to the Huanan South China Seafood Market, a live animal or "wet" market, suggesting a zoonotic origin of the virus.[47][48][49] An initial assessment of the transmission dynamics in the first 425 confirmed cases found that 55% of cases before 1 January 2020 were linked to the market, whereas only 8.6% of cases after this date were linked to the market. This suggests that person-to-person spread was occurring among close contacts since the middle of December 2019.[49] More recent studies suggest that the virus may have emerged earlier than previously thought.[50]

  • A zoonotic origin has still not been confirmed. Some studies suggest that SARS-CoV-2 may be a recombinant virus between a bat coronavirus and an origin-unknown coronavirus, with pangolins and minks suggested as possible intermediate hosts. However, there is currently no evidence to demonstrate the possible route of transmission from a bat reservoir to human through one or several intermediary animal species.[51] Further research is required to determine the origin of SARS-CoV-2.

Transmission dynamics

  • Respiratory transmission is the dominant mode of transmission, with proximity and ventilation being the key determinants of transmission risk.[52] Available evidence suggests that transmission between people occurs primarily when an infected person is in close contact with another person. The virus can spread from an infected person’s mouth or nose in small liquid particles (ranging in size from larger droplets to smaller aerosols) when the person coughs, sneezes, sings, breathes heavily, or talks. Close-range contact can result in inhalation of, or inoculation with, the virus through the mouth, nose, or eyes.[53]

  • Aerosol transmission can occur in healthcare settings during aerosol-generating procedures. There are also some outbreak reports that suggest aerosol transmission is possible in the community under certain conditions; however, these reports relate to enclosed indoor crowded spaces with poor ventilation where the infected person may have been breathing heavily (e.g., restaurants, choir practice, fitness classes). A detailed investigation of these clusters suggests that droplet and fomite transmission could also explain the transmission in these reports.[53] While the air close to, and distant from, patients has been found to frequently be contaminated with SARS-CoV-2 RNA, few of these samples contained viable virus.[54] The risk of transmission is much lower outdoors compared with indoors, with a limited number of studies estimating a transmission rate of <1%.[55] Evidence that nebulizer treatments increase the risk of transmission of coronaviruses similar to SARS-CoV-2 is inconclusive, and there is minimal direct evidence about the risk for transmission of SARS-CoV-2.[56]

  • Fomite transmission (from direct contact with fomites) may be possible, but there is currently no conclusive evidence for this mode of transmission. In the few cases where fomite transmission has been presumed, respiratory transmission has not been completely excluded.[52] While the majority of studies report identification of the virus on inanimate surfaces, there is a lack of evidence to demonstrate recovery of viable virus.[57] 

  • Fecal-oral transmission (or respiratory transmission through aerosolized feces) may be possible, but there is only limited circumstantial evidence to support this mode of transmission.[52]

  • Transmission via other body fluids (including sexual transmission or bloodborne transmission) has not been reported.[52] While the virus has been detected in body fluids (e.g., semen, urine, cerebrospinal fluid, ocular fluids), the presence of virus or viral components does not equate with infectivity.[58]

  • Vertical transmission occurs rarely and transplacental transmission has been documented. There is limited evidence on the extent of vertical transmission and its timing.[59] Viral fragments have been detected in breast milk; however, this finding is uncommon and, when it occurs, has been associated with mild symptoms in infants.[60] 

  • Nosocomial transmission was reported in 44% of patients in one systematic review; however, this review was limited to case series conducted early in the outbreak in Wuhan before the institution of appropriate infection prevention and control measures.[61] Hospital-acquired infections accounted for approximately 11.3% of infections in the UK between February and August 2020. This peaked at 15.8% in the middle of May. Rates as high as 25% were reported in some areas in October 2020. Rates were notably higher in residential community care hospitals (61.9%) and mental health hospitals (67.5%) compared with acute and general care hospitals (9.7%).[62][63] Studies of healthcare workers exposed to index cases (not in the presence of aerosol-generating procedures) found little to no nosocomial transmission when contact and droplet precautions were used.[64]

  • BMJ: visualising SARS-CoV-2 transmission routes and mitigations Opens in new window

