COVID-19, caused by SARS-CoV-2, has been linked to multiple systemic complications, including
potential effects on the male reproductive system. Evidence suggests that the virus may impair
spermatogenesis, alter hormone levels, and disrupt testicular architecture through direct viral entry,
immune-mediated mechanisms, and oxidative stress. While many studies report transient effects,
particularly in mild cases, severe and long-COVID may result in prolonged dysfunction. This review
summarizes the biological pathways by which SARS-CoV-2 may impair testicular function, highlights
clinical and experimental evidence, and discusses implications for fertility preservation, reproductive
counseling, and therapeutic interventions.
