1.1 Coronaviruses (CoV)
CoV, of which there are four genera (alpha, beta, gamma, and delta), are a family of enveloped, positive-sense, single-stranded, and highly diverse RNA viruses.(Zhu et al. 2020) Three beta coronaviruses have been identified to cause severe respiratory illness in humans including SARS-CoV, and MERS-CoV (Middle Eastern respiratory syndrome CoV) and SARS-CoV-2.(McFadyen, Stevens, and Peter 2020) Although bats have been suggested to be the primary origin of SARS-CoV and SARS-CoV-2, the precise origin and mechanism by how SARS-CoV-2 manifested in humans is still unclear, with other possible hosts (such as the Malayan pangolins [Manis javanica ]), under investigation.(Lam et al. 2020)
SARS-CoV-2 is a single-stranded RNA virus and entry into host cells initiates with their transmembrane spike (S) glycoproteins (GP) encompassing S1 and S2 subunits. The S1 unit binds to host cell receptors, while the S2 subunit aids in viral and host cell fusion.(Walls et al. 2020) Like SARS-CoV, SARS-CoV-2 binds via the human angiotensin-converting enzyme 2 (ACE-2) receptor expressed on the endothelial surface.(Davidson, Wysocki, and Batlle 2020; Hoffmann et al. 2020) In comparison to SARS-CoV, SARS-CoV-2 has different amino acid residues within the receptor-binding domain (RBD) of the S protein and a polybasic furin cleavage site at the junction of S1 and S2. In addition, transmissibility and pathogenicity of SARS-CoV-2 is linked to cellular proteases such as furin and transmembrane protease serine 2 (TMPRSS-2).(McFadyen, Stevens, and Peter 2020) Although the functionality of these specific features of SARS-CoV-2 has yet to be fully elucidated, they could provide key information to the pro-thrombotic phenotype associated with SARS-CoV-2 and why patients with this specific Co-V have higher thrombosis rates vs. SARS-CoV and MERS-CoV infections.