Transmission dynamics in relation to symptoms

  • Transmission is more likely if contacts are exposed shortly before or after symptom onset in the index patient. In one study, the risk of transmission to close contacts was higher if exposure occurred between -2 and 3 days from symptom onset in the index patient. Among contacts who became infected, asymptomatic infection was more common if they were exposed to an asymptomatic index patient, suggesting that disease severity in the index patient may be associated with the clinical presentation of disease.[65]

  • Symptomatic transmission

    • Transmission mainly occurs via respiratory droplets or aerosols during close contact with an infected symptomatic case. Transmissibility depends on the amount of viable virus being shed and expelled by a person, the type of contact, the setting, and what infection prevention and control measures are in place.[53]

  • Presymptomatic transmission

    • Transmission may occur during the incubation period before symptom onset. Only 7% of people exposed to a presymptomatic index case became infected in one systematic review.[66] People without symptoms may be presymptomatic, or they may remain persistently asymptomatic.

  • Asymptomatic transmission

    • Transmission from asymptomatic cases (laboratory-confirmed cases who never develop symptoms) has been reported; however, most of the evidence is based on early data from China and has limitations (e.g., small number of cases, cases may have been presymptomatic).[67][68][69][70][71][72][73] Numerous studies have reported no evidence of asymptomatic transmission from carriers of SARS-CoV-2, including a large study in nearly 10 million residents in Wuhan.[74][75][76][77] Only 1% of people exposed to an asymptomatic index case became infected in one systematic review, suggesting limited infectiousness.[66]

    • Estimating the prevalence of asymptomatic cases in the population is difficult. A meta-analysis of over 130,000 people found that 21.7% remained asymptomatic throughout the course of the infection (after excluding presymptomatic cases). Subgroup analysis showed that the overall rate of asymptomatic infections was higher in pregnant women (48.8%) and children (32.1%). African studies reported the highest asymptomatic infection rate, while Asian studies reported the lowest.[78] 

    • Healthcare workers may play a role in asymptomatic transmission. About 7.6% of healthcare workers who worked in hospital units with infected patients tested positive for SARS-CoV-2 antibodies; however, only 58% of these workers reported prior symptoms.[79] 

    • Although there is some evidence that older children have higher rates of asymptomatic disease than infants <1 year of age, the majority of children present with symptomatic disease and do not appear to be silent spreaders of infection.[27]

Superspreading events

  • Superspreading events have been reported. These events are associated with explosive growth early in an outbreak and sustained transmission in later stages. Examples include church/religious gatherings, family or social gatherings, choir practices, indoor recreational sporting activities, nightclubs, restaurants, business conferences, and working in call centers. Widespread transmission has also been reported in long-term care facilities, homeless shelters, prisons, and meat and poultry processing facilities, as well as on board cruise ships.[80]

  • Limited transmission has been reported in childcare, school, and university settings.[81][82] There is limited high-quality evidence to quantify the extent of transmission in schools, or to compare it with community transmission. However, evidence suggests a lower overall infection attack rate in school staff (1.18%) compared with students (1.66%). Emerging evidence suggests the overall infection attack rate and SARS-CoV-2 positivity rate in school settings are low.[83] During periods of low incidence of infection in the local population in schools with nonpharmaceutical interventions in place, the risk to school staff is not generally higher than that of the general population and not comparable to other high-risk professions (e.g., healthcare workers). Studies reporting periods of high incidence of infection are limited, but do show a higher risk to school staff in these circumstances.[84] In one study, infection in close contacts in secondary schools and colleges in England was uncommon (approximately 2%).[85]

  • Some individuals are supershedders of virus, but the reasons underlying superspreader events are often more complex than just excess virus shedding and can include a variety of behavioral, host, and environmental factors.[86]

Viral transmission factors

  • Incubation period

    • The incubation period is estimated to be between 1 and 14 days, with a median of 5 to 7 days (9.6 days in children).[87][88][89]

  • Reproduction number (R₀)

    • A systematic review and analysis estimates the reproduction number to be 2.69 (based on published literature from January to August 2020).[90] The Centers for Disease Control and Prevention estimates the R₀ to be 2.5.[91]

