NOVEL MUTATIONS IN THE NON-STRUCTURE PROTEIN 2 OF SARS-CoV-2: Sequence analysis NSP2 of SARS-CoV-2
Year: 2023
Type: article
Study design: Observational Study
Abstract: Background: 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 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, prediction of homology models, phylogeny tree. Results: The patients' mean age wa Background: 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 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, prediction of homology models, 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 as K337D and G392D modulate the stability of nsp2 and tracking viral evolution should be implemented and vaccine development updated. s 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 as K337D and G392D modulate the stability of nsp2 and tracking viral evolution should be implemented and vaccine development updated.
Authors: Mohsen Nakhaei, Zohreh-Al-Sadat Ghoreshi, Mohammad Rezaei Zadeh Rukerd, Hedyeh Askarpour, Nasir
Language: English
Subfield: Infectious Diseases
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $647
OpenAlex ID: W4388049068
