Is SARS-COV-2 biased?

Wondering why some countries are more intensely hit by COVID-19 and some not? Could it be different strategies adopted by their government, quarantine, different genetic population herd immunity? Or could the answer lie within the virus itself?

Let`s look at it together!

A recent report published on 22 April 2020 (Emerging SARS-CoV-2 mutation hot spots include a novel RNA-dependent-RNA polymerase variant) tells us that differences in viral infection could be due to various reasons but it may also be dependent on the virus mutations and evolution over the course of time. Just like everyone else RNA viruses also want to survive but as we find various ways to tackle them, they also come up with new strategies to survive in the form of mutations. These mutations help them adapt to new environment and have been linked with their virulence, rate of evolution and their adaptation to new environment. This may be the cause of the virus moving so rapidly across the countries. These mutations can be beneficial to trace the evolution of the virus and their transmission. Moreover they can help design a cure. These mutations are a result of either the error incorporated by the replicating enzymes of the virus or the host enzymes, spontaneous nucleic acid damages due to physical and chemical mutagens or recombination events. Mutation rates are modulated by other factors such as determinants of the template sequence and structure involved in viral replication.

The SARS-CoV-2 just like the other RNA viruses have RNA-dependent RNA polymerases (RdRps) which help in replication and transcription of the genome. The RdRps in coronaviruses are controlled by non-structural proteins (nsps). nsp12 present in SARS-CoV-2 and SARS-CoV share a high homology pointing towards the similarity of their mechanism of action and function. A homologue of nsp14 present in SARS-COV is found in SARS-CoV-2 too. The nsp14 of SARS-CoV has exonuclease activity which when targeted resulted in significant reduction in replication fidelity. Also a supercomplex found in SARS-CoV formed with RdRp along with nsp7 and nsp8 have been identified in SARS-CoV-2. This point towards the conserved replication machinery coronaviruses have acquired over the years, which needs to be targeted. There are wide variety of antiviral drugs under development that target RdRps as primary targets, however the docking site is not located close to the catalytic domain of the RdRp. This may give rise to naturally occurring mutations which can in turn lead to drug resistance phenomena, and the binding affinity of the drug to the RdRp could be significantly lost.

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