Abstract
The pandemic caused by Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) has led to several concerns on male fertility. Nowadays, there are numerous unanswered questions, for example: is the virus present or not in the seminal fluid of infected subjects? Could the seminal fluid represent a way of sexual transmission for the virus? Why do men appear to be more susceptible than women? Several studies have been carried out to ascertain the presence of SARS−CoV−2 in the seminal fluid, with contrasting results; the expression of angiotensin-converting enzyme-2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) in the testes and in the male genital tract led to speculation about the possible presence of the virus in the seminal fluid. However, it was found that ACE2 and TMPRSS2, used by the virus to enter host cells, are expressed differently in certain testicle cells (stem germ cells, Leydig and Sertoli cells), yet the testicle cells in which ACE2 and TMPRSS2 molecules are simultaneously expressed are rare. This fact would suggest that the virus is not able to enter testicular cells, that it is not present in the seminal fluid and that it cannot infect male germ cells. However, the direct influence of SARS-CoV-2 on the testes is still to be evaluated, and recent results are very controversial. SARS-CoV-2 could enter the testicle using alternative paths and lead to alterations in testicular functionality. Another plausible consideration is that the COVID-19 disease could also indirectly cause alterations to testicular activity, since the fever and the cytokinic storm generated by the immune system can lead to damage of the testicular activity, consequently compromising male fertility. Although the literature provides controversial evidence, the purpose of this review is to lend a general overview about the state of the art. Despite the lack of studies, it would represent a starting point for further investigation about the effect of this coronavirus on male fertility.
Highlights
Multiple cases of severe pneumonia provoked by a β coronavirus termed Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) were reported in Wuhan, China, in December 2019 (Wu and McGoogan, 2020)
Given that clinical features of COVID-19 appear to be widely determined by the cells and tissues with co-expression of angiotensin-converting enzyme-2 (ACE2) and TMPRSS2 in their constituent cells, it is fitting to evaluate the activity of the virus on those male and female reproductive cells in which there is a co-expression of the two proteins, and if SARS-CoV-2 could have a negative impact on fertility
It is argued that testicular cells expressing both ACE2 and TMPRRS2 are rare, and this fact suggests that the virus may not harm male gametes
Summary
Multiple cases of severe pneumonia provoked by a β coronavirus termed Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) were reported in Wuhan, China, in December 2019 (Wu and McGoogan, 2020). Given that clinical features of COVID-19 appear to be widely determined by the cells and tissues with co-expression of ACE2 and TMPRSS2 in their constituent cells, it is fitting to evaluate the activity of the virus on those male and female reproductive cells in which there is a co-expression of the two proteins, and if SARS-CoV-2 could have a negative impact on fertility. As ACE2 is highly expressed in human testes, it is relevant to evaluate whether COVID-19 in males, via ACE2, might damage fertility. SARS-CoV-2 might indirectly compromise male fertility due to the fever produced and the infiltration of inflammatory molecules that damage Leydig cell functions. Apart from finding co-expression of ACE-2 and TMPRSS2 in sperm cells, there would seem to be evidence that COVID-19 could indirectly affect male fertility (Figure 2). Viruses able to cause viremia can pass the blood-testes barriers (e.g., anti-sperm antibodies) and can survive in the male reproductive system because the testicular immune response is related to sperm survival (Li et al, 2012; Salam and Horby, 2017)
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