Sex-based dimorphism in the SARS-CoV2 virulence
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Whilst men and women have similar risk of getting SARS-CoV2 infection, the mortality rate for COVID-19 is almost the double in men as compared with women.

This sex-based difference of immune response reflects complex interactions between hormones, genes, environment and commensal microbiome.

Different features of the host, such as hormonal milieu, could also force pathogens to adapt some of their traits that ultimately leads to a different virulence in men and women.

The SARS CoV2 spike protein binds to ACEII receptor on pneumocytes II, and the human protease TMPRSS2 activates the spike protein and allows the viral entry, being paramount for viral spread and pathogenesis in the infected host.

The human TMPRSS2 gene promoter has an androgen response element (ARE) and androgens are positive regulators of its transcription.

Finally, according to an evolutionary theory postulating that pathogens evolve becoming less virulent in hosts in which both horizontal and vertical transmission routes can be exploited as compared with hosts in which only the horizontal route is available, sex-dimorphism of SARS-CoV2 virulence could further increase overtime as a consequence of evolutionary dynamics.

Taken together all these factors, in addition to some behavioural habits such as smoking that are more common in men, could explain the higher virulence of SARS-Cov2 observed in males.

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