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Virions are then able to enter and release their RNA into infected cells, where it is replicated and translated into new viral proteins. Once the virus has attached to the ACE2 receptors, the TMPRSS2 protease cleaves the spike protein to expose a fusion peptide. These cells also possess the TMPRSS2 serine protease, which is needed to cleave the spike protein and facilitate cell entry by SARS-CoV-2. These receptors are present on many types of cells throughout the body – including lungs, heart, liver, intestines, kidneys, testes, and blood vessels. Specifically, the RBD of the spike protein mediates recognition of the ACE2 receptor. The spike protein is functionally divided into the S1 domain, responsible for receptor binding, and the S2 domain, responsible for cell membrane fusion. SARS-CoV-2 virions attach to human cells with their densely glycosylated spike protein and bind with high affinity to the angiotensin-converting enzyme 2 (ACE2) receptor on human cells. The virion contains four structural proteins (spike, envelope, membrane, and nucleocapsid) and single-stranded RNA (see Figure 2).
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However, unlike bat coronaviruses, SARS-CoV-2 has a spike protein optimized for high-affinity binding to human ACE2 receptors and a functional polybasic cleavage site at the junction of the spike protein’s S1 and S2 subunits (a feature that enhances spike protein cleavage and increases viral infectivity). SARS-CoV-2 is a betacoronavirus (an enveloped, single-stranded RNA virus) that shares 79 percent of its genetic sequence with SARS-CoV and has 96 percent homology with the RATG13 coronavirus strain in bats. The virus was initially referred to as “novel coronavirus 2019” (2019-nCoV) by the WHO – but, on February 11, 2020, was given the official name of SARS-CoV-2 by the International Committee on Taxonomy of Viruses (2).
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By January 2, 2020, the full genome of a new coronavirus (SARS-CoV-2) had been sequenced by Shi Zhengli, a coronavirus expert at the Wuhan Institute of Virology just over a week later, the sequence had been published and the Chinese National Health Commission warned of its potential danger. On December 30, 2019, a cluster of patients with pneumonia of unknown etiology was observed in Wuhan, China, and reported to the World Health Organization (WHO)’s China bureau in Beijing. Almost all cases have been linked to people in or near the Arabian Peninsula. Explosive nosocomial transmission has been linked to single super-spreaders of infection. MERS is characterized by sporadic zoonotic transmission from camels and limited episodes of person-to-person transmission. Nine years later, MERS-CoV – which causes Middle Eastern Respiratory Syndrome (MERS) – emerged in Saudi Arabia. Although the virus infected 8,069 persons and caused 774 deaths, the last known case of SARS was detected in September 2003. SARS-CoV has a R 0 of 4, meaning that each infected person spreads the disease to an average of four others, and a case fatality rate of 9.5 percent. In SARS, peak viral shedding occurs approximately 10 days after the onset of illness, when many patients are hospitalized, which explains why health care professionals have a particularly high risk of becoming infected. Transmission occurred person-to-person through droplets produced by coughing or sneezing, via personal contact, and by touching contaminated surfaces. Early cases of SARS were linked to human and animal contact at live game markets. Bats are the natural hosts of SARS-CoV its intermediate hosts are palm civets and raccoon dogs. Severe Acute Respiratory Syndrome (SARS), caused by a coronavirus termed SARS-CoV, started in 2003 in Guangdong, China, and spread to many countries in southeast Asia, North America, Europe, and South Africa. In the past two decades, there have been three global coronavirus outbreaks (1).
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Six strains of coronavirus have infected humans, four of which are together responsible for about one-third of common colds.