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Across the world so far, we have three truncated ORF3a proteins in SARS-CoV2 in India only.
Can you illuminate me how does a protein (here accessory protein of SARS-COV2) generally get such nonsense mutations and what happens to such proteins in protein-protein interactions?

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Your question couldn't be answered using just suggestions: we need proofs. In this study (from which I've quoted the sentence below) authors suggest an implication for inflammation response in patient.

Among the mutations, the ORF3a-Type-3 and ORF3a-Type-4 mutations are restricted to only the Indian patients based in Ahmedabad so far it is identified. These mutations (Q to H, D to Y, S to L) are located near TRAF, ion channel, and caveolin binding domains respectively, suggesting that Type-3 and Type-4 might have effect on NLRP3 inflammasome activation. This unique non-synonymous mutations might affect the virulence of the virus and this needs a special attention from pathogenesis perspective by the medical scientists

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