  • Serial interval

    • The serial interval has been estimated to be approximately 5.45 days (range 4.2 to 6.7 days).[92] Emerging evidence does not support a significant difference in serial interval between the Delta and wild-type variants.[93]

  • Secondary attack rate

    • The pooled secondary attack rate among all close contacts of an index case has been estimated to be 7%, based on data from early in the pandemic.[94] The pooled rate varies between contact settings with an estimated rate of 18.9% to 21.1% in household settings (as of 17 June 2021), 3.6% in healthcare facilities, 1.2% to 5.9% in social settings, and 1.9% in workplaces. The rate is higher for symptomatic index cases compared with asymptomatic cases, and adults compared with children.[95][96][97] A higher overall secondary attack rate of 37.3% has been reported in household settings in a more recent meta-analysis due to circulating SARS-CoV-2 variants.[98] The overall pooled secondary attack rate in aged-care facilities was much higher: 42% among residents and 22% among staff.[99] The rate in children and young people was higher in household settings compared with school settings.[100] Secondary attack rates for SARS-CoV-2 variants may differ. The secondary attack rate for the Omicron variant is higher compared with other SARS-CoV-2 variants.[98][101] See the Classification section for more information.

  • Viral load

    • Viral load appears to be a leading driver of virus transmission; higher viral loads are associated with increased secondary attack rates and a higher risk of developing symptomatic disease.[102] Viral load is highest in the upper respiratory tract (nasopharynx and oropharynx) early in the course of infection (usually peaks in the first week of illness), and then increases in the lower respiratory tract (sputum). Viral load decreases after symptom onset. Patients with severe disease have higher viral loads compared with those with mild disease. Viral load in the upper respiratory tract is comparable in asymptomatic and symptomatic patients; however, most studies demonstrate faster viral clearance among asymptomatic people compared with symptomatic people.[103]

  • Viral shedding

    • The mean duration of viral shedding depends on the specimen: 17 days in the upper respiratory tract (maximum 83 days); 14.6 days in the lower respiratory tract (maximum 59 days); and 17.2 days in stool (maximum 126 days). Duration of shedding was longer in symptomatic patients compared with asymptomatic patients, and in patients with severe illness compared with those with nonsevere illness.[103] Immunocompromised patients may shed for at least 2 months.[104] There is no convincing evidence that duration of viral shedding correlates with duration of infectivity.[105] No viable virus has been isolated in patients with mild or moderate disease after 10 days of symptoms, or after 20 days in those with severe or critical disease, despite ongoing viral shedding.[52]

  • Human challenge study

    • The first human challenge study has been published on a preprint server (not peer reviewed). A total of 36 volunteers ages 18 to 29 years without evidence of previous infection or vaccination were inoculated with an intranasal dose of wild-type SARS-CoV-2 virus. Eighteen volunteers (53%) became infected. Most (89%) had either no or mild to moderate symptoms. In those infected, viral shedding became quantifiable in throat swabs from 40 hours. Viral load rose steeply and peaked at 5 days post-inoculation. Virus was first detected in the throat, but rose to significantly higher levels in the nose for up to 10 days post-inoculation.[106]

Pathophysiology

The exact pathophysiology remains unknown, partly due to the scarcity of postmortem studies.[107] The pathophysiology resembles that of other coronavirus infections. However, emerging evidence indicates that COVID-19 has distinctive pathophysiological features that set it apart from respiratory failure of other origins.[108]

SARS-CoV-2 attaches to the angiotensin-converting enzyme-2 (ACE2) receptor on target host cells, followed by internalization and replication of the virus. ACE2 receptors are highly expressed in the upper and lower respiratory tract cells, but are also expressed in myocardial cells, renal epithelial cells, enterocytes, and endothelial cells in multiple organs, which may explain the extrapulmonary manifestations associated with the disease.[109] Viral RNA has been identified in many organs in postmortem studies.[107]

