Abstract
Coronavirus belongs to the family of Coronaviridae, comprising single-stranded, positive-sense RNA genome (+ ssRNA) of around 26 to 32 kilobases, and has been known to cause infection to a myriad of mammalian hosts, such as humans, cats, bats, civets, dogs, and camels with varied consequences in terms of death and debilitation. Strikingly, novel coronavirus (2019-nCoV), later renamed as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), and found to be the causative agent of coronavirus disease-19 (COVID-19), shows 88% of sequence identity with bat-SL-CoVZC45 and bat-SL-CoVZXC21, 79% with SARS-CoV and 50% with MERS-CoV, respectively. Despite key amino acid residual variability, there is an incredible structural similarity between the receptor binding domain (RBD) of spike protein (S) of SARS-CoV-2 and SARS-CoV. During infection, spike protein of SARS-CoV-2 compared to SARS-CoV displays 10–20 times greater affinity for its cognate host cell receptor, angiotensin-converting enzyme 2 (ACE2), leading proteolytic cleavage of S protein by transmembrane protease serine 2 (TMPRSS2). Following cellular entry, the ORF-1a and ORF-1ab, located downstream to 5′ end of + ssRNA genome, undergo translation, thereby forming two large polyproteins, pp1a and pp1ab. These polyproteins, following protease-induced cleavage and molecular assembly, form functional viral RNA polymerase, also referred to as replicase. Thereafter, uninterrupted orchestrated replication-transcription molecular events lead to the synthesis of multiple nested sets of subgenomic mRNAs (sgRNAs), which are finally translated to several structural and accessory proteins participating in structure formation and various molecular functions of virus, respectively. These multiple structural proteins assemble and encapsulate genomic RNA (gRNA), resulting in numerous viral progenies, which eventually exit the host cell, and spread infection to rest of the body. In this review, we primarily focus on genomic organization, structural and non-structural protein components, and potential prospective molecular targets for development of therapeutic drugs, convalescent plasm therapy, and a myriad of potential vaccines to tackle SARS-CoV-2 infection.
Highlights
In late December 2019, an acute case of respiratory diseases was reported in Wuhan, Hubei People’s Republic of China
We primarily focus on multiple features of SARS-CoV-2, including genomic organization, structural and non-structural protein components, and potential prospective molecular targets, against which either various FDA approved drugs used for other diseaseare being repurposed, or novel drugs under various phases of clinical trial are being tested
The SARS-CoV-2 is the causative pathogen for the current pandemic, and is evolving through recombination and mutation into several strains over a period of time
Summary
In late December 2019, an acute case of respiratory diseases was reported in Wuhan, Hubei People’s Republic of China. 2019-nCoV was renamed as SARS-CoV-2 by the International Committee on Taxonomy of Viruses (ICTV) owing to its genetic similarity to an earlier known coronavirus (SARS-CoV) [2]. This coronavirus-induced disease was officially announced as Coronavirus Disease-19 (COVID-19), and on 11 March 2020, World. SARS-CoV vis-à-vis MERS-related CoV and SARS-related CoV, indicating that it might have evolved from bats [7] This knowledge of similarities and differences of SARS-CoV-2 with viruses, which are known to have caused earlier outbreaks, may help in developing better understanding of etiology, and design curative strategy to tackle current pandemic. We focus on plasma therapy and antibody cocktail, as well as 13 approved/authorized vaccines being administered worldwide to tackle current pandemic
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