Abstract

The current coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome virus 2 (SARS-CoV-2), has resulted in a major global pandemic, causing extreme morbidity and mortality. Few studies appear to suggest a significant impact of gender in morbidity and mortality, where men are reported at a higher risk than women. The infectivity, transmissibility, and varying degree of disease manifestation (mild, modest, and severe) in population studies reinforce the importance of a number of genetic and epigenetic factors, in the context of immune response and gender. The present review dwells on several contributing factors such as a stronger innate immune response, estrogen, angiotensin-converting enzyme 2 gene, and microbiota, which impart greater resistance to the SARS-CoV-2 infection and disease progression in women. In addition, the underlying importance of associated microbiota and certain environmental factors in gender-based disparity pertaining to the mortality and morbidity due to COVID-19 in women has also been addressed.

Highlights

  • The coronaviruses belong to the subfamily Coronavirinae, which cause respiratory and gastrointestinal infections [1]

  • Another study involving 1,019 COVID-19 patients revealed greater susceptibility of men compared to women to SARS-CoV-2, indicating that gender is as a risk factor for morbidity and mortality [6]

  • Menopause is an individual risk factor for COVID-19 as it causes a sudden reduction in estrogen levels which could minimize the risk difference between men and women, the case studies have revealed that the gender disparity still exists in elderly people

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Summary

Introduction

The coronaviruses belong to the subfamily Coronavirinae, which cause respiratory and gastrointestinal infections [1]. Another study involving 1,019 COVID-19 patients revealed greater susceptibility of men compared to women to SARS-CoV-2, indicating that gender is as a risk factor for morbidity and mortality [6]. The observed resistance to SARS-CoV-2 in women can be attributed to sex hormones, estrogen, which is known to enhance the immune activity of both B as well as Thelper cells [16].

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