[Figure caption and citation for the preceding image starts]: Multi-organ complications of COVID-19 and long COVID. The SARS-CoV-2 virus gains entry into the cells of multiple organs via the ACE2 receptorBMJ. 2021;374:n1648 [Citation ends].com.bmj.content.model.Caption@57f89113

The virus uses host transmembrane protease serine 2 (TMPRSS2) for viral spike protein priming and fusion of viral and host cell membranes.[110] The SARS-CoV-2 spike protein plays a key role in the recognition of the ACE2 receptor and cell membrane fusion process. A unique structural feature of the spike glycoprotein receptor-binding domain confers potentially higher binding affinity for ACE2 on host cells compared with SARS-CoV-1.[111] This furin-like cleavage site does not appear to exist in other coronaviruses.[112] The binding energy between the spike protein and ACE2 was highest for humans out of all species tested in one study, suggesting that the spike protein is uniquely evolved to bind to and infect human cells expressing ACE2.[113] Emerging evidence suggests that the spike protein alone may damage endothelial cells by downregulating ACE2 and consequently inhibiting mitochondrial function. Further research is required on whether the spike protein can by itself trigger cell signaling that could lead to various biologic processes.[114][115] SARS-CoV-2 variants may be more transmissible, at least in part, due to enhanced spike protein binding affinity for the ACE2 receptor.[116]

[Figure caption and citation for the preceding image starts]: Virus replication cycleBMJ. 2020;371:m3862 [Citation ends].com.bmj.content.model.Caption@6285ea4e

In addition to direct cytopathic viral injury, severe disease is frequently complicated by an infection-induced microangiopathy or hypercoagulable state that causes capillary, venous, and/or arterial thrombosis, which may lead to end-organ damage due to distant thrombotic or embolic disease. Widespread microthrombi have been identified in almost every organ in postmortem studies. The predominant pathologic findings in fatal cases were diffuse alveolar damage, coagulopathy, and hemodynamic compromise. Involvement of nonpulmonary organs was limited to mild parenchymal inflammation (e.g., myocarditis, hepatitis, encephalitis). Direct viral cytopathic injury of extrapulmonary organs in general was not regarded as the cause of organ failure.[109][107] Three major tissue phenotypes have emerged in postmortem lung tissue: a classic phenotype characterized by progressive diffuse alveolar damage; bronchopneumonia from secondary infection; and tissue thrombosis. These phenotypes are not mutually exclusive and may overlap.[117] SARS-CoV-2-induced endotheliitis may play a role in both the respiratory and nonrespiratory manifestations.[118]

SARS-CoV-2 placentitis is a distinct pathologic entity that has been reported in pregnant women, and is characterized by massive perivillous fibrin deposition and chronic histiocytic intervillositis. It is associated with increased risk of pregnancy loss.[119]

Genetic factors may play a role in susceptibility to infection and disease severity; however, further research is required.[120][121][122][123]

Classification

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variant classification

All viruses, including SARS-CoV-2, change over time. Most changes have little to no impact on the virus’ properties; however, some changes may affect virus transmission, disease severity, and performance of diagnostic tests, therapeutics, or vaccines.

These variants have been emerging and circulating around the world since the beginning of the pandemic, and are routinely monitored and classified as either variants under monitoring, variants of interest, or variants of concern by the World Health Organization (WHO).[2] These classification systems may vary between countries. For example, in the UK, variants are only classified as variants of concern by the UK Health Security Agency (UKHSA). The classifications of variants in monitoring and variants under investigation were used previously but have since been retired.[3] In the US, variants are classified by the Centers for Disease Control and Prevention (CDC) as variants being monitored, variants of interest, variants of concern, or variants of high consequence.[4] 

The WHO has assigned simple labels for key variants using letters of the Greek alphabet. This does not replace existing scientific names (e.g., Pango, Nextstrain, GISAID), which continue to be used in research.[2]

Variant of interest

  • The WHO defines a variant of interest as a variant with genetic changes that are predicted or known to affect virus characteristics such as transmissibility, disease severity, immune escape, or diagnostic or therapeutic escape; and that has been identified to cause significant community transmission or multiple case clusters, in multiple countries with increasing relative prevalence alongside increasing number of cases over time, or other apparent epidemiologic impacts to suggest an emerging risk to global public health.[2]

