ArticleResearch square2026
SARS-CoV-2 infection reduces the number of spermatogonial stem cells and dysregulates the transcriptional landscape of the human testis.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
SARS-CoV-2 coronavirus emerged in 2019, leading to the Coronavirus disease 2019 (COVID-19). Expression of viral entry factors such as ACE2 and TMPRSS2 is higher in the testis, particularly in Sertoli cells, Leydig cells, and spermatogonia. To understand COVID-19's impact on testicular cell populations and gene expression, we analyzed testicular tissue samples from 28 COVID-19 patients and compared them with 23 non-diseased controls. COVID-19 samples showed increased immune cell infiltration, thrombosis, and reduced numbers of testicular cells. There was a significant decrease in Sertoli cells and spermatogonial stem cells (SSC) among COVID-19 patients, associated with high levels of DNA damage and apoptosis in these cell types. To explore the pathways through which the virus affects testicular function, we profiled 112,657 single-nucleus transcriptomes from the testes of 4 COVID-19 patients and 4 controls. We found that COVID-19 infection alters multiple transcriptome clusters and induces a new COVID-19-specific cluster. To confirm that these transcriptome changes are COVID-19-specific, we compared our results with those from the brains of patients with COVID-19 and influenza. We observed an average of 144 dysregulated genes unique to COVID-19, regardless of tissue type. Lastly, we examined whether the SSC phenotype seen in fatal COVID-19 cases was also present in recovered patients. Indeed, recovered patients also exhibited high DNA damage and a reduced SSC population at 3, 6, and 12 months post-infection. Additionally, embryos derived from recovered patients' sperm showed lower fertilization rates compared to control-derived embryos and fewer live births. Overall, our findings demonstrate that SARS-CoV-2 disrupts spermatogenesis, alters the transcriptional landscape, and affects human testicular architecture and function well after the acute phase of infection, with potential long-term consequences for male fertility.
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