COVID-19 and male infertility - A review

Abstract Background: Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, is a systemic illness capable of influencing the male reproductive system through fever, inflammation, oxidative stress, vascular injury and endocrine disturbance. Because spermatogenesis is temperature-sensitive and spermatozoa are vulnerable to oxidative damage, semen quality may be altered during acute infection and early recovery. Objective: This systematic review evaluates the association between COVID-19 and male reproductive function, with a focus on conventional semen parameters, sperm DNA fragmentation and oxidative stress, reproductive hormones, SARS-CoV-2 detection in semen, and the time course of recovery. Methods: Published human studies of confirmed or previous SARS-CoV-2 infection were identified through structured searches of electronic literature sources. Eligible observational studies reported at least one male reproductive outcome, including semen quality, sperm functional integrity, reproductive hormones, or viral detection in semen/testicular material. Findings were synthesised qualitatively in accordance with PRISMA 2020 reporting principles (Page et al., 2021). Results: Across the available evidence, the clearest pattern is a short-term reduction in sperm concentration, total sperm count and motility after infection, although individual studies differ in magnitude and not all report persistent abnormalities. Longitudinal and pre/post-infection studies indicate improvement over subsequent months in many men (Guo et al., 2021; Hu et al., 2022; Zhao et al., 2025). Sperm DNA fragmentation and seminal oxidative/inflammatory markers may also increase after COVID-19 (Hajizadeh Maleki and Tartibian, 2021; Yuan et al., 2025). Endocrine studies report transient reductions in testosterone or altered gonadotrophin relationships, particularly during symptomatic disease (Ma et al., 2021; Majzoub et al., 2024). SARS-CoV-2 RNA is rarely detected in semen; one early study reported positive samples, whereas most subsequent cohorts did not (Li et al., 2020; Pan et al., 2020; Ruan et al., 2021). Conclusion: COVID-19 can act as a temporary reproductive stressor in men, particularly after symptomatic or febrile illness. Current evidence supports predominantly indirect mechanisms such as fever, inflammation, oxidative stress and endocrine disturbance, rather than persistent seminal infection. The evidence is insufficient to conclude that COVID-19 commonly causes permanent infertility. When semen results are abnormal soon after infection, repeat assessment after approximately one spermatogenic cycle may help distinguish transient suppression from persistent dysfunction.