Immune-Mediated SARS-CoV-2-Induced Orchitis Leading to Complete Testicular Failure: A Report of a Rare Case
Autoimmune orchitis is a rare cause of male infertility characterized by immune-mediated impairment of spermatogenesis. SARS-CoV-2 infection has been implicated in testicular inflammation and immune dysregulation, but reports of virus-associated autoimmune orchitis remain exceedingly uncommon. We describe a 40-year-old man with rapidly progressive infertility leading to azoospermia and testicular failure, occurring in the context of a balanced chromosomal translocation that may have conferred genetic susceptibility. Histological findings were consistent with autoimmune orchitis, and serological evidence indicated prior asymptomatic exposure to SARS-CoV-2 in the absence of recent vaccination, suggesting a potential immunological trigger. This case supports the hypothesis of a "second-hit" mechanism whereby virus-induced immune activation may accelerate testicular damage in genetically vulnerable individuals. To our knowledge, only a single-digit number of cases of SARS-CoV-2-associated autoimmune orchitis have been reported. Early fertility preservation, genetic and immunological evaluation, and long-term endocrine follow-up should be considered in men presenting with unexplained, rapidly progressive infertility. Further studies are needed to clarify the relationship between SARS-CoV-2, testicular autoimmunity, and male reproductive health.
Authors
- Menelaos Ioannidis
- Eleftherios Anagnostou
- Michail Stratis
- Ioannis Moysidis
- Theodosia Zegkiniadou
- Georgios Chytas
- Nasos Ioannidis
- Vasileios Malasidis
Institutions
- Aristotle University of Thessaloniki (GR)
- CARE Fertility (US)
- St. Luke's Hospital (GR)
- Hellenic Agency for Local Development and Local Government (GR)
- IS practice (BE)
- Polyclinic General Hospital (GR)
Publication Details
- Journal
- Cureus
- Published
- 2026-02-13
- DOI
- https://doi.org/10.7759/cureus.103527
- Primary Topic
- COVID-19 Impact on Reproduction
- Type
- article
- Field-Weighted Citation Impact
- 0.00