Abstract text
Since the very early days of the COVID-19 pandemic, concern has been raised about the possibility of damage to the male reproductive system in those men who are infected with SARS-CoV-2. This was first raised by the early observation (January 2020) that the route of infection was via the Angiotensin Converting Enzyme 2 (ACE-2) receptor present on host cells. ACE-2 was first described in the year 2000 and subsequently shown in 2004 to be selectively expressed in the Leydig cells of the adult testis. This opens up the possibility that although COVID-19 is primarily a respiratory infection, it may also infect the male reproductive system. The authors of several review articles have proposed that male fertility may be theoretically impacted by SARS-CoV-2 in a number of ways. This includes alteration of: (i) testicular architecture; (ii) reproductive hormone profiles (LH/FSH); (iii) spermatogenesis as evidenced by changes to ejaculate quality; (iv) sperm function (e.g., DNA damage); (v) sexual/erectile function; or a combination of all five. Clearly each of these individually may impact on the chance of pregnancy or live birth either in natural or medically assisted reproduction. There is also the possibility that SARS-CoV-2 may be transmitted sexually if sufficient numbers of SARS-CoV-2 are found in semen. Reassuringly, of 14 studies published to date, there is little evidence to suggest that SARS-CoV-2 is present in semen and so the possibility of sexual transmission in patient or donor samples can probably be discounted. However, there is currently an incomplete picture of whether semen quality is affected by SARS-CoV-2 infection as studies are often limited by the fact that no pre-infection control samples are available for direct comparison or they are too short to identify any long-term effects. Nevertheless, the few case-controlled studies published which compare semen quality infected with non-infected (control) individuals suggest that there may be a statistically significant alteration in sperm concentration and motility, although it is not clear whether this is linked to infection by the SARS-CoV-2 virus or simply a consequence of febrile illness and fever (or medication given to combat the infection). There is currently a lack of long-term data on any impact of COVID-19 on male reproductive hormones (although much speculation about the role that testosterone might play in the severity of disease). There are also emerging reports of increased risk of erectile dysfunction in men following SARS-CoV-2. In terms of birth rates, it is simply too early to tell whether these have been affected by the pandemic, given the possibility of lockdown affecting sexual behaviour in fertile couples and IVF clinic closures in infertile couples. In conclusion, although the COVID-19 pandemic has infected over 130 million people worldwide we still know too little about the impact of SARS-CoV-2 on the male reproductive system. Given the incidence of long-COVID, and the asymptomatic nature of the infection for some, it is important to commission and conduct long-term studies which can monitor the reproductive outcomes of young men who have survived a SARS-CoV-2 infection.
Comparison of Serum Inhibin B and Follicle-Stimulating Hormone (FSH) Level between Normal and Infertile Men in Yaoundé
