Coronavirus disease 2019

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"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)

 The coronavirus
Other names
 2019-nCoV acute respiratory disease

 Novel coronavirus pneumonia[1][2]

 Severe pneumonia with novel

pathogens[3]

False-color transmission electron microscope image of coronavirus

Pronunciation
/kəˈroʊnəˌvaɪrəs dɪˈziːz/
/ˌkoʊvɪdnaɪnˈtiːn, ˌkɒvɪd-/[4]

Specialty Infectious disease

Symptoms Fever, cough, fatigue, shortness of breath, loss of

taste or smell; sometimes no symptoms at all[5][6]
Complications Pneumonia, viral sepsis, acute respiratory distress
syndrome, kidney failure, cytokine release
syndrome

Usual onset 2–14 days (typically 5) from infection

Duration 5 days to 6+ months known

Causes Severe acute respiratory syndrome coronavirus

2 (SARS-CoV-2)

Diagnostic rRT-PCR testing, CT scan

method

Prevention Hand washing, face coverings, quarantine, social

distancing[7]

Treatment Symptomatic and supportive

Frequency 62,265,915[8] confirmed cases

Deaths 1,452,608[8]

Part of a series on the

COVID-19 pandemic

 SARS-CoV-2 (virus)
 COVID-19 (disease)

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 COVID-19 Portal

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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.
Common symptoms of COVID-19 include fever, cough, fatigue, breathing difficulties,
and loss of smell and taste. Symptoms begin one to fourteen days after exposure to
the virus. While most people have mild symptoms, some people develop acute
respiratory distress syndrome (ARDS). ARDS can be precipitated by cytokine storms,
[9]
 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. [10][11][12][13]
COVID-19 spreads via a number of means, primarily involving saliva and other bodily
fluids and excretions. These fluids can form small droplets and aerosols, which can
spread as an infected person breathes, coughs, sneezes, sings, or speaks. The virus
may also spread by direct contact and it is unknown how often it spreads
via fomites (contaminated surfaces).[14][15] The exact route of transmission is rarely proven
conclusively,[16] but infection mainly happens when people are near each other for long
enough, which is known as "close contact".[a] It can spread as early as two days before
infected persons show symptoms (presymptomatic), and from asymptomatic individuals.
People remain infectious for up to ten days in moderate cases, and two weeks in severe
cases. The standard diagnosis method is by real-time reverse transcription polymerase
chain reaction (rRT-PCR) from a nasopharyngeal swab.
Preventive measures include 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.
 There are currently no proven vaccines or specific treatments for COVID-19, though
several are in development. Management involves the treatment of
symptoms, supportive care, isolation, and experimental measures.

Contents

 1Signs and symptoms

 2Cause
o 2.1Transmission
o 2.2Virology
 3Pathophysiology
o 3.1Immunopathology
 4Diagnosis
o 4.1Pathology
 5Prevention
o 5.1Personal protective equipment
o 5.2Social distancing
o 5.3Hand-washing and hygiene
 6Management
 7Prognosis
o 7.1Comorbidities
o 7.2Complications
o 7.3Longer-term effects
o 7.4Immunity
 8History
o 8.1Possible earlier cases
 9Epidemiology
o 9.1Infection fatality rate
o 9.2Sex differences
o 9.3Ethnic differences
 10Name
 11Misinformation
 12Other animals
 13Research
o 13.1Vaccine
o 13.2Medications
o 13.3Cytokine storm
o 13.4Passive antibodies
o 13.5Laminoid antibodies
o 13.6BCG vaccine
 14See also
 15Notes
 16References
 17Further reading
 18External links
o 18.1Health agencies
o 18.2Directories
o 18.3Medical journals
o 18.4Treatment guidelines

Signs and symptoms

Main article: Symptoms of COVID-19

Symptoms of COVID-19[20]

Symptoms of COVID-19 are variable, but usually include fever and a cough. [21][22] 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%.[23]
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. [24] 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. [24][25]
Around one in five people are infected with the virus but do not develop noticeable symptoms at
any point in time.[26][27] These asymptomatic carriers tend not to get tested, and they can spread
the disease.[28][29][27] Other infected people will develop symptoms later (called pre-symptomatic) or
have very mild symptoms, and can also spread the virus.[30]

Cause
COVID-19 is caused by infection with the severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) virus strain.
Transmission
Main article: Transmission of COVID-19
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.[31][32]
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. 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. [32]
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.[33] This is more infectious than influenza, but less so than measles.[34] 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.

Virology
Main article: Severe acute respiratory syndrome coronavirus 2

Illustration of SARSr-CoV virion

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.[35] All
features of the novel SARS-CoV-2 virus occur in related coronaviruses in nature.[36]
Outside the human body, the virus is destroyed by household soap, which bursts
its protective bubble.[37]
SARS-CoV-2 is closely related to the original SARS-CoV.[38] 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).[39][40] 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. [41]

Pathophysiology
COVID-19 can affect the upper respiratory tract (sinuses, nose, and throat) and the
lower respiratory tract (windpipe and lungs).[42] 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.[43] The virus uses a special surface glycoprotein called a "spike" (peplomer) to
connect to ACE2 and enter the host cell.[44] 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,[45] though another view is that increasing
ACE2 using angiotensin II receptor blocker medications could be protective.[46] As the
alveolar disease progresses, respiratory failure might develop and death may follow. [47]
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. [48] 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. [49][50]
[51]
 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.[48]
The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in
the glandular cells of gastric, duodenal and rectal epithelium[52] as well
as endothelial cells and enterocytes of the small intestine.[53]
The virus can cause acute myocardial injury and chronic damage to the cardiovascular
system.[54] An acute cardiac injury was found in 12% of infected people admitted to the
hospital in Wuhan, China,[55] and is more frequent in severe disease.[56] 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. [54] ACE2 receptors are highly
expressed in the heart and are involved in heart function. [54][57] 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.[58] 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 blood
vessels within the pulmonary circulation has also been posited as a mechanism in
which oxygenation decreases alongside the presentation of viral pneumonia. [59]
Another common cause of death is complications related to the kidneys.[59] Early reports
show that up to 30% of hospitalized patients both in China and in New York have
experienced some injury to their kidneys, including some persons with no previous
kidney problems.[60]
Autopsies of people who died of COVID-19 have found diffuse alveolar damage (DAD),
and lymphocyte-containing inflammatory infiltrates within the lung. [61]
Immunopathology
Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the
respiratory tract, patients 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-γ inducible protein 10 (IP-
10), monocyte chemoattractant protein 1 (MCP-1), Macrophage inflammatory protein 1-
α (MIP-1α), and tumour necrosis factor-α (TNF-α) indicative of cytokine release
syndrome (CRS) suggest an underlying immunopathology.[55]
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.[62]
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 COVID-19 patients.[63] Lymphocytic
infiltrates have also been reported at autopsy. [61]