Concise Update on Genomics of COVID-19: Approach to Its latest Mutations, Escalated Contagiousness, and Vaccine Resistance.

Abstract

The novel coronavirus disease 2019 (COVID-19) that started to invade the world from the Chinese fish market, causes an acute respiratory distress syndrome. COVID-19 is a dreadful infectious disease that surfaced only less than 8 months ago and caused the deadly COVID-19 pandemic. In this new species with a positive, single-strand RNA genome and a huge size, from the proteomics point view, there are no changes in sequences of amino acids in NSP7, 13, matrix, or envelope or other proteins including 8b and p6 and excluding NSP2 and NSP3. P6 is a multifunctional golgi–endoplasmic reticulum membrane-associated protein. This complex has a key duty to increase the replication rate of the virus and also causes intrinsic immune system responses by suppressing the signal transducer and activator of transcription factor 1 (STAT 1) translocated to the nucleus. Palmitoylated proteins elevate hydrophobicity which helps in membrane connection. Inside the N-linked glycosylation, moieties oligosaccharide is adhering to Asn-X-Ser/Thr canonical sequence. This helps for exact enfolding and carrying viral proteins by industriously using host's chaperon proteins including calreticulin and calnexin. 2B proteins encourage the internalization of major histocompatibility complex, class-I (MHC-I) protein and meanwhile inhibit their transfer to the surface of the cell as a recognition side. The deubiquitination of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) has precise modification apparatus in the posttranslational stage. In this article, we outlined the recent and up-to-date data on genomic and molecular structures, epidemiology, vaccine development, and, last but not least, the clinical features, diagnostics, and treatment of the novel coronavirus.