infection could reduce male fertility

One year after the start of the pandemic, the effects of the coronavirus on the body are not yet all known. In recent months, researchers have found that the infection can spread to the brain, digestive system, and heart. And a recent study suggests that the virus may also impact male fertility by infecting the male reproductive system and reducing the quality of sperm. Results which, if confirmed, would impose a new axis of therapeutic monitoring of male patients.

COVID-19 can damage sperm quality and reduce fertility in men, according to a new study based on experimental evidence. Infection can cause increased sperm death, inflammation and oxidative stress, researchers report in the journal Reproduction. « These results provide the first direct experimental evidence that the male reproductive system could be targeted and damaged by COVID-19 », Write the authors.

Experts commenting on the research, however, said the ability of the virus to compromise fertility in men remains to be proven. Targeting the respiratory tract, intestinal system, heart and brain, the virus can also infect male reproductive organs, interfere with sperm development and disrupt reproductive hormones, previous studies have shown. The same receptors that the virus uses to access lung tissue are also found in the testes.

Inflammation, oxidative stress and lower sperm quality

But the effects of the virus on the ability of humans to reproduce have been unclear. Behzad Hajizadeh Maleki and Bakhtyar Tartibian from Justus-Liebig University in Germany, looked for biomarkers that could indicate a negative impact on fertility. Analysis performed at 10-day intervals for 60 days in 84 infected men was compared with data from 105 healthy men.

diagram impact infection coronavirus reproductive system
Potential pathways of SARS-CoV-2 affecting the male reproductive system. SARS-CoV-2 and elevated levels of cytokines can enter testicular tissues by hematogenous spread. LCs could be attacked by cytokines (or the SARS-CoV-2 virus), which would influence testosterone secretion and spermatogenesis. In addition, BTB which normally prevents viral invasion is susceptible to cytokine-mediated inflammation. The severe cytokine storm associated with SARS-CoV-2 infection could cause orchitis and epididymitis. Additional factors, including hyperpyrexia and inflammatory destruction of BTB, may increase the likelihood that the virus will cross BTB. In view of the low co-expression of ACE2 and TMPRSS2 in SCs and germ cells, further investigation will be needed to determine the possibility of sexual transmission. Sperm DNA fragmentation, epigenome alterations, and semen tsRNAs may be indirectly mediated by fever, inflammation, and psychological factors. Studies to investigate possible adverse effects on future pregnancies and offspring are also warranted. BV: blood vessel; Mφ: macrophage; DC: dendritic cell; SG: spermatogonia; PS: primary spermatocyte; SS: secondary spermatocyte; RS: round spermatid; ES: elongated spermatid.

In patients, sperm showed significant increases in markers of inflammation and oxidative stress, a chemical imbalance that can damage the body’s DNA and proteins. ” These effects on sperm are associated with inferior sperm quality and reduced fertility potential. Although these effects tended to improve over time, they remained significantly and abnormally higher in infected patients. », Explains Maleki.

The more severe the form of COVID-19, the greater the changes. The male reproductive system “should be considered a vulnerable pathway to infection and declared a high risk organ by the World Health Organization,” according to Maleki. Experts not involved in the study welcomed the research, but cautioned that more work was needed before any firm and rapid conclusions were drawn.

Results subject to caution

« Men should not be overly alarmed. There is currently no definitive evidence of lasting damage from COVID-19 to semen or male reproductive potential Says Alison Campbell, director of embryology at CARE Fertility Group in Great Britain. The results could have been skewed because the men recovering from COVID were treated with corticosteroids and antiviral therapy, while the control group was not.

Allan Pacey, a male reproductive medicine specialist at the University of Sheffield, raises a “strong caveat” about how the data has been interpreted. Some of the indicators of declining sperm quality could be due to factors other than COVID, noting that more men in the infected group were overweight.

Sources : Reproduction

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