The COVVI-19 virus diverts the machinery from testicular cells that produce hormonal testosterone in order to reproduce. He also appropriates the metabolic pathways of these cells and cholesterol, a precursor of testosterone, thus modifying the metabolism of lipids for his formation. This was verified in a study conducted in Brazil by researchers from the Araraquara dentistry school of the State University of São Paulo (Foar-Unesp), in partnership with the Ribeirão Preto School of Medicine of the University of São Paulo (FMRP-USP), in transgenic mice testicles.
The study, which was supported by FAPESP, revealed the presence of SAR-COV-2 particles in lipid inclusions and organelles responsible for the production of testosterone in Leydig cells for the first time. In addition, the researchers described the mechanism by which the virus interferes with the functioning of these testicular cells. Discovery helps to explain why male patients with severe COVIR-19 have lower testosterone levels and perhaps cholesterol.
“After having infected Leydig cells in the testicles, the virus uses lipid metabolism and the cellular structure to reproduce, which alters the production of testosterone. Borders in cell microbiology and infection. “In addition, cells are responsible for storing cholesterol – essential for the synthesis of testosterone – and contain specialized cellular machines for the production of steroid hormones, making it a favorable target for infection. »»
Research was carried out using transgenic mice that have been developed in the laboratory and express the viral receiver ACE2. When infected, they develop COVID-19 in the same way as humans, which allows a better understanding of the mechanism used by the virus.
“We have observed that both in the transgenic mouse testicle and in the human testicle, there was an intense concentration of ACE2 in the same types of cells. The result therefore validates the model used in the study and confirms that the testicle is a target organ for the SRAS-COV-2, ”explains the researcher.
In experience, researchers have discovered that SARS-COV-2 can change the lipid metabolism of Leydig cells. This happens because the virus uses cholesterol stored by the cell for testosterone production to reproduce. Thus, despite the low levels of testosterone in infected Leydig cells, they were full of lipids because the virus also induced an increase in the internalization of cholesterol for its own replication and training.
Immunological character
The study also observed changes in the functional profile of Leydig cells. After being infected with the virus, they stopped producing steroid hormones from cholesterol and took an immunological profile.
Sras-COV-2 infection has also induced Leydig cells to produce large amounts of pro-inflammatory cytokines, a process that they normally do not allow. This increase in cytokines may also have interfered with the production of testosterone, altering this main function. “”
Salmo Azambuja de Oliveira, student in the structural and functional biology program (BEF) at the Federal University of São Paulo (Unifesp), recipient of a Fapesp scholarship and first author of the study
These results advance our understanding of cellular and molecular processes associated with the testicular endocrine dysfunction caused by viral infection. “The results corroborate the low cholesterol levels observed clinically in patients with severe covid-19 and can shed light on the vulnerability of men to COVID-19 and their higher mortality rate compared to women.Lipid clearance) Medicines that interfere with lipid metabolism and inhibit viral action, ”explains Sasso-Cerri.
