Impaired spermatogenesis in COVID-19 patients

The first time that human coronaviruses caused by SARS-CoV were recognized as pathogens was in 2002, though these diseases weren’t called coronavirus yet then. Now, the world is again facing an imminent health threat from COVID-2019, caused by another novel coronavirus (SARS-CoV-2).

COVID-19 affects men more than women compared to its original form. SARS-CoV-2 can stay in human bodies longer than SARS-CoV. Its clinical characteristics are similar to SARS, but the male reproductive system is seriously affected by it. The male reproductive system is vulnerable to viral infections, and previous viral epidemics had documented varying impacts on male reproductive functions. There is substantial recorded evidence that the male reproductive system is vulnerable to viral infections like MUMPS, ZIKA, Hepatitis B virus (HBV), Hepatitis C Virus (HCV), Human Immunodeficiency Virus (HIV), Human papillomavirus (HPV), Herpes, EBOLA.

During active viremia, the possibility of viral access to the male reproductive tract is possible. Persistent high body temperatures, as such during viral infections, may tamper with the blood-testis barrier (BTB), the experimental evidence also suggests that even mild scrotal heat stress could lead to the BTB leakages and allowing the passage for macromolecular substances to the testis.

The current study is to identify significant impacts of SARS-CoV-2 on male reproductive health. In this study autopsy specimens of testis and epididymis obtained from patients who died from СОVID -19 and semen samples of recovering patients were investigated. Samples were subjected to histopathological studies and immunohistochemistry.

All participants have never suffered from infertility and have not been treated for it. The semen samples were tested for parameters and immune factors.

Histopathological assessments of testes and epididymis from the deceased revealed the presence of interstitial edema, congestion, red blood cell exudation, and thinning of the seminiferous tubules. Also, the number of apoptotic cells was high in the seminiferous tubules with massive destruction of spermatozoa. An increased concentration of CD3 + and CD68 + was found in the interstitial cells of the testicular tissue and the presence of IgG in the seminiferous tubules.
As for inpatients: their semen showed oligozoospermia and a significant increase in leukocytes in semen. Along with this, decreased sperm concentration was found.

Thus, we were able to observe the disruption of sperm production, which can be partially explained by the result of an increased immune response from the testes. In addition to this, autoimmune inflammation of the testicles occurred in some COVID-19 patients.

The current study observed a significant impact on male fertility and pathological changes in male gonads that might impact healthy reproductive well-being in male COVID-19 patients in the long-term. It is connected with impaired spermatogenesis with low sperm count, inflammatory responses in the testes and epididymis, and altered markers of seminal immunity indicating impaired immunity due to COVID-19 disease.

Impaired human spermatogenesis and delayed sperm maturation may be the result of an immune response in the testes and epididymis of COVID-19 patients, these factors are vital and determinant for healthy male fertility. It requires further care and support of males infected with SARS-CoV-2. It may indicate an increase in male infertility as a consequence.
This study was supported by the Ministry of Science and Technology of China Plan, Hubei Science and Technology Plan, National Key Research and Development Program of China, HUST COVID-19 Rapid Response Call, China and National Natural Science Foundation of China.