Abstract
Background/Objectives: Premature ovarian insufficiency (POI) is a disorder that affects women under the age of 40. It is characterized by decreased ovarian function, elevated gonadotropin levels, and decreased estradiol. SARS-CoV-2 disrupts ovarian function largely through oxidative stress, inflammation, and immunological dysregulation, which are enhanced by its entrance into ovarian tissues via ACE2 receptors. The purpose of this comprehensive review was to investigate the molecular pathways that link SARS-CoV-2 infection to POI and analyze their consequences for ovarian reserve and fertility. Methods: We searched databases such as PubMed, Scopus, EMBASE, and Google Scholar for papers published between 2020 and 2024. Eligible studies investigated the effects of SARS-CoV-2 on ovarian function, including the hormonal indicators anti-Müllerian hormone (AMH) and follicle-stimulating hormone (FSH), oocyte quality, and ovarian reserve. The data were compiled into a complete examination of molecules and clinical findings. Increased inflammatory indicators, such as interleukin-6 and NLRP3 inflammasome activation, impaired ovarian homeostasis. Anti-SARS-CoV-2 antibodies in follicular fluid could have impaired oocyte quality. Observational studies showed transitory decreases in AMH and changed FSH levels following infection, with variable effects on antral follicle count and IVF results. Changes in lipid profiles and VEGF expression emphasized the virus's influence on ovarian angiogenesis and the ovarian microenvironment. Conclusions: SARS-CoV-2 infection impairs ovarian function by causing oxidative stress, inflammation, and hormonal disruption, thereby increasing the incidence of POI. While most alterations are temporary, the long-term reproductive consequences remain unknown. Continuous monitoring and specific treatments are required to reduce the reproductive risks associated with COVID-19.