Coronavirus disease 2019 (COVID-19)

Publish Date : 2020-12-20

Coronavirus disease 2019 (COVID-19)

Coronavirus disease 2019

"COVID" and "COVID-19" redirect here. For diseases caused by coronaviruses, see Coronavirus diseases. For the ongoing pandemic, see COVID-19 pandemic.

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first case was identified in Wuhan, China, in December 2019. It has since spread worldwide, leading to an ongoing pandemic.

Symptoms of COVID-19 are variable, but often include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. Symptoms begin one to fourteen days after exposure to the virus. Around one in five infected individuals do not develop any symptoms.[9] While most people have mild symptoms, some people develop acute respiratory distress syndrome (ARDS). ARDS can be precipitated by cytokine storms,[10] multi-organ failure, septic shock, and blood clots. Longer-term damage to organs (in particular, the lungs and heart) has been observed. There is concern about a significant number of patients who have recovered from the acute phase of the disease but continue to experience a range of effects—known as long COVID—for months afterwards. These effects include severe fatigue, memory loss and other cognitive issues, low-grade fever, muscle weakness, and breathlessness.[11][12][13][14]

The virus that causes COVID-19 spreads mainly when an infected person is in close contact[a] with another person.[18][19] Small droplets and aerosols containing the virus can spread from an infected person's nose and mouth as they breathe, cough, sneeze, sing, or speak. Other people are infected if the virus gets into their mouth, nose or eyes. The virus may also spread via contaminated surfaces, although this is not thought to be the main route of transmission.[19] The exact route of transmission is rarely proven conclusively,[20] but infection mainly happens when people are near each other for long enough. It can spread as early as two days before infected persons show symptoms, and from individuals who never experience symptoms. People remain infectious for up to ten days in moderate cases, and two weeks in severe cases. Various testing methods have been developed to diagnose the disease. The standard diagnosis method is by real-time reverse transcription polymerase chain reaction (rRT-PCR) from a nasopharyngeal swab.

Preventive measures include physical or social distancing, quarantining, ventilation of indoor spaces, covering coughs and sneezes, hand washing, and keeping unwashed hands away from the face. The use of face masks or coverings has been recommended in public settings to minimise the risk of transmissions. Several vaccines have been developed and various countries have initiated mass vaccination campaigns.

Although work is underway to develop drugs that inhibit the virus, the primary treatment is currently symptomatic. Management involves the treatment of symptoms, supportive care, isolation, and experimental measures.

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Signs and symptoms

Symptoms of COVID-19 are variable, ranging from mild symptoms to severe illness.[22][23] Common symptoms include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. People with the same infection may have different symptoms, and their symptoms may change over time. For example, one person may have a high fever, a cough, and fatigue, and another person may have a low fever at the start of the disease and develop difficulty breathing a week later. However, in people without prior ears, nose, and throat (ENT) disorders, loss of taste combined with loss of smell is associated with COVID-19 with a specificity of 95%.[24]

As is common with infections, there is a delay, known as the incubation period, between the moment a person first becomes infected and the appearance of the first symptoms. The median incubation period for COVID-19 is four to five days.[25] Most symptomatic people experience symptoms within two to seven days after exposure, and almost all symptomatic people will experience one or more symptoms before day twelve.[25][26]

Around one in five people are infected with the virus but do not develop noticeable symptoms at any point in time.[27][28][29] These asymptomatic carriers tend not to get tested, and they can spread the disease.[30][31][29] Other infected people will develop symptoms later (called pre-symptomatic) or have very mild symptoms, and can also spread the virus

COVID-19 spreads from person to person mainly through the respiratory route after an infected person coughs, sneezes, sings, talks or breathes. A new infection occurs when virus-containing particles exhaled by an infected person, either respiratory droplets or aerosols, get into the mouth, nose, or eyes of other people who are in close contact with the infected person.[33][34] During human-to-human transmission, an average 1000 infectious SARS-CoV-2 virions are thought to initiate a new infection.