  • There are currently no circulating variants of interest, according to the WHO and the CDC. Previously circulating variants of interest include the Epsilon, Zeta, Eta, Theta, Iota, Kappa, Lambda, and Mu variants.[2][4]

Variant of concern

  • The WHO defines a variant of concern as a variant that has been demonstrated to be associated with one or more of the following changes at a degree of global public health significance:[2]

    • Increase in transmissibility or detrimental change in epidemiology

    • Increased virulence or change in clinical disease presentation

    • Decrease in effectiveness of public health and social measures, or available diagnostics, therapeutics, or vaccines.

  • Current variants of concern according to the WHO and the CDC are the Delta and Omicron variants. Previously circulating variants of concern include the Alpha, Beta, and Gamma variants.[2][4]

Alpha variant

The Alpha variant was previously classified as a variant of concern.[2][3][4]

  • Pango lineage: B.1.1.7.

  • Earliest documented samples: UK (September 2020).

  • Transmissibility: appears greater than the wild type virus.[3] 

  • Disease severity: appears to be associated with an increased risk of hospitalization and intensive care unit admission (suggesting more severe disease), but not mortality, compared with the wild-type virus, although data are conflicting. Not associated with changes in the symptoms reported or their duration.[5][6][7][8]

Beta variant

The Beta variant was previously classified as a variant of concern.[2][3][4]

  • Pango lineage: B.1.351.

  • Earliest documented samples: South Africa (May 2020).

  • Transmissibility: no more transmissible than Alpha.[3] 

  • Disease severity: insufficient information available.[3]

Gamma variant

The Gamma variant was previously classified as a variant of concern.[2][3][4]

  • Pango lineage: P.1.

  • Earliest documented samples: Brazil (November 2020).

  • Transmissibility: appears greater than the wild type virus.[3] 

  • Disease severity: insufficient information available.[3]

Delta variant

The Delta variant is currently classified as a variant of concern by the WHO, but is no longer classified as a variant of concern by the UKHSA and the CDC.[2][3][4]

  • Pango lineage: B.1.617.2 (including all AY sublineages).

  • Earliest documented samples: India (October 2020).

  • Transmissibility: appears greater than the wild type virus and Alpha. In the UK, the secondary attack rate among household contacts of cases that have not traveled was 11.3% (12.3% for the AY.4.2 sublineage based on limited data), compared with 10.2% with Alpha (as of 22 November 2021).[3] 

  • Disease severity: appears to be associated with an increased risk of hospitalization (suggesting more severe disease) compared with contemporaneous Alpha cases; however, there is a high level of uncertainty in these findings. The crude case fatality rate is estimated to be 0.53%, considerably less than the Alpha variant (as of 26 October 2021). There is no evidence that the AY.4.2 sublineage causes more severe disease than other Delta variants.[3] Observational evidence suggests that infection with Delta was associated with more severe disease compared with Beta.[9]

Omicron variant

The Omicron variant (Pango lineage B.1.1.529) is currently classified as a variant of concern by the WHO, the UKHSA, and the CDC.[2][3][4] Omicron is a highly divergent variant with a high number of mutations. There is no path of transmission linking Omicron to its predecessors (Alpha, Delta), and it has been estimated that its closest-known genetic ancestor likely dates back to some time after mid-2020.[10] Cases were first reported in South Africa in November 2021. The Omicron variant has become the dominant variant in many countries. 

The Omicron variant comprises several known lineages including the parental lineage B.1.1.529, and the descendent sublineages (or subvariants) BA.1, BA.1.1, BA.2, BA.3, BA.4, and BA.5. The BA.2 lineage has become the dominant subvariant in some countries, while the incidence of BA.4 and BA.5 lineages is currently increasing in some countries.

