COVID-19

Coronavirus disease 2019 (COVID-19) is a

COVID‑19 transmission occurs when infectious particles are breathed in or come into contact with the eyes, nose, or mouth. The risk is highest when people are in close proximity, but small airborne particles containing the virus can remain suspended in the air and travel over longer distances, particularly indoors. Transmission can also occur when people touch their eyes, nose or mouth after touching surfaces or objects that have been contaminated by the virus. People remain contagious for up to 20 days and can spread the virus even if they do not develop symptoms.^[23]

Several COVID-19 vaccines have been approved and distributed in various countries, many of 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 drugs have been developed to inhibit the virus, the primary treatment is still symptomatic, managing the disease through supportive care, isolation, and experimental measures.

During the initial outbreak in

The

breathing difficulties.^[47] 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.^[47] 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.^[48][49][50]

Published data on the neuropathological changes related with COVID-19 have been limited and contentious, with neuropathological descriptions ranging from moderate to severe

hemorrhagic and hypoxia phenotypes, thrombotic consequences, changes in acute disseminated encephalomyelitis (ADEM-type), encephalitis and meningitis. Many COVID-19 patients with co-morbidities have hypoxia and have been in intensive care for varying lengths of time, confounding interpretation of the data.^[51]

Of people who show symptoms, 81% develop only mild to moderate symptoms (up to mild

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.^{[52][needs update}

]

At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time.^[53][54][55] These asymptomatic carriers tend not to get tested and can still spread the disease.^{[55][56][57][58]} Other infected people will develop symptoms later (called "pre-symptomatic") or have very mild symptoms and can also spread the virus.^[58]

As is common with infections, there is a delay, or incubation period, 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^[59] possibly being infectious on 1-4 of those days.^[60] Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.^[59][61]

Most people recover from the acute phase of the disease. However, some people continue to experience a range of effects, such as fatigue, for months, even after recovery.^[62] This is the result of a condition called long COVID, which can be described as a range of persistent symptoms that continue for weeks or months at a time.^[63] 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.^[64]

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.^[65]

Complications may include

Fungal infections such as aspergillosis, candidiasis, cryptococcosis and mucormycosis have been recorded in patients recovering from COVID‑19.^[85][86]

COVID‑19 is caused by infection with a strain of coronavirus known as "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2).^[87]

Outside the human body, the virus is destroyed by household soap which bursts its protective bubble.^[106] Hospital disinfectants, alcohols, heat, povidone-iodine, and ultraviolet-C (UV-C) irradiation are also effective disinfection methods for surfaces.^[107]

SARS-CoV-2 is closely related to the original

The many thousands of SARS-CoV-2 variants are grouped into either clades or lineages.^[113][114] 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".^[115] 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).^[116] The Pango tool groups variants into lineages, with many circulating lineages being classed under the B.1 lineage.^[114][117]

Several notable variants of SARS-CoV-2 emerged throughout 2020.^[118][119] Cluster 5 emerged among minks and mink farmers in Denmark.^[120] After strict quarantines and the slaughter of all the country's mink, the cluster was assessed to no longer be circulating among humans in Denmark as of 1 February 2021.^[121]

As of December 2021^[update], 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),^[122] and the Omicron variant (B.1.1.529), which had spread to 57 countries as of 7 December.^[123][124]

On December 19, 2023, the WHO declared that another distinctive variant, JN.1, had emerged as a "variant of interest". Though the WHO expected an increase in cases globally, particularly for countries entering winter, the overall global health risk was considered low.^[125][126]

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).

Following viral entry, COVID‑19 infects the ciliated epithelium of the nasopharynx and upper airways.[130] Autopsies of people who died of COVID‑19 have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung.^[131]

From the CT scans of COVID-19 infected lungs, white patches were observed containing fluid known as ground-glass opacity (GGO) or simply ground glass.^[132] This tended to correlate with the clear jelly liquid found in lung autopsies of people who died of COVID-19. One possibility addressed in medical research is that hyuralonic acid (HA) could be the leading factor for this observation of the clear jelly liquid found in the lungs, in what could be hyuralonic storm, in conjunction with cytokine storm.^[133]

One common symptom, loss of smell, results from

Research conducted when Alpha was the dominant variant has suggested COVID-19 may cause brain damage.^[140] Later research showed that all variants studied (including Omicron) killed brain cells, but the exact cells killed varied by variant.^[141] It is unknown if such damage is temporary or permanent.^[142][143] 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.^[144]

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium^[145] as well as endothelial cells and enterocytes of the small intestine.^[146]

