(A–D) Photomicrographs of testicular sections of animals from CG and IG submitted to CD68 (A, B) and CD163 (C, D) immunohistochemistry. Nuclear staining with hematoxylin. In (A) the interstitial tissue reveals a couple of CD68+ macrophages (arrows) compared to the excessive incidence of those cells noticed in IG (B). In (C, D), CD163-immunolabeled macrophages are seen (arrows); nonetheless, in (D), word the excessive incidence of those macrophages (arrows) compared to CG. (E, F) The variety of CD68 and CD163-immunolabeled macrophages per µm2 of interstitial tissue is increased in IG compared to CG. (G) Western blot evaluation of MIF ranges in testicular extracts reveals robust bands at 9KDa in IG compared to CG. β-tubulin sign is noticed in each teams. A big enhance in MIF ranges optical density (OD) is noticed within the animals from the IG when in comparison with CG. *p worth. Credit score: Frontiers in Mobile and An infection Microbiology (2025). DOI: 10.3389/fcimb.2025.1538461
The COVID-19 virus hijacks the equipment of testicular cells that produce the hormone testosterone with a view to replicate. It additionally appropriates the metabolic pathways of those cells and ldl cholesterol, a precursor of testosterone, thereby altering lipid metabolism for its formation.
This has been verified in a research carried out in Brazil by researchers from the Araraquara College of Dentistry at São Paulo State College (FOAr-UNESP), in partnership with the Ribeirão Preto College of Medication on the College of São Paulo (FMRP-USP), within the testicles of transgenic mice. The analysis is revealed within the journal Frontiers in Mobile and An infection Microbiology.
The research revealed the presence of SARS-CoV-2 particles in lipid inclusions and organelles accountable for testosterone manufacturing in Leydig cells for the primary time. As well as, the researchers described the mechanism by which the virus interferes with the functioning of those testicular cells. The invention helps clarify why male sufferers with extreme COVID-19 have decrease ranges of testosterone, and probably ldl cholesterol.
“After infecting the Leydig cells in the testicles, the virus uses lipid metabolism pathways and the cell structure to replicate, which impairs testosterone production. This happens because these cells, responsible for producing testosterone, express high concentrations of the ACE2 receptor, facilitating the entry of the virus,” explains Estela Sasso-Cerri, a professor at FOAr-UNESP who coordinated the research.
“In addition, the cells are responsible for storing cholesterol—essential for testosterone synthesis—and contain specialized cellular machinery for producing steroid hormones, making them a favorable target for infection.”
The analysis was carried out utilizing transgenic mice that had been developed in a laboratory and expressed the viral receptor ACE2. When contaminated, they develop COVID-19 in an analogous option to people, which permits for a greater understanding of the mechanism utilized by the virus.
“We observed that both in the transgenic mouse testicle and in the human testicle, there was an intense concentration of ACE2 in the same cell types. The result therefore validates the model used in the study and confirms that the testicle is a target organ for SARS-CoV-2,” says the researcher.
Within the experiment, the researchers discovered that SARS-CoV-2 can alter the lipid metabolism of Leydig cells. This happens as a result of the virus makes use of the ldl cholesterol saved by the cell for testosterone manufacturing to copy itself. Thus, regardless of the low testosterone ranges in contaminated Leydig cells, they had been stuffed with lipids as a result of the virus additionally induced a rise in ldl cholesterol internalization for its personal replication and formation.
Immunological character
The research additionally noticed adjustments within the practical profile of Leydig cells. After being contaminated by the virus, they ceased producing steroid hormones from ldl cholesterol and took on an immunological profile.
“Infection with SARS-CoV-2 also induced the Leydig cells to produce large amounts of pro-inflammatory cytokines, a process they don’t normally perform. This increase in cytokines may also have interfered with testosterone production, impairing this main function,” explains Salmo Azambuja de Oliveira, a scholar within the Structural and Practical Biology Program (BEF) on the Federal College of São Paulo (UNIFESP) and the primary writer of the research.
These findings advance our understanding of the mobile and molecular processes related to testicular endocrine dysfunction attributable to viral an infection.
“The outcomes corroborate the clinically noticed low levels of cholesterol in sufferers with extreme COVID-19 and will make clear males’s vulnerability to COVID-19 and their increased mortality price in comparison with ladies.
“The study also paves the way for developing markers that indicate the severity of COVID-19, as well as therapies for treating the disease based on [lipid-lowering] drugs that interfere with lipid metabolism and inhibit viral action,” says Sasso-Cerri.
Extra info:
Salmo Azambuja de Oliveira et al, SARS-CoV-2 exploits steroidogenic equipment, triggers lipid metabolism for viral replication and induces immune response in Leydig cells of K18-hACE2 mice, Frontiers in Mobile and An infection Microbiology (2025). DOI: 10.3389/fcimb.2025.1538461
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SARS-CoV-2 infects testicular cells and makes use of mobile equipment to copy, research finds (2025, August 21)
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