Transmissibility

  • Omicron has substantial growth advantage over Delta, and has rapidly replaced Delta globally. There is significant evidence that immune evasion contributes to its rapid spread, but it is unknown how much intrinsic increased transmissibility contributes and further research is required. The growth of the BA.2 lineage is increasing in some countries, but it is currently unclear what the drivers of transmission are.[11] Although data suggest that BA.2 is more transmissible than BA.1, the difference in transmissibility appears to be much smaller than the difference between BA.1 and Delta.[12] BA.2 has demonstrated an increased growth rate compared with BA.1.[3] There is preliminary evidence from South Africa that the BA.4 and BA.5 lineages have a growth advantage compared with BA.2.[3]

  • In the UK, the secondary attack rate was 11.4% for lineage BA.1 among household contacts (14.3% for lineage BA.2), and 4.6% for lineage BA.1 in nonhousehold contacts (6.1% for lineage BA.2) as of 21 February 2022. These rates decrease over time as more data is accumulated. Secondary attack rates for Alpha and Delta were 10.2% and 11.3% (see above).[3]

Disease severity

  • Data from South Africa, the UK, Canada, and Denmark suggest a reduced risk of hospitalization for Omicron compared with Delta. Epidemiologic trends continue to show a decoupling between cases and hospital admissions and deaths compared with previous variants, likely due to a lower intrinsic severity of the variant and preserved vaccine efficacy against severe disease.[11]

  • Data from the US also supports this trend, but acknowledges that a higher number of cases (5 times higher than the Delta wave) due to increased transmissibility of the variant is resulting in a record number of hospitalizations (1.8 times higher compared with the Delta wave).[13]

  • Observational data from long-term care facilities in England found that the risk of hospitalization and death was lower during the Omicron period compared with the pre-Omicron period.[14]

  • Evidence from animal studies suggests that Omicron does not infect cells deep in the lung as readily as it does cells in the upper airways.[15]

  • There is no reported difference in severity or hospitalization between BA.2 and BA.1.[3][12] There is insufficient data to determine whether BA.4 or BA.5 lineages cause more severe disease or an increased risk of hospitalization compared with BA.1 or BA.2.[3]

Vaccine efficacy

  • There is growing (not peer reviewed) evidence on vaccine effectiveness for Omicron, with data available from South Africa, the UK, the US, Canada, and Denmark. Early data suggests that the efficacy is significantly lower against Omicron infection and symptomatic disease compared with Delta, with homologous and heterologous booster doses increasing vaccine effectiveness. Vaccine efficacy estimates against severe outcomes (e.g., hospitalization) are lower for Omicron compared with Delta, but mostly remain >50% after the primary series and improve with a booster dose to >80%. However, it is uncertain how long this increased protection lasts for.[11]

  • Specific vaccines for the Omicron variant are currently in clinical trials, but have not shown promise in animal studies.[16][17]

  • There is no reported difference in vaccine efficacy between BA.2 and BA.1.[3] There is insufficient data to determine whether BA.4 or BA.5 lineages affect vaccine efficacy.[3]

Diagnosis

  • The diagnostic accuracy of polymerase chain reaction and rapid antigen tests does not appear to be influenced by the Omicron variant.[11]

Therapeutics

  • Treatments for severe or critical disease are expected to remain effective. However, monoclonal antibodies may have decreased neutralization against Omicron based on preliminary preprint (not peer reviewed) data. Monoclonal antibodies will need to be tested individually for their antigen binding and virus neutralization.[11][18]

  • Preclinical evidence suggests that casirivimab/imdevimab and bamlanivimab/etesevimab lack neutralization activity against the Omicron variant in vitro. Sotrovimab and bebtelovimab appear to retain activity against Omicron; however, sotrovimab is not active against the BA.2 subvariant.[19][20][21]

Reinfection

  • Increased risk of reinfection has been reported by South Africa, the UK, the US, Denmark, and Israel.[11][22]

Recombinant variants

Several recombinant SARS-CoV-2 variants have been identified over the course of the pandemic, and the vast majority do not confer any advantage to the virus and die out relatively quickly.[3]

Recombinant lineages involving the Omicron variant have been reported. A combination of the BA.1 omicron variant and the Delta variant (also known as BA.1 x AY.4 recombinant, XD and XF, or "deltacron") is being monitored, but there is currently limited information available. A recombinant of Omicron BA.1 and BA.2 (known as XE) has also been reported.[3]

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