The virus can cause acute myocardial injury and chronic damage to the cardiovascular system.^[147][148] An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China,^[149] and is more frequent in severe disease.^[150] 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.^[148] ACE2 receptors are highly expressed in the heart and are involved in heart function.^[148][151]

A high incidence of

Another common cause of death is complications related to the kidneys.^[153] 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.^[158]

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‑6, IL‑7, as well as the following suggest an underlying immunopathology:^[149]

• 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)
• Tumour necrosis factor (TNF‑α) indicative of cytokine release syndrome
  (CRS)

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.^[162]

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.^[163] Lymphocytic infiltrates have also been reported at autopsy.^[131]

Multiple viral and host factors affect the pathogenesis of the virus. The

• 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

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.[165] The N and E protein are accessory proteins that interfere with the host's immune response.^[165]

Human

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.^[167]

Among healthy adults not exposed to SARS-CoV-2, about 35% have

It is unknown whether different persons use similar antibody genes in response to COVID‑19.[169]

The severity of the inflammation can be attributed to the severity of what is known as the

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.[173]

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.^[173]
• 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.^[173]
• 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.^[173]

However, from the evidence base, it is difficult to conclude whether pregnant women are at increased risk of grave consequences of this virus.^[173]

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.^[173] For preterm birth, a 2023 review indicates that there appears to be a correlation with COVID-19.^[174]

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.^[175]

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.^[27][176] Along with laboratory testing, chest CT scans may be helpful to diagnose COVID‑19 in individuals with a high clinical suspicion of infection.^[177] Detection of a past infection is possible with serological tests, which detect antibodies produced by the body in response to the infection.^[27]

The standard methods of testing for presence of SARS-CoV-2 are nucleic acid tests,^[27][178] which detects the presence of viral RNA fragments.^[179] As these tests detect RNA but not infectious virus, its "ability to determine duration of infectivity of patients is limited".^[180] The test is typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab or sputum sample may also be used.^[181][182] Results are generally available within hours.^[27] The WHO has published several testing protocols for the disease.^[183]

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.^[184]

The University of Oxford's CEBM has pointed to mounting evidence^[185][186] 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"^[187] 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".^[188]

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.

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.^[194]

The main pathological findings at autopsy are:

• lung consolidation and pulmonary oedema^[131]
• Lung findings:
  • Minor serous exudation, minor fibrin exudation^[131]
  • Pulmonary oedema,
    lymphocytic infiltration and multinucleated giant cell formation^[131]
  • exudates. DAD is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxaemia.^[131]
  • Organisation of exudates in alveolar cavities and pulmonary interstitial fibrosis^[131]
  • Plasmocytosis in bronchoalveolar lavage (BAL)^[195]
• Blood and vessels:
  leukoerythroblastic reaction,^[197] endotheliitis,^[198] hemophagocytosis^[198]
• Heart:
  cardiac muscle cell necrosis^[198]
• Liver: microvesicular steatosis^[131]
• Nose: shedding of olfactory epithelium^[134]
• Brain: infarction^[198]
• Kidneys: acute tubular damage.^[198]
• Spleen: white pulp depletion.^[198]

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,^[200] 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.^[201][202]

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.^[203][204]

The first

This article needs attention from an expert in Mathematics. The specific problem is: Preprint cited by 2024 paper criticizes methodology of 2007 paper, updated 2023. See the talk page for details. WikiProject Mathematics may be able to help recruit an expert. (September 2024)

Sung Kim accompanied by local officials at the Presidential Palace

wearing face masks amid the COVID-19 pandemic

In community and healthcare settings, the use of face masks is intended as source control to limit transmission of the virus and for personal protection to prevent infection.^[229] Properly worn masks both limit the respiratory droplets and aerosols spread by infected individuals and help protect healthy individuals from infection.^[230][231]

Reviews of various kinds of scientific studies have concluded that masking is effective in protecting the individual against COVID-19.^{[230][232][233]} Various case-control and population-based studies have also shown that increased levels of masking in a community reduces the spread of SARS-CoV-2,^[232][233] though there is a paucity of evidence from randomized controlled trials (RCTs).^[234][235] Masks vary in how well they work. Fitted N95s outperform surgical masks,^[236][237] while cloth masks provide marginal protection.^[238][239]

During the public health emergency, governments widely recommended and mandated mask-wearing, and prominent national and intergovernmental health agencies and their leaders recommended the use of masks to reduce transmission, including the

European, and Chinese

Centers for Disease Control and Prevention.

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.^[240]

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.^[245]

Thorough hand hygiene after any cough or sneeze is required.

