Are sars-cov-2 infection and transmission study on humans rather than animal models and ethical?
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11 February 2020, the International Committee on Taxonomy of Viruses adopted the official name "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2).
The World Health Organization (WHO) has decided to name the disease caused by the novel coronavirus "COVID-19" and refers to the virus that causes it as the "COVID-19 virus." CO for corona, VI for virus, D for disease, and 19 for the year the outbreak was first recognized, late in 2019.
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SARS-CoV-2 is a beta-coronavirus closely related to SARS-CoV that caused a relatively small outbreak in the early 2000s.2,10 Similar to SARS-CoV, SARS-CoV-2 binds the ACE2 receptor and requires proteases such as serine TMPRSS2 to cleave the viral spike (S) protein required for SARS-CoV and SARS-CoV-211,12 cell entry.2 This step may be facilitated by endosomal proteases such as cathepsin-L and enhanced by the protein furin,13 the virus then enters the host cell by endocytosis.
A critical element of SARS-CoV-2 tropism in humans is the abundance of ACE2 in the upper respiratory tract (URT) especially the nasopharynx.14 The molecular configuration of the SARS-CoV-2 membrane binding component of the S protein binds with greater affinity to ACE2 than does SARS-CoV, which likely contributes to the higher infectivity of the former.15
The clinical course commences with an incubation period with a median of 5.1 days, with illness typically developing by 11 days.16 This phase is characterized by mild symptoms, with most people remaining asymptomatic and infection thought to be confined to the URT, although they are capable of transmitting infection. Symptoms when they do occur are typically acute viral respiratory illness with fever, cough, dyspnoea, fatigue, anosmia, myalgia and confusion.17
In ~80% of people, the course remains mild and disease does not extend to the lower respiratory tract (LRT). However, ~20% develop more severe symptoms, with diffuse widespread pneumonia, with 5% having severe gas exchange problems, acute lung injury and progress onto acute respiratory distress syndrome (ARDS).18,19 The clearest predictor of mortality is age, with the case fatality rate rising dramatically over 60 years of age.20 Other predisposing factors for heightened mortality are male sex, social deprivation, and chronic disease particularly chronic obstructive pulmonary disease (COPD), cardiovascular disease (CVD), obesity and diabetes.21
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