Potential mechanisms of SARS-CoV-2 action on male gonadal function and fertility: Current status and future prospects

Area of Science:

• Reproductive Endocrinology
• Virology
• Immunology

Background:

• The novel coronavirus (SARS-CoV-2) utilizes the angiotensin-converting enzyme 2 (ACE2) receptor for cell entry.
• ACE2 is expressed in various organs, including the testis, raising concerns about male reproductive system involvement.
• The long-term effects of SARS-CoV-2 on male fertility are not fully understood.

Purpose of the Study:

• To explore potential mechanisms by which SARS-CoV-2 may affect the male reproductive system.
• To investigate the role of the ACE2 axis in the testis.
• To examine hormonal alterations, anti-sperm antibody formation, and subsequent infertility in COVID-19 patients.

Main Methods:

• Review of existing literature on SARS-CoV-2, ACE2 expression, and male reproductive physiology.
• Analysis of potential pathways including ACE2 signaling, oxidative stress, and inflammation.
• Discussion of diagnostic markers for male fertility impairment.

Main Results:

• SARS-CoV-2 invasion of spermatogonia, Leydig cells, and Sertoli cells can disrupt testicular function.
• Infection may lead to sex hormonal alterations, impaired spermatogenesis, abnormal sperm parameters, and DNA fragmentation.
• Oxidative stress and inflammation are implicated in virus-induced testicular damage.

Conclusions:

• SARS-CoV-2 infection poses a risk to male fertility through direct testicular invasion and disruption of reproductive functions.
• Sperm DNA fragmentation index (DFI), alongside hormonal assays and semen analysis, should be considered for evaluating fertility in COVID-19 survivors.
• Further research is needed to fully elucidate the long-term reproductive consequences of SARS-CoV-2 infection.