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Updated: Jul 13, 2025
Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry
Published on: December 28, 2021
SARS-CoV-2 replicates in the human testis with slow kinetics and has no major deleterious effects ex vivo
Dominique Mahé1, Salomé Bourgeau1,2,3, Janaina da Silva1
1Institut National de la Santé et de la Recherche Médicale, Ecole des Hautes Etudes en Santé Publique, Institut de recherche en santé, environnement et travail, Université de Rennes, UMR_S1085 , Rennes, France.
Importance:
SARS-CoV-2 is a new virus responsible for the Covid-19 pandemic. Although SARS-CoV-2 primarily affects the lungs, other organs are infected. Alterations of testosteronemia and spermatozoa motility in infected men have raised questions about testicular infection, along with high level in the testis of ACE2, the main receptor used by SARS-CoV-2 to enter host cells. Using an organotypic culture of human testis, we found that SARS-CoV-2 replicated with slow kinetics in the testis. The virus first targeted testosterone-producing Leydig cells and then germ-cell nursing Sertoli cells. After a peak followed by the upregulation of antiviral effectors, viral replication in the testis decreased and did not induce any major damage to the tissue. Altogether, our data show that SARS-CoV-2 replicates in the human testis to a limited extent and suggest that testicular damages in infected patients are more likely to result from systemic infection and inflammation than from viral replication in the testis.
Insights
The SARS-CoV-2 virus can infect the human testis, primarily targeting Leydig and Sertoli cells. However, viral replication is limited and unlikely to cause significant testicular damage.
Area of Science:
- Virology
- Reproductive Biology
- Pathology
Background:
- The COVID-19 pandemic, caused by SARS-CoV-2, has demonstrated multi-organ involvement.
- Alterations in testosterone levels and sperm motility in infected males suggest potential testicular impact.
- The presence of ACE2 receptors in the testis indicates a possible route for SARS-CoV-2 entry.
Purpose of the Study:
- To investigate the replication kinetics and cellular targets of SARS-CoV-2 within human testicular tissue.
- To determine the extent of viral replication and potential for testicular damage during SARS-CoV-2 infection.
Main Methods:
- Organotypic culture of human testis explants.
- Infection of testicular tissue with SARS-CoV-2.
- Analysis of viral replication, cellular tropism, and host antiviral responses.
Main Results:
- SARS-CoV-2 demonstrated slow replication kinetics in the human testis.
- The virus initially infected Leydig cells (testosterone production) and subsequently Sertoli cells (spermatogenesis support).
- Viral replication peaked, followed by an upregulation of antiviral effectors, leading to decreased viral load and minimal tissue damage.
Conclusions:
- SARS-CoV-2 can replicate in the human testis, but to a limited extent.
- Testicular damage observed in COVID-19 patients is more likely attributable to systemic inflammation and infection rather than direct viral replication within the testis.
