4. Conclusion
A large number of different kinds of non-synonymous mutations in CoV-2
structural proteins, S (4725), E (259), M (627), and N (1631) are
present, covering the entire coding sequences, showing that antiviral
and vaccines efficacy might be compromised. This will make it difficult
to design particular drugs against structural targets. Further,
investigating the stability of these mutation on structural dynamics
will enhance our understanding about the viral pathogenicity and
transmission pattern. The variants may also affect drug interactions,
diagnostics, and virulence of CoV-2, especially the N which is being
considered as alternative to S. Geographic genome specific therapy might
be useful. Alternatively, immune boosting agents against CoV-2 might be
a more successful strategy in the current scenario.