Abstract
The novel coronavirus disease 2019 (COVID-19) shows a wide spectrum of clinical presentations, severity, and fatality rates. The reason older patients and males show increased risk of severe disease and death remains uncertain. Sex hormones, such as estradiol, progesterone, and testosterone, might be implicated in the age-dependent and sex-specific severity of COVID-19. High testosterone levels could upregulate transmembrane serine protease 2 (TMPRSS2), facilitating the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into host cells via angiotensin-converting enzyme 2 (ACE2). Data from patients with prostate cancer treated with androgen-deprivation therapy seem to confirm this hypothesis. Clinical studies on TMPRSS2 inhibitors, such as camostat, nafamostat, and bromhexine, are ongoing. Antiandrogens, such as bicalutamide and enzalutamide, are also under investigation. Conversely, other studies suggest that the immune modulating properties of androgens could protect from the unfavorable cytokine storm, and that low testosterone levels might be associated with a worse prognosis in patients with COVID-19. Some evidence also supports the notion that estrogens and progesterone might exert a protective effect on females, through direct antiviral activity or immune-mediated mechanisms, thus explaining the higher COVID-19 severity in post-menopausal women. In this perspective, we discuss the available evidence on sex hormones and hormone therapy in patients infected with SARS-CoV-2, and we highlight the possible implications for cancer patients, who can receive hormonal therapies during their treatment plans.
Highlights
Lessons from 2002–2003 SARS-CoVFewobserved experimental data areinfected currently on SARS-CoV-2, experiences with
Chinese study showed that the ratio of testosterone to luteinizing hormone was significantly reduced in patients with COVID-19 [69]
These data support the notion that reduced testosterone levels in pre-existing or potentially virus-induced hypogonadism might be associated with an adverse prognosis in COVID-19 [70]
Summary
Fewobserved experimental data areinfected currently on SARS-CoV-2, experiences with. Weight authors that the viral spike protein induces to produce proinflammatory loss wasdemonstrated significantly reduced in mice treated with the ERmacrophages modulator tamoxifen compared with the cytokines (IL-6 and TNF-α) via activation of theor nuclear factor κBthe (NF-κB). This protein complex is control or ER antagonist. The authors demonstrated that the viral spike protein induces macrophages to produce proinflammatory cytokines (IL-6 and TNF-α) via activation of the nuclear factor κB (NF-κB) This protein complex is activated by angiotensin II to induce lung vasoconstriction and inflammation [38], whereas it is inhibited by androgens and estrogens. Similar in vitro antiviral effects on SARS-CoV and MERS-CoV have been described with protease inhibitors targeting the transmembrane serine protease 2 (TMPRSS2), an androgen-regulated gene commonly known in prostate cancer biology [42]
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