Severe acute respiratory syndrome coronavirus 2 for physicians: Molecular characteristics and host immunity (Review)

Recently, severe acute respiratory syndrome (SARS) coronavirus (CoV) 2 (SARS‑CoV‑2)‑causing CoV disease 2019 (COVID‑19) emerged in China and has become a global pandemic. SARS‑CoV‑2 is a novel CoV originating from β‑CoVs. Major distinctions in the gene sequences between SARS‑CoV and SARS‑CoV‑2 include the spike gene, open reading frame (ORF) 3b and ORF 8. SARS‑CoV‑2 infection is initiated when the virus interacts with angiotensin‑converting 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 SARS‑CoV‑2 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 COVID‑19 remains to be elucidated. By studying other SARS and Middle East respiratory syndrome coronaviruses, it is hypothesized that patients with COVID‑19 may lack sufficient antiviral T‑cell 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.