Social distancing (also known as physical distancing) includes

In 2020, outbreaks occurred in prisons due to crowding and an inability to enforce adequate social distancing.[251]^[252] 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.^[251]

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.^[253] Evidence indicates that contact with infected surfaces is not the main driver of COVID‑19,^{[254][255][256]} 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.^[257][258] 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.^[259][260]

The amount of time that the virus can survive depends significantly on the type of surface, the temperature, and the humidity.

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.[261]^[262] On some surfaces, including cotton fabric and copper, the virus usually dies after a few hours.^[261] The virus dies faster on porous surfaces than on non-porous surfaces due to capillary action within pores and faster aerosol droplet evaporation.^{[263][256][261]} 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.^[261]

The CDC says that in most situations, cleaning surfaces with soap or detergent, not disinfecting, is enough to reduce risk of transmission.^[256][264] 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.^[265] Surfaces may be decontaminated with the following:

• 62–71% ethanol
• 50–100%
  isopropanol
• 0.1% sodium hypochlorite
• 0.5% hydrogen peroxide
• 0.2–7.5% povidone-iodine
• 50–200 ppm hypochlorous acid

Other solutions, such as

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.[270] Additionally, symptom/exposure-based screening measures at borders may miss many positive cases.^[270] 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.^[270]

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

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.[310]^[311]

According to

It is also assumed that those that are immunocompromised are at higher risk of getting severely sick from SARS-CoV-2.[323] One research study that looked into the COVID‑19 infections in hospitalised kidney transplant recipients found a mortality rate of 11%.^[324]

Men with untreated hypogonadism were 2.4 times more likely than men with eugonadism to be hospitalised if they contracted COVID-19; Hypogonad men treated with testosterone were less likely to be hospitalised for COVID-19 than men who were not treated for hypogonadism.^[325]

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.^[332][333] Children are likely to have milder symptoms and are at lower risk of severe disease than adults.^[334] The CDC reports that in the US roughly a third of hospitalised children were admitted to the ICU,^[335] while a European multinational study of hospitalised children from June 2020, found that about 8% of children admitted to a hospital needed intensive care.^[336] 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.^[337][338]

Around 10% to 30% of non-hospitalised people with COVID-19 go on to develop long COVID. For those that do need hospitalisation, the incidence of long-term effects is over 50%.^[21] Long COVID is an often severe multisystem disease with a large set of symptoms. There are likely various, possibly coinciding, causes.^[21] Organ damage from the acute infection can explain a part of the symptoms, but long COVID is also observed in people where organ damage seems to be absent.^[339]

By a variety of mechanisms, the lungs are the organs most affected in COVID‑19.

The

As of August 2021, reinfection with COVID‑19 was possible but uncommon. The first case of reinfection was documented in August 2020.[349] A systematic review found 17 cases of confirmed reinfection in medical literature as of May 2021.^[349] With the Omicron variant, as of 2022, reinfections have become common, albeit it is unclear how common.^[350] COVID-19 reinfections are thought to likely be less severe than primary infections, especially if one was previously infected by the same variant.^{[350][additional citation(s) needed]}

Several measures are commonly used to quantify mortality.^[351] 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.^[352]

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.^{[353][354][355]} 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.^[356]

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 1.02% (6,881,955/676,609,955) as of 10 March 2023.^[357] The number varies by region.^[358][352]

• 
  Total confirmed cases over time
• 
  Total confirmed cases of COVID‑19 per million people^[359]
• 
  Total confirmed deaths over time
• 
  Total confirmed deaths due to COVID‑19 per million people^[360]

A key metric in gauging the severity of COVID‑19 is the

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.^[365] 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.^[365] These results were also highlighted in a December 2020 report issued by the WHO.^[366]

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.^[365]

At an early stage of the pandemic, the World Health Organization reported estimates of IFR between 0.3% and 1%.^[367][368] 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%.^[369][370] In August, the WHO found that studies incorporating data from broad serology testing in Europe showed IFR estimates converging at approximately 0.5–1%.^[371] 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).^[372] 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).^[373] Antibody testing in New York City suggested an IFR of ≈0.9%,^[374] and ≈1.4%.^[375] In Bergamo province, 0.6% of the population has died.^[376] 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.^[377]

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.^[356] Globally, men are more likely to be admitted to the ICU and more likely to die.^[379][380] 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).^[381]

The Chinese Center for Disease Control and Prevention reported the death rate was 2.8% for men and 1.7% for women.^[382] Later reviews in June 2020 indicated that there is no significant difference in susceptibility or in CFR between genders.^[383][384] 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.^[385] 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.^[356] 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.^[386] In Europe as of February 2020, 57% of the infected people were men and 72% of those died with COVID‑19 were men.^[387] As of April 2020, the US government is not tracking sex-related data of COVID‑19 infections.^[388] Research has shown that viral illnesses like Ebola, HIV, influenza and SARS affect men and women differently.^[388]

In the US, a greater proportion of deaths due to COVID‑19 have occurred among African Americans and other minority groups.

