The Blog

2020-

2020-12-15 d
SYNTHETIC VIRUS COUNTERS MALE FERTILITY
"Spermatogenesis damage was observed in COVID-19 patients."

Pathological and molecular examinations of postmortem testis biopsies reveal SARS-CoV-2 infection in the testis and spermatogenesis damage in COVID-19 patients

In late December 2019, the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), was identified in Wuhan, China, and the ensuing pandemic has led to more than 50 million infected individuals and more than one million deaths by November 10, 2020 (https://covid19.who.int/). Pathologic investigations of autopsy tissue have focused primarily on the lung, heart, and kidney, whereas morphologic data on testis injury and the effects of SARS-CoV-2 infection on spermatogenesis are limited. Although two groups did not detect SARS-CoV-2 in the semen or testes of recovered COVID-19 patients,1,2 another group confirmed SARS-CoV-2 in the semen of patients.3 Therefore, it is currently unknown whether SARS-CoV-2 infection impacts spermatogenesis and male fertility. In the present study, we evaluated the effects of SARS-CoV-2 infection on spermatogenesis by examining the pathophysiology and molecular features of testes obtained from five male COVID-19 patients at autopsy.

... Spermatogenesis damage was observed in COVID-19 patients. (a) Histological analyses of testicular sections from COVID-19 patients (patients 1, 2, 3, 4, and 5) and uninfected controls (controls 1, 2, and 3) showing numerous degenerated germ cells sloughing into the lumen of the seminiferous tubules of all five COVID-19 patients; normal spermatogenesis was observed in control patients.

... SARS-CoV-2 can induce cellular and humoral immune changes and destroy antiviral immunity at an early stage in COVID-19 patients.4,5 To ascertain how male GC loss occurs in patients with COVID-19, we investigated the presence of apoptosis and inflammatory reactions in the testicular cells. TUNEL assays revealed that the number of apoptotic cells in COVID-19 testes was significantly higher than that in control testes (Supplementary Fig.Â S1e, f), raising the possibility that SARS-CoV-2 damages the immune privilege and innate immune homeostasis of the testis.

... The SARS-CoV-2 spike protein binds to the angiotensin-converting enzyme 2 (ACE2) receptor through its receptor-binding domain. In turn, ACE2 employs the serine protease TMPRSS2 to activate the S protein, allowing its HR1 and HR2 domains to interact with each other and form a six-helical bundle (6-HB) to mediate membrane fusion between the virus and a target cell.7,8,9 Therefore, we next examined the protein and mRNA levels of ACE2 and TMPRSS2 in the testes. Although both ACE2 and TMPRSS2 proteins were predominantly expressed in the cytoplasm and membrane of spermatocytes, spermatids, and Sertoli cells in control testes, elevated ACE2 and TMPRSS2 levels were observed in the seminiferous tubules of all patients with COVID-19.

... Collectively, our findings provide direct evidence that SARS-CoV-2 can infect the testis and GCs, indicating the potential impact of the COVID-19 pandemic on spermatogenesis and male fertility. Nevertheless, further study is essential to reveal the underlying mechanism of SARS-CoV-2 infection of testicular cells and the correlation of testis infection with the clinical course of COVID-19. (read more)

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