PMC:7264098 / 7141-10365 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7264098","sourcedb":"PMC","sourceid":"7264098","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7264098","text":"Are We All Affected the Same Way by Coronavirus?\nCoronavirus-related infections can cause a variety of illnesses, which range from asymptomatic or mild such as a common cold, to severe including Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and now, COVID-19. The severity of these infections also varies widely between age-groups and different ethnic populations. Older people are at increased risk of acquiring the infection and are likely to develop severe symptoms culminating in death.\nInterestingly, there appears to also be gender disparity in the number of acquired cases of COVID-19 with higher percentage of men (~60%) than women being infected, as was first reported in China (Li et al., 2020); other countries have also reported higher case fatality rate (CFR) in men1. Similar observations were reported in a meta-analysis in relation to the MERS-CoV, where the number of infected men was double that of females (Badawi and Ryoo, 2016). Epidemiological studies tracing SARS-CoV showed that SARS-CoV was also more prevalent in men and associated with increased CFR (Karlberg, 2004). A number of proposed explanations for these gender differences in terms of both the incidence and CFR of MERS-CoV, SARS-CoV, and now COVID-19 infections, include past smoking history, work-environmental factors, different treatment regimens, and underlying biological differences such as gender-specific innate and adaptive immune responses (Karlberg, 2004; Klein and Flanagan, 2016). Clear biological differences between male and female gender include the presence of different steroid hormones and two instead of one X-chromosomes in females, which influences the number of immune response X-linked genes and genetic susceptibility to viral infections (Klein and Flanagan, 2016). Notably, experiments in mice, which seem to represent responses in humans well in this particular study, demonstrated greater susceptibility of male mice to enhanced viral titres, vascular leakage, and alveolar edema, compared to age-matched female mice infected with SARS-CoV (Channappanavar et al., 2017). This was attributed to differential immune cells and inflammatory responses including inflammatory monocyte macrophages, neutrophils, T- and B-cells. Notably, in this pre-clinical study, sex-dependent differences in susceptibility to SARS-CoV infection became more prominent with advancing age. In fact, once female mice underwent ovariectomy or were administered estrogen receptor antagonist treatment, the mortality associated with SARS-CoV infection increased, suggesting a protective effect of estrogen receptor signaling. Although experimental and mechanistic data is lacking in relation to the novel COVID-19 sex-specific differences, it is likely that similar factors and biological differences will be applicable as with MERS-CoV and SARS-CoV. It is important for these differences to be clearly elucidated particularly in the context of the treatment response, with certain treatments potentially being more effective in a specific gender group. Nevertheless, other confounding factors need to be taken into the account such as age, smoking, comorbidities and work-environmental 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