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.^[401] Evidence stemming from meta-analysis of several smaller research papers also suggests that smoking can be associated with worse outcomes.^[402][403] When someone with existing respiratory problems is infected with COVID‑19, they might be at greater risk for severe symptoms.^[401] COVID‑19 also poses a greater risk to people who misuse opioids and amphetamines, insofar as their drug use may have caused lung damage.^[404]

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.^[405]

This section needs to be updated. The reason given is: excessive detail about the very early pandemic while missing an overview of the later pandemic. Please help update this article to reflect recent events or newly available information. (July 2023)

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COVID-19 portal
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The virus is thought to be of natural animal origin, most likely through

The Wuhan Municipal Health Commission made the first public announcement of a pneumonia outbreak of unknown cause on 31 December, confirming 27 cases[446]^[447][448] – enough to trigger an investigation.^[449]

During the early stages of the outbreak, the number of cases doubled approximately every seven and a half days.

Italy had its first confirmed cases on 31 January 2020, two tourists from China.[455] Italy overtook China as the country with the most deaths on 19 March 2020.^[456] By 26 March the United States had overtaken China and Italy with the highest number of confirmed cases in the world.^[457] 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.^[458] Retesting of prior samples found a person in France who had the virus on 27 December 2019,^[459][460] and a person in the United States who died from the disease on 6 February 2020.^[461]

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.^[462] 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.^[463]

As of 1 October 2021^[update], Reuters reported that it had estimated the worldwide total number of deaths due to COVID‑19 to have exceeded five million.^[464]

The Public Health Emergency of International Concern for COVID-19 ended on May 5, 2023. By this time, everyday life in most countries had returned to how it was before the pandemic.^[465][466]

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.^{[467][468][469]}

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.^[377][470]

Humans appear to be capable of spreading the virus to some other animals,

The virus does not appear to be able to infect pigs, ducks, or chickens at all.^[475] Mice, rats, and rabbits, if they can be infected at all, are unlikely to be involved in spreading the virus.^[477]

Tigers and lions in zoos have become infected as a result of contact with infected humans.

International research on vaccines and medicines in COVID‑19 is underway by government organisations, academic groups, and industry researchers.

As of December 2020[update], hundreds of clinical trials have been undertaken, with research happening on every continent except Antarctica.^[483] As of November 2020^[update], more than 200 possible treatments have been studied in humans.^[484]

Repurposed

In March 2020, the World Health Organization (WHO) initiated the Solidarity trial to assess the treatment effects of some promising drugs:^[497][498]

• An experimental drug called remdesivir
• Anti-malarial drugs chloroquine and hydroxychloroquine
• Two
  interferon-beta

More than 300 active clinical trials are underway as of April 2020.^[78]

Research on the antimalarial drugs hydroxychloroquine and chloroquine showed that they were ineffective at best,^[499][500] and that they may reduce the antiviral activity of remdesivir.^[501] By May 2020^[update], France, Italy, and Belgium had banned the use of hydroxychloroquine as a COVID‑19 treatment.^[502]

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.^[503] 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.^[504][505] 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.^[506]

In September 2020, the WHO released updated guidance on using corticosteroids for COVID‑19.^[507][508] 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).^[507] The WHO suggests not to use corticosteroids in the treatment of people with non-severe COVID‑19 (conditional recommendation, based on low certainty evidence).^[507] The updated guidance was based on a meta-analysis of clinical trials of critically ill COVID‑19 patients.^[509][510]

In September 2020, the

In November 2020, the US Food and Drug Administration (FDA) issued an emergency use authorisation for the investigational monoclonal antibody therapy bamlanivimab for the treatment of mild-to-moderate COVID‑19.^[513] 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.^[513] This includes those who are 65 years of age or older, or who have chronic medical conditions.^[513]

In February 2021, the FDA issued an emergency use authorisation (EUA) for bamlanivimab and

In April 2021, the FDA revoked the emergency use authorisation (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.[515]

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.^[516] 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.^[517]

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.^[525]

Transferring purified and concentrated

• 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