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Vimentin as a contributing factor in SARS-CoV-2-induced orchitis on postmortem testicular autopsy of COVID-19 cases: A case-control study. | LitMetric

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Article Abstract

Background: Coronavirus disease 2019 (COVID-19) was identified in China in late December 2019 and led to a pandemic that resulted in millions of confirmed cases and deaths. The causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), uses distinct receptors and co-receptors to enter host cells. Vimentin has emerged as a potential co-receptor for SARS-CoV-2 due to the high level of vimentin expression in testis tissue.

Objective: The present study investigated the link between vimentin expression level and SARS-CoV-2-induced orchitis.

Materials And Methods: In this case-control study, testis autopsy samples were collected immediately after the death of both COVID-19 cases and a control group that included individuals who died due to accidental causes. Gene expression and immunohistochemical assays were conducted to evaluate the level of vimentin expression, cell proliferation, and leukocyte infiltration.

Results: A significant expression of vimentin and infiltration of immune cells (CD68+, CD38+, and CD138+) in the testicular tissue of COVID-19 cases, along with extensive immunoglobulin G precipitation and reduced inhibin expression (p = 0.001) were observed. Additionally, gene expression analysis revealed increased expression of vimentin and decreased expression of the proliferation markers Ki67 and proliferating cell nuclear antigen, suggesting that SARS-CoV-2 may disrupt spermatogenesis through immune responses and the arrest of cell proliferation.

Conclusion: There may be a strong link between vimentin expression and COVID-19-induced orchitis. Further studies are needed to confirm these findings. Considering some limitations, vimentin can be used as a biomarker option for testicular damage following COVID-19-induced orchitis.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11757669PMC
http://dx.doi.org/10.18502/ijrm.v22i11.17822DOI Listing

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