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TL;DR
The central result was that infection caused testicular tissue damage, including inflammation and reduced spermatogenic cells, with a correlation between higher viral load and lower gonadosomatic index.
Viruses · 19 authors, 10 centres
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The central result was that infection caused testicular tissue damage, including inflammation and reduced spermatogenic cells, with a correlation between higher viral load and lower gonadosomatic index.
The authors monitored infection kinetics, including fever, viremia, and immune response, and analyzed testicular outcomes at 21 days post-infection. Central results indicated that infection led to histopathological damage, including inflammatory infiltrate, tubular retraction, and a reduction in spermatogenic cells, alongside an increase in Sertoli cells. An inverse correlation was found between testicular viral load and the gonadosomatic index. Limitations include the use of sexually immature animals, a single collection time point of 21 days, and the inability to determine if damage is reversible or leads to permanent infertility.