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.