Variation in COVID-19 mortality rate across populations, polymorphism in genes, and gender-associated genetic patterns

Kousain Kousar; Hafiz Muhammad Imran Aziz; Tahir Ahmad; Rameesha Abid

doi:10.32593/jstmu/Vol5.Iss2.221

Kousain Kousar Department of Industrial Biotechnology, Atta ur Rahman School of Applied Biosciences, National University of Science and Technology, Islamabad, Pakistan
Hafiz Muhammad Imran Aziz Department of Pharmacology, Abwa Medical College, Faisalabad, Pakistan
Tahir Ahmad Department of Industrial Biotechnology, Atta ur Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad, Pakistan
Rameesha Abid Department of Microbiology, Quaid-i-Azam University, Islamabad, Pakistan

DOI: https://doi.org/10.32593/jstmu/Vol5.Iss2.221

Keywords: COVID-19, TMPRSS2, ACE2, Gene polymorphism, Blood group susceptibility, Gender

Abstract

A severe onset of COVID-19 leads to death due to respiratory failure and ARDS is the common finding of lung histopathology in different people with different comorbidities. It can invade the nervous system leading to the manifestation of neurological symptoms and brain damage including encephalitis and stroke. Genetic polymorphism, comorbidities, and gender differences is playing a pivotal role in conferring resistance and susceptibility to COVID-19. Despite almost the same ACE2 expression profile in males and females, males have shown a high mortality rate due to higher expression of TMPRSS2 (pivotal for S protein binding) as these genes are androgen responsive. While women have shown higher expression of ADAM17, ADAM10 genes are associated with the shedding of ACE2 receptors and are estrogen-responsive, leading to low levels of membrane-bound ACE2 which is indispensable for SARS-Cov2 entry into the cell. People with blood Groups A, and AB are comparatively more susceptible to COVID-19 than people with blood group O, the reason for the O group is attributed to the presence of Anti A antibodies.

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Author Biographies

Kousain Kousar, Department of Industrial Biotechnology, Atta ur Rahman School of Applied Biosciences, National University of Science and Technology, Islamabad, Pakistan

Research Assistant

Hafiz Muhammad Imran Aziz, Department of Pharmacology, Abwa Medical College, Faisalabad, Pakistan

Assistant Professor

Tahir Ahmad, Department of Industrial Biotechnology, Atta ur Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad, Pakistan

Associate Professor

Rameesha Abid, Department of Microbiology, Quaid-i-Azam University, Islamabad, Pakistan

PhD Scholar

References

Daniel G, Paola AR, Nancy G, Fernando SO, Beatriz A, Zulema R, et al. Epigenetic mechanisms and host factors impact ACE2 gene expression: Implications in COVID-19 susceptibility. Infect Genet Evol. 2022; 104:105357.

DOI: https://doi.org/10.1016/j.meegid.2022.105357.

Sargin G, Yavaşoğlu Sİ, Yavasoglu I. Is Coronavirus Disease 2019 (COVID-19) seen less in countries more exposed to Malaria? Med Hypotheses. 2020; 140:109756.

DOI: https://doi.org/10.1016/j.mehy.2020.109756

Darbani B. The expression and polymorphism of entry machinery for COVID-19 in human: juxtaposing population groups, gender, and different tissues. Int J Environ Res. Public Health. 2020; 17(10):3433.

DOI: https://doi.org/10.3390/ijerph17103433

Paniri A, Hosseini MM, Akhavan-Niaki H. First comprehensive computational analysis of functional consequences of TMPRSS2 SNPs in susceptibility to SARS-CoV-2 among different populations. J Biomol Struct Dyn. 2021; 39(10):3576-93.

DOI: https://doi.org/10.1080/07391102.2020.1767690

Schurz H, Salie M, Tromp G, Hoal EG, Kinnear CJ, Möller M. The X chromosome and sex-specific effects in infectious disease susceptibility. Hum Genomics. 2019; 13(1):1-2.

DOI: https://doi.org/10.1186/s40246-018-0185-z

Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020; 181(2):271-80.

DOI: https://doi.org/10.1016/j.cell.2020.02.052

Chen J, Jiang Q, Xia X, Liu K, Yu Z, Tao W, et al. Individual variation of the SARS‐CoV‐2 receptor ACE2 gene expression and regulation. Aging Cell. 2020; 19(7):e13168.

DOI: https://doi.org/10.1111/acel.13168

Clinckemalie L, Spans L, Dubois V, Laurent M, Helsen C, Joniau S, Claessens F. Androgen regulation of the TMPRSS2 gene and the effect of a SNP in an androgen response element. Mol Endocrinol. 2013; 27(12):2028-40.

DOI: https://doi.org/10.1210/me.2013-1098

Jia HP, Look DC, Tan P, Shi L, Hickey M, Gakhar L, et al. Ectodomain shedding of angiotensin converting enzyme 2 in human airway epithelia. Am J Physiol Lung Cell. 2009; 297(1):L84-96.

DOI: https://doi.org/10.1152/ajplung.00071.2009

Golinelli D, Boetto E, Maietti E, Fantini MP. The association between ABO blood group and SARS-CoV-2 infection: A meta-analysis. PLoS One. 2020; 18;15(9):e0239508.

DOI: https://doi.org/10.1371/journal.pone.0239508.

Sijjeel F, Khalid A, Khan MY, Khurshid R, Habiba UE, Majid H, et al. Prevalence of ABO and Rh Blood Groups and Their Association with Transfusion-Transmissible Infections (TTIs) among Blood Donors in Islamabad, Pakistan. BioScientific Rev. 2021; 3(4),13-26.

DOI: https://doi.org/10.32350/BSR.0304.02

Li J, Wang X, Chen J, Cai Y, Deng A, Yang M. Association between ABO blood groups and risk of SARS‐CoV‐2 pneumonia. Br J Haematol. 2020; 190(1): 24-27

DOI: https://doi.org/10.1111/bjh.16797

Cheng Y, Cheng G, Chui CH, Lau FY, Chan PK, Ng MH, et al. ABO blood group and susceptibility to severe acute respiratory syndrome. J Am Med Assoc 2005; 293(12):1447-51.

DOI: https://doi.org/10.1001/jama.293.12.1