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).