Sex-hormones and chromosomal roles in host cells toward males and females’ susceptibilities to SARS-CoV-2

Abstract

Due to the SARS-CoV-2 outbreak in Wuhan, there are rising global concerns due to increasing numbers of fatalities. SARS-CoV-2 is an enveloped, RNA virus and classified within beta coronaviruses which include MERS-CoV and SARS 2003. SARS-CoV-2 is transmitted between individuals through coughing, sneezing and contacting contaminated surfaces. Several studies indicate mortality rate and serious health outcomes among males than females. Biased males’ susceptibilities to COVID-19 have attributed to androgen regulation in host cells, poor expression of immune cells by the chromosomes. Additionally, males have high susceptibilities to comorbidities such as cardiovascular disease (CVD), hypertension and other symptoms such as respiratory disease which mostly ends with cytokines storm followed by death. In contrast, females survive from COVID-19 as oestrogen can protects the host through mediating immune cells into the host. Herein, published studies are critically analysed to determine why males have increased susceptibility to SARS-CoV2 relative to females. This includes the role of androgen receptors in induction of TMPRSS2 which is a part of SARS-CoV-2 entry. The alternative possibility that androgen mediated effects on immune cells increases susceptibility of males to SARS-CoV2 is also explored. Moreover, oestrogen roles in modulating immune cells may influence the susceptibility to SARS-CoV-2. The potential outcomes due to the variations of genes on sex-chromosomes are considered as impacting of immune cells and the host of SARS-CoV-2. Together, findings reported here indicate that androgen suppresses immunity in males and oestrogen augments the immune response in the female host. X- Linked genes protects the host and enhance immune cells.