The closer people interact, and the longer they interact, the more likely they are to transmit COVID-19. Closer distances can involve larger droplets (which fall to the ground) and aerosols, whereas longer distances only involve aerosols. The larger droplets may also evaporate into the aerosols (known as droplet nuclei). The relative importance of the larger droplets and the aerosols is not clear as of November 2020, however the virus is not known to transmit between rooms over long distances such as through air ducts. Airborne transmission is able to particularly occur indoors, in high risk locations, such as in restaurants, choirs, gyms, nightclubs, offices, and religious venues, often when they are crowded or less ventilated. It also occurs in healthcare settings, often when aerosol-generating medical procedures are performed on COVID-19 patients.

Social distancing and the wearing of cloth face masks, surgical masks, respirators, or other face coverings are controls for droplet transmission. Transmission may be decreased indoors with well maintained heating and ventilation systems to maintain good air circulation and increase the use of outdoor air.[34]

The number of people generally infected by one infected person varies; as of September 2020 it was estimated that one infected person will, on average, infect between two and three other people.[35] This is more infectious than influenza, but less so than measles.[36] It often spreads in clusters, where infections can be traced back to an index case or geographical location. There is a major role of "super-spreading events", where many people are infected by one person.

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.[37] All features of the novel SARS-CoV-2 virus occur in related coronaviruses in nature.[38]

Outside the human body, the virus is destroyed by household soap, which bursts its protective bubble.[39]

SARS-CoV-2 is closely related to the original SARS-CoV.[40] 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).[41][42] 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 98.6% similar to the M protein of bat SARS-CoV, maintains 98.2% homology with pangolin SARS-CoV, and has 90% homology with the M protein of SARS-CoV; whereas, the similarity is only 38% with the M protein of MERS-CoV. In silico analyses showed that the M protein of SARS-CoV-2 has a triple helix bundle, forms a single 3-transmembrane domain, and is homologous to the prokaryotic sugar transport protein SemiSWEET.[43]

SARS-CoV-2 has at least six main strains as of August 2020. The main strains are L, S, V, G, GR, and GH.[44] Strain L was the first strain, discovered in Wuhan in December 2019. As of August 2020, strain G (and related strains GR and GH) are the most widespread. Strains L and V are gradually disappearing. In addition, there are some infrequent mutations. Cluster 5 was a rare but virulent strain that was discovered in mink farms and mink farmers in Denmark. Denmark engaged in a mink euthanasia campaign[45], and is believed to have eradicated Cluster 5. The number of SARS-CoV-2 serotypes is currently unknown.


COVID-19 can affect the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs).[46] The lungs are the organs most affected by COVID-19 because the virus accesses host cells via the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant in type II alveolar cells of the lungs.[47] The virus uses a special surface glycoprotein called a "spike" (peplomer) to connect to ACE2 and enter the host cell.[48] The density of ACE2 in each tissue correlates with the severity of the disease in that tissue and some have suggested decreasing ACE2 activity might be protective,[49] though another view is that increasing ACE2 using angiotensin II receptor blocker medications could be protective.[50] As the alveolar disease progresses, respiratory failure might develop and death may follow.[51]

Whether SARS-CoV-2 is able to invade the nervous system remains unknown. The virus is not detected in the 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 patients who died from COVID-19, but these results need to be confirmed.[52] SARS-CoV-2 may cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. 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.[53][54][55] 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 by a "Trojan horse" mechanism.[52]

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium[56] as well as endothelial cells and enterocytes of the small intestine.[57]

The virus can cause acute myocardial injury and chronic damage to the cardiovascular system.[58] An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China,[59] and is more frequent in severe disease.[60] 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.[58] ACE2 receptors are highly expressed in the heart and are involved in heart function.[58][61] A high incidence of thrombosis and venous thromboembolism have been found in intensive care unit (ICU)-transferred patients with COVID-19 infections, and may be related to poor prognosis.[62] Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in patients infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blo

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