Moreover, its genome comprises eight accessory proteins, namely, 3a, 3b, p6, 7a, 7b, 8b, 9b, and orf1 [12]. There is an ample amount of M glycoproteins in the SARS-CoV-2 genome that are responsible for the formation of virus particles and conduce virus assembly. It consists of a small -NH₂ terminal domain uncovered to the outside of the virion, three transmembrane domains and a much longer -COOH terminus that resides inside the virion [13]. The N protein is the only protein present in the nucleocapsid. Although it is predominantly intricated in various viral genome-related processes, particularly in virus assembly and the formation of nucleocapsids, it is also involved in replication-transcription complexes in infected cells and host cellular responses to viral infection [14, 15]. The smallest structural protein E is involved in various processes related to virus replication cycles, such as virus assembly, budding, envelope formation and pathogenesis [16]. The S protein mainly paves the way for the virus to bind and enter into the host cell membrane and results in infection. It consists of two subunits: the S1 subunit, which contains a signal peptide and the receptor-binding domain, and the S2 subunit, which contains conserved fusion proteins, a transmembrane domain and the cytoplasmic domain [17]. Hoffmann M. et al. demonstrated that the S protein of the virus, similar to SARS-CoV, has a strong propensity to bind with human angiotensin-converting enzyme 2 (ACE2) and targets ACE2 as a receptor for entry and undergoes structural changes to merge with the host [18]. However, SARS-CoV-2 is more dangerous because its affinity towards ACE2 is more than 10-fold higher than that of SARS-CoV [19]. Furthermore, novel coronavirus also utilizes the cellular protease TMPRSS2 (transmembrane protease, serine 2) because the S protein needs to be primed first before entering host cells. Generally, SARS-CoV-2 has less sequence homology with SARS-CoV (approximately 79%) and MERS-CoV (approximately 50%) [20].

Analysis of the genome sequence conducted by Lu R. et al. showed that its genome possesses 88% sequence homology with two bat coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21 [20]. All the genome sequencing data of SARS-CoV-2 from all over the world are being uploaded to the Global Initiative on Sharing All Influenza Data (GISAID), which facilitates the process of analyzing and understanding its genomic biology. A total of 71,000 genomic sequences were available on the website until 24 July 2020 [21]. Following the entry and denudation of the virus, its genome commences the transcription process followed by the translation process. The replication and transcription processes of coronaviruses occur in the cytoplasm. The mechanism of replication requires continuous RNA synthesis to determine whether transcription involves discontinuous synthesis [22]. These mechanisms are stimulated by the replication-transcription complex encoded by a 20 kb replicase gene and presumed to consist of as many as 16 viral proteins and different proteins involved with cellular processes [23]. The expression of the replicase gene is stimulated by the translation of the genomic RNA. After an individual is exposed to a potential virus source such as bat or pangolins or persons infected by the virus, human antigen processing cells (APCs) and virus-specific T lymphocytes counter the entry of the virus. APC, along with human MHC (major histocompatibility complex) molecules known as human leukocyte antigens (HLAs), responds to and mediates defense against novel coronavirus attacks [24]. Genetic polymorphism in HLA genes elucidates why individual susceptibility to novel coronavirus varies in a diverse population, and this difference among individual susceptibility is also promoted by genetic polymorphisms in mannose-binding lectin (MBL).