Immunity, Inflammation and Disease (Feb 2024)

Genetic determinants of SARS‐CoV‐2 and the clinical outcome of COVID‐19 in Southern Bangladesh

  • Md. Mahbub Hasan,
  • Chayan Kumar Saha,
  • H. M. Hamidullah Mehedi,
  • Kallyan Chakma,
  • Asma Salauddin,
  • Md. Shakhawat Hossain,
  • Farjana Sharmen,
  • S. M. Rafiqul Islam,
  • Afroza Akter Tanni,
  • Farhana Yasmin,
  • Al‐Shahriar Akash,
  • Mohammad Enayet Hossain,
  • Mojnu Miah,
  • Sanjoy Kanti Biswas,
  • Nahid Sultana,
  • Adnan Mannan

DOI
https://doi.org/10.1002/iid3.1171
Journal volume & issue
Vol. 12, no. 2
pp. n/a – n/a

Abstract

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Abstract Background The coronavirus disease 2019 (COVID‐19) pandemic has had a severe impact on population health. The genetic determinants of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) in southern Bangladesh are not well understood. Methods This study aimed to determine the genomic variation in SARS‐CoV‐2 genomes that have evolved over 2 years of the pandemic in southern Bangladesh and their association with disease outcomes and virulence of this virus. We investigated demographic variables, disease outcomes of COVID‐19 patients and genomic features of SARS‐CoV‐2. Results We observed that the disease severity was significantly higher in adults (85.3%) than in children (14.7%), because the expression of angiotensin‐converting enzyme‐2 (ACE‐2) diminishes with ageing that causes differences in innate and adaptive immunity. The clade GK (n = 66) was remarkable between June 2021 and January 2022. Because of the mutation burden, another clade, GRA started a newly separated clustering in December 2021. The burden was significantly higher in GRA (1.5‐fold) highlighted in mild symptoms of COVID‐19 patients than in other clades (GH, GK, and GR). Mutations were accumulated mainly in S (22.15 mutations per segment) and ORF1ab segments. Missense (67.5%) and synonymous (18.31%) mutations were highly noticed in adult patients with mild cases rather than severe cases, especially in ORF1ab segments. Moreover, we observed many unique mutations in S protein in mild cases compared to severe, and homology modeling revealed that those might cause more folding in the protein's alpha helix and beta sheets. Conclusion Our study identifies some risk factors such as age comorbidities (diabetes, hypertension, and renal disease) that are associated with severe COVID‐19, providing valuable insight regarding prioritizing vaccination for high‐risk individuals and allocating health care and resources. The findings of this work outlined the knowledge and mutational basis of SARS‐CoV‐2 for the next treatment steps. Further studies are needed to confirm the effects of structural and functional proteins of SARS‐CoV‐2 in detail for monitoring the emergence of new variants in future.

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