Severe acute respiratory syndrome coronavirus 2 for physicians: Molecular characteristics and host immunity (Review).
2021
Recently, severe acute respiratory syndrome (SARS) coronavirus (CoV) 2 (SARSCoV2)causing CoV disease 2019 (COVID19) emerged in China and has become a global pandemic. SARSCoV2 is a novel CoV originating from sCoVs. Major distinctions in the gene sequences between SARSCoV and SARSCoV2 include the spike gene, open reading frame (ORF) 3b and ORF 8. SARSCoV2 infection is initiated when the virus interacts with angiotensinconverting enzyme 2 (ACE2) receptors on host cells. Through this mechanism, the virus infects the alveolar, esophageal epithelial, ileum, colon and other cells on which ACE2 is highly expressed, causing damage to target organs. To date, host innate immunity may be the only identified direct factor associated with viral replication. However, increased ACE2 expression may upregulate the viral load indirectly by increasing the baseline level of infectious virus particles. The peak viral load of SARSCoV2 is estimated to occur ~10 days following fever onset, causing patients in the acute stage to be the primary infection source. However, patients in the recovery stage or with occult infections can also be contagious. The host immune response in patients with COVID19 remains to be elucidated. By studying other SARS and Middle East respiratory syndrome coronaviruses, it is hypothesized that patients with COVID19 may lack sufficient antiviral Tcell responses, which consequently present with innate immune response disorders. This may to a certain degree explain why this type of CoV triggers severe inflammatory responses and immune damage and its associated complications.
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