A Reviewof SARS-CoV-2Genetic and Structure: Hot Cellular Targets for Virus Entry

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) usesseveral molecules such as angiotensin-converting enzyme 2 (ACE2), cluster of differentiation 26 (CD26), Ezrin,and Neuropilin-1 (NRP-1)for viral entry. In this review,the entire structural and genomic combination and the mechanism of virus entry, are discussed. This study might be useful for further drug design studies.SARS-CoV-2 neutralizationallowsthe immune system to fight the virus before its entry. COVID-19 enters the host bloodstream by infecting endothelial cells via a cluster of differentiation 147 (CD147).SARS-CoV-2 not only usesACE2 for its entry but also affectsACE-2 and its enzymatic activity on AngII and bradykinin, it also imbalancesthe RAAS and bradykinin system and elevatesthe inflammation. High levels of bradykinin, cause nonproductive cough as the result of fluid extravasation and leukocyte recruitment to the lung.Accordingly,we suggest replicase transcriptase complex (RTC) and specific non-structural proteins (Nsps)such as Nsp7,8,Nsp10, Nsp12,and Nsp16 are perfect targets of study becauseRTC and Nspsare the golden elements in the maintenance of COVID-19 appearance and masking. Base on this evidence COVID-19 usesvarious receptors for its entry and it might block these receptors'activity to evade the immune system and spread to other cells.