Novel Mutations in the Non-Structure Protein 2 of SARS-CoV-2

Abstract

Introduction: Mutation in the genome of SARS-CoV-2 may play a role in immune evasion, pathogenicity, and speed of its transmission. Our investigation aimed to evaluate the mutations that exist in the NSP2. Materials and Method: RNA was extracted from nasopharyngeal swabs from 100 COVID-19 patients. RT-PCR was performed on all samples using NSP2-specific primers. Following gel electrophoresis, the bands were cut, purified, and sequenced using the Sanger method. After sequencing, 90 sequences could be used for further analysis. Bioinformatics analysis was conducted to investigate the effect of mutations on protein structure, stability, prediction of homology models, and phylogeny tree. Results: The patients' mean age was 51.08. The results revealed that 8 of the 17 NSP2 mutations (R207C, T224I, G262V, T265I, K337D, N348S, G392D, and I431M) were missense. One deletion was also found in NSP2. Among NSP2 missense mutations studied, K337D and G392D increased structural stability while the others decreased it. The homology-designed models demonstrated that the homologies were comparable to the sequences of the Wuhan-HU-1 virus. Conclusion: Our study suggested that the mutations K337D and G392D modulate the stability of NSP2, and tracking viral evolution should be implemented and vaccine development updated.