tetano
Editor, Senior Moderator
Hum Fertil (Camb)
. 2021 Jan 13;1-6.
doi: 10.1080/14647273.2020.1867902. Online ahead of print.
COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms
Pallav Sengupta[SUP] 1 [/SUP], Sulagna Dutta[SUP] 2 [/SUP]
Affiliations
Abstract
Men show higher vulnerability to severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection (COVID-19) and present with depleted testosterone levels. Reports pertaining to high luteinizing hormone (LH), while diminished levels of in COVID-19 patients negate the hypothalamic-pituitary-testicular (HPT) axis mediated lowering of testosterone. Although not evidenced, high testicular expression of angiotensin-converting enzymes-2 (ACE2), that aids viral entry into cells, may suggest direct viral-testicular invasion. However, secondary inflammation and oxidative stress (OS), owing to SARS-CoV-2 infection, are more likely to impair steroidogenesis. Moreover, blockage of ACE2 aided angiotensin II into angiotensin (1-7) conversion may also affect testosterone synthesis. SARS-CoV-2, by mimicking adrenocorticotrophic (ACTH) hormones, may trigger host antibodies against the ACTH molecules to suppress host stress response. This commentary concisely presents the possible mechanisms by which SARS-CoV-2 infection may affect testosterone levels, which possibly result in compromised male reproductive health.
Keywords: COVID-19; SARS-CoV-2; inflammation; oxidative stress; testosterone.
. 2021 Jan 13;1-6.
doi: 10.1080/14647273.2020.1867902. Online ahead of print.
COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms
Pallav Sengupta[SUP] 1 [/SUP], Sulagna Dutta[SUP] 2 [/SUP]
Affiliations
- PMID: 33439057
- DOI: 10.1080/14647273.2020.1867902
Abstract
Men show higher vulnerability to severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection (COVID-19) and present with depleted testosterone levels. Reports pertaining to high luteinizing hormone (LH), while diminished levels of in COVID-19 patients negate the hypothalamic-pituitary-testicular (HPT) axis mediated lowering of testosterone. Although not evidenced, high testicular expression of angiotensin-converting enzymes-2 (ACE2), that aids viral entry into cells, may suggest direct viral-testicular invasion. However, secondary inflammation and oxidative stress (OS), owing to SARS-CoV-2 infection, are more likely to impair steroidogenesis. Moreover, blockage of ACE2 aided angiotensin II into angiotensin (1-7) conversion may also affect testosterone synthesis. SARS-CoV-2, by mimicking adrenocorticotrophic (ACTH) hormones, may trigger host antibodies against the ACTH molecules to suppress host stress response. This commentary concisely presents the possible mechanisms by which SARS-CoV-2 infection may affect testosterone levels, which possibly result in compromised male reproductive health.
Keywords: COVID-19; SARS-CoV-2; inflammation; oxidative stress; testosterone.