When it comes to coronavirus and biology - sex matters
Scott M Nelson, MD PhD1,2
Martina Capuzzo3
Antonio La Marca, MD PhD3
1School of Medicine, University of Glasgow, UK
2NIHR Bristol Biomedical Research Centre, Bristol, UK
3Department of Medical and Surgical Sciences for
Children and Adults, University of Modena and Reggio Emilia, Modena,
Italy
Corresponding author:
Prof Scott M Nelson
University of Glasgow
New Lister Building
Glasgow Royal Infirmary
Glasgow G31 2ER, UK
+44 (0)141 201 8581
Scott.Nelson@glasgow.ac.uk
Word count: Text 1058
The male dominance in COVID19 morbidity and mortality figures has been a
consistent feature from the early reports emerging from Wuhan, to
national intensive care data, through to more recent comprehensive
population mortality data. Men are more than twice as likely to become
severely ill and require intensive care than women and at least twice as
likely to die, with further widening of the mortality discordance with
increasing age. These differences do not appear to be caused by
differential rates of infection, as equal numbers of men and women catch
SARS-CoV-2. Nor do they appear to reflect clustering of unhealthy
behaviour and comorbidities in men, as even after adjustment, male sex
is associated with a hazard ratio (HR) of death from COVID19 of HR 1.99,
(95%CI 1.88-2.10)1. These sex-specific differences in
severity and fatality were also observed for the 2002-2003 SARS-CoV
outbreak, and the Middle East respiratory syndrome
(MERS)-CoV2. So, what underlies this sex-specific
susceptibility difference for pathogenic coronaviruses? Several early
lifestyle theories were proposed, but rather more fundamental
sex-specific discordances in steroid hormones, x-linked genes and the
innate immune response are likely to underlie this sexual dimorphism.