SARS-CoV-2: Epidemiology, Genome, Replication and Future Research

review article also discusses potential future research studies to elucidate critical information on SARS-CoV-2 cell entry mechanisms.

reveals that both the alphacoronaviruses and the betacoronaviruses originated in bats and jumped to humans via zoonotic transfer.
Civet cats (Paguma larvata) and dromedary camels (Camelus dromedarius) are the intermediate hosts for the original SARS and MERS, respectively [4]. The reservoir host for the latest coronavirus is unknown; however, amino acid analysis revealed that the spike glycoprotein for SARS-CoV-2 bears a 97% homology to pangolin coronaviruses, suggesting that it may be an intermediate host of the pandemic virus [5]. SARS-CoV-2 is a member of the betacoronaviruses. SARS-CoV-2, similar to other members of the family Coronaviridae, is a single-stranded (positive polarity) RNA enveloped virus [6].

Structure of SARS-CoV-2
A genetic comparison of SARS-CoV-1 and SARS-CoV-2 revealed that their genomes share 80% homology. Figure 1 shows the critical structural features of SARS-CoV-2. The four structural proteins are the membrane protein (M), an envelope protein (E), nucleocapsid protein (N), and the spike glycoprotein (S) (Figure 1) [1]. The membrane protein is a transmembrane protein that connects the helical nucleocapsid to the nuclear envelope through its C-terminal region and represents the most abundant structural polypeptide.
Envelope proteins maintain the lipid bilayer's stability and play a role during viral maturation and virion release. Nucleocapsid proteins bind to and protect the viral genome. The nucleocapsid protein and RNA complex are found in the viral core. Spike glycoproteins are responsible for host cell attachment and viral cellular entry. Unbound S molecules are proproteins that convert the S glycoprotein into its active fusogenic state [7]. The SARS-CoV-2 viral lipid envelope, like other enveloped viruses, is derived from host cell membranes. specific and largely contribute to the pathogenesis of the novel coronavirus. Both the 5′ end and the 3′ end contain untranslated regions. A cap structure and a poly (A) tail are found on the 5′ and 3′ end, respectively [9]. The presence of transcription regulatory sequences (TRS) in the genome facilitates transcription of the viral genome and the production of subgenomic mRNAs, which leads to the generation of structural and accessory proteins.

Cell Entry Research Studies
Investigating the fundamental virology of SARS-CoV-2, the invisible pathogenic culprit responsible for COVID-19, remains a high priority on the global scientific landscape. Future research projects that explore the underlying molecular mechanisms involved in viral entry into the intracellular host environment would greatly benefit the scientific community. Moreover, to gain a greater understanding of the specific molecular networks and signaling pathways associated with viral cell entry, microarray technology or next-generation RNA sequencing and bioinformatics analysis should be employed to analyze gene expression profiles during viral entry events in human cell types known to be susceptible to SARS-CoV-2 [11,12]. A detailed experimental examination of viral cell entry will enhance our comprehension of viral host range, viral replication, and immune evasion. It may also augment our knowledge of endocytosis and the cellular uptake of exogenous material across the Domain Eukarya. In the short term, an increased understanding of attachment, fusion, and penetration processes will help scientists to develop specific drugs to treat infections that work by disrupting essential replication mechanisms [13,14]. replication cycle. The aggressive study of the many biological processes employed by the virus will undoubtedly bring about the development of drugs to inhibit attachment, penetration, biosynthesis, maturation, and expulsion. The main strategy being employed regarding drug identification is therapeutic repurposing.
Using this strategy, scientists can determine the efficacy of already approved drugs to stop the growth of the virus in human cells.