Abstract
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) has infected >235 million people and killed over 4.8 million individuals worldwide. Although vaccines have been developed for prophylactic management, there are no clinically proven antivirals to treat the viral infection. Continuous efforts are being made all over the world to develop effective drugs but these are being delayed by periodic outbreak of mutated SARS-CoV-2 and a lack of knowledge of molecular mechanisms underlying viral pathogenesis and post-infection complications. In this regard, the involvement of Annexin A2 (AnxA2), a lipid-raft related phospholipid-binding protein, in SARS-CoV-2 attachment, internalization, and replication has been discussed. In addition to the evidence from published literature, we have performed in silico docking of viral spike glycoprotein and RNA-dependent RNA polymerase with human AnxA2 to find the molecular interactions. Overall, this review provides the molecular insights into a potential role of AnxA2 in the SARS-CoV-2 pathogenesis and post-infection complications, especially thrombosis, cytokine storm, and insulin resistance.
Highlights
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), a single known causative agent of coronavirus disease 2019 (COVID-19), has infected more than 235 million people worldwide
It has recently been discovered that high levels of circulating angiotensin-converting enzyme 2 (ACE2) in severe COVID-19 patients are linked to a higher risk of serious cardiovascular events such heart failure and aortic stenosis [17]
In this review, we considered the evidence from the published literature and in silico docking analysis data to provide the molecular insights into the potential role of Annexin A2 (AnxA2) in the SARS-CoV-2 pathogenesis and post-infection complications, especially thrombosis, cytokine storm, and hyperglycemia
Summary
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), a single known causative agent of coronavirus disease 2019 (COVID-19), has infected more than 235 million people worldwide. There is a lack of knowledge about the molecular mechanisms involved in SARS-CoV-2 replication as well as its interaction with human host cells, except angiotensin-converting enzyme 2 (ACE2), a cell membrane receptor protein for the viral entry [10,11,12]. It has been observed that Sglycoprotein has a furin cleavage site at the S1/S2 boundary and mediates the cleavage through the type II transmembrane serine protease TMPRSS2 at S2 site to activate the membrane fusion [10] This fusion is a molecular mimic of SNARE-mediated cellular membrane fusion, and it generates a channel that allows the virus’s RNA and RNA-associated nucleocapsid proteins to gain access to the cytosol, causing infection [36]. In this review, we considered the evidence from the published literature and in silico docking analysis data to provide the molecular insights into the potential role of AnxA2 in the SARS-CoV-2 pathogenesis and post-infection complications, especially thrombosis, cytokine storm, and hyperglycemia
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