Covid-19 could cause male infertility by harming testicular cells that produce sperm, study claims

• Sperm production dropped to half its normal levels in male patients, study said
• More than one-in-ten sperm were also shown to be infected with the virus
• Covid-19 is able to infect the testes as they have ACE2 receptors like the lungs
• But to do this it must travel in the bloodstream which scientists say is unlikely
• The virus was found within the sperm of some 13% of screened male COVID-19 patients

Coronavirus may lead to infertility in men — even if they only suffer a mild form of the disease, a doctor has claimed.

Sperm counts of infected men halved 30 days after they were diagnosed with Covid-19, according to an Israeli study.

And Dr Dan Aderka, from the Sheba Medical Centre in Tel Aviv, also alleged sperm motility — or its ability to move by itself — was also hampered.

Scientists studying the effect of coronavirus on fertility have, however, made similar claims in the past.

But doctors insist reports of men having lower sperm counts are likely down to them having had a fever — a tell-tale symptom of coronavirus.

This, scientists say, makes it harder for the body to produce sperm. They also argue that production can bounce back after an infection has passed.

Professor Allan Pacey, an andrologist at the University of Sheffield and former chair of the British Fertility Society, told MailOnline he wouldn’t be surprised if coronavirus caused a temporary drop in sperm production.

But the jury is still out on whether or not the effect could be long-lasting, harming the fertility of men.

‘People who get coronavirus are probably quite unwell, even influenza will cause a decline in sperm count temporarily,’ he said.

‘The question is whether it is permanent and whether it is recoverable.’

Research is yet to reveal whether long-term damage can be caused to testicles by coronavirus, and it could take several years before scientists have the answer.

Previous research has indicated, however, that any damage caused to the testes by an infection is not long-term.

Professor Pacey cautioned against the finding in the new Israeli research that coronavirus can damage cells in the testicles responsible for making semen and the male hormone testosterone.

The doctors claimed that was the case after examining 12 men who had died from the virus. The Jerusalem Post did not expand on this observation in any greater clarity.

But Professor Pacey pointed out deceased patients would have been much sicker than the average infected man, and are likely to have been older, which would also cause a drop in the amount of sperm they produce.

‘There’s a bit of caution there because if you’re in ICU and you die you’re very sick, so we shouldn’t be surprised if there are changes in the testicles,’ he said. ‘Also, men who get very sick and are in ICU tend to be older.’

He also poured cold water on the finding that 13 per cent of sperm samples taken of infected men contained the virus, as reported by the Jerusalem Post.

‘I think that’s very difficult to prove and I’d like to read the paper,’ he said.

‘We’ve done work on other viruses, for example chlamydia, a bacteria that behaves like a virus, and it’s really difficult to prove if the virus is inside the sperm.’

It is unclear whether the virus could be transmitted through this route, but there is no evidence that it can be passed via semen or vaginal fluids.

The virus, scientifically called SARS-CoV-2, could be passed through kissing during sex, however.

Dr Aderka, from the Sheba Medical Center, who carried out the study, claimed that coronavirus could harm the testicles by binding to the ACE2 receptors on their cells.

These receptors, which act as a gateway for the virus to enter cells, are the same as those on the lungs, heart and intestines.

But scientists have previously pointed out that to do this the coronavirus would need to enter the bloodstream, and there’s no ‘clear mechanism’ for it to do this.

Professor Ian Jones, a virologist at the University of Reading, told MailOnline in April that coronaviruses do not generally travel in the blood.

‘The main site of virus replication is the respiratory tract,’ he said. ‘(Travel in the bloodstream) has been reported for the virus but it is not generally what coronaviruses do.’

Professor Pacey said he can’t see a mechanism whereby coronavirus would become blood-borne. ‘I may be wrong, this is a new virus, we’re learning all the time,’ he said.

When the team of Inventiva investigated this matter further, we found a research paper on NCBI website.

Multiple cases of pneumonia caused by a novel corona virus (SARS-COV2) have been reported in Wuhan city in China in December 2019. Since then, the infection has spread world-wide, leading to acute respiratory distress syndrome (SARS) named as “COVID-19” by the World Health Organization (WHO). On 11/03/2020, the disease has been declared as a global pandemic by WHO. Angiotensin converting enzymes 2 (ACE2) receptors play a key role in pathogenesis of COVID-19. Binding of SARS-COV2 virus to ACE2 receptors facilitate its cell entry and replication. Therefore, cells that show high level of ACE2 expression have the potential to be targeted and damaged by the virus. Multiple studies detected high ACE2 expression level in testicular cells, mainly in seminiferous duct cells, spermatogonia, Leydig cell and Sertoli cells. Based on the results of these studies, it is concluded that the testis could be a potential target for direct damage by SARS-COV2 virus. Another study performed following the outbreak of SARS-COV infection in 2002 showed that orchitis was a recognised complication of SARS. The main question is whether COVID-19 has the potential to cause testicular damage and infertility in male patients.

SARS-cov2 virus binds to ACE2 receptors and enter the cells to complete its replication cycle. This is considered as the main pathological mechanism of direct cell infection and damage by the virus. Therefore, cells with increased ACE2 expression are potential target of viral invasion. Among different body tissues, testis shows nearly the highest level of ACE2 mRNA and protein expression. At the level of testicular cells, four main cell types; seminiferous duct cells, spermatogonia, Leydig cells and Sertoli cells, show higher rate of ACE2 mRNA expression. If the virus causes damage to these cells, the process of spermatogenesis could be affected which might pose risk to male fertility. Interestingly, the testicular expression of ACE2 is age related. The highest expression recorded in patients aged 30, which is higher than those in their twenties, whereas 60-year-old patients show the lowest level of expression. This might indicate that young male patients are at higher risk of testicular damage by COVID-19 than older patients. In one study, examination of autopsy specimen of testis of six patients who died due to SARS-Cov infection in 2002 showed an evidence of orchitis. Histopathological examination revealed inflammatory infiltrates, mainly in seminiferous tubules. Immunohistochemistry showed IgG deposition mainly in seminiferous epithelium, interstitium, degenerated germ cells and Sertoli cells. These are almost the same cell types that show high ACE2 expression. Interestingly, in-situ hybridization does not detect viral genomic materials in the testicular tissue specimens. This indicates that testicular damage is due to inflammatory and immunological response rather than direct damage by the virus.

There is a theoretical possibility of testicular damage and subsequent infertility following COVID-19 infection. The possibility of testicular damage is caused by either direct viral invasion through binding of SARS-COV2 virus to ACE2 receptors or secondary to immunological and inflammatory response.

COVID-19 is harming the sperm of patients, even weeks after recovery, Israeli doctors have concluded, raising concerns that the disease could reduce fertility.

“Men who had the mild disease had a broadly normal sperm quality,” Prof. Dan Aderka of Sheba Medical Center, told The Times of Israel this week. “But those who had the disease in moderate or serious form often didn’t, even after recovery.

“These men had a reduction of around 50% on average of the number of sperm per milliliter, total volume of ejaculate, and motility of sperm,” he said. This figure reflects testing that was carried out around a month after diagnosis.