Abstract
Although much has been published since the
first cases of COVID-19, there remain unanswered questions regarding
SARS-CoV-2 impact on testes and the potential consequences for
reproductive health. We investigated testicular alterations in deceased
COVID-19-patients, the precise location of the virus, its replicative
activity, and the molecules involved in the pathogenesis. We found that
SARS-CoV-2 testicular tropism is higher than previously thought and that
reliable viral detection in the testis requires sensitive nanosensoring
or RT-qPCR using a specific methodology. Macrophages and spermatogonial
cells are the main SARS-CoV-2 lodging sites and where new virions form
inside the Endoplasmic Reticulum Golgi Intermediate Complex. Moreover,
we showed infiltrative infected monocytes migrating into the testicular
parenchyma. SARS-CoV-2 maintains its replicative and infective abilities
long after the patient infection, suggesting that the testes may serve
as a viral sanctuary. Further, infected testes show thickening of the
tunica propria, germ cell apoptosis, Sertoli cell barrier loss, evident
hemorrhage, angiogenesis, Leydig cell inhibition, inflammation, and
fibrosis. Finally, our findings indicate that high angiotensin II levels
and activation of mast cells and macrophages may be critical for
testicular pathogenesis. Importantly, our data suggest that patients who become critically ill exhibit severe damages and may harbor the active virus in testes.
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