COVID-19 and female reproductive health: pathophysiological mechanisms and clinical reproductive outcomes.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has raised important concerns regarding its potential effects on female reproductive health. This review aimed to synthesize current evidence on the biological mechanisms, clinical manifestations, ovarian reserve, fertility potential, and assisted reproductive technology (ART) outcomes associated with COVID-19. A comprehensive literature search of PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar was conducted for studies published between January 2020 and March 2026. Current evidence suggests that SARS-CoV-2 may affect female reproductive tissues through multiple interconnected pathways, including ACE2/TMPRSS2-mediated tissue susceptibility, immune dysregulation, oxidative stress, endothelial dysfunction, neuroendocrine disturbances, and potentially autoimmune mechanisms. Menstrual disturbances, such as changes in cycle length, menstrual flow, and dysmenorrhea, are among the most frequently reported reproductive manifestations, although most appear transient and reversible. Several studies have reported reductions in anti-Müllerian hormone (AMH) and hormonal alterations, particularly following severe infection; however, findings remain inconsistent. Importantly, most investigations demonstrate preserved ovarian reserve, fertility potential, and ART outcomes, including ovarian response, embryo development, clinical pregnancy, and live birth rates. Overall, current evidence suggests that COVID-19 may cause temporary reproductive alterations rather than permanent impairment of female fertility. Nevertheless, large prospective longitudinal studies are required to clarify long-term reproductive consequences and identify women at increased risk of persistent reproductive dysfunction.