Follicular oocyte as a potential target for severe acute respiratory syndrome coronavirus 2 infection

• Published in: Reviews in medical virology 2024-07, Vol.34 (4), p.e2568-n/a
• Main Authors: Yadav, Pramod K., Pandey, Ashutosh N., Premkumar, Karuppanan V., Tiwari, Meenakshi, Pandey, Ajai K., Chaube, Shail K.
• Format: Article
• Language: English
• Subjects: ACE2; Angiotensin; Angiotensin-converting enzyme 2; Angiotensin-Converting Enzyme 2 - metabolism; Basigin - metabolism; Cathepsin L; Cathepsin L - metabolism; CD147 antigen; cell death pathways; Coronaviruses; COVID-19; COVID-19 - virology; Cysteine proteinase; Female; Follicles; follicular oocyte; Humans; Hypoxia; Infections; Meiosis; meiotic instability; Oocytes; Oocytes - virology; Ovarian Follicle - metabolism; Ovarian Follicle - virology; Ovaries; Oxidative Stress; psychological stress; Reactive oxygen species; Reactive Oxygen Species - metabolism; Reproductive status; ROS; SARS-CoV-2 - physiology; SARS‐CoV‐2; Serine Endopeptidases - metabolism; Serine proteinase; Severe acute respiratory syndrome coronavirus 2; Somatic cells; Viral infections; Virus Internalization
• ISSN: 1052-9276; 1099-1654; 1099-1654
• DOI: 10.1002/rmv.2568

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) was reported in December 2019 and rapidly became a pandemic as coronavirus disease 2019 (COVID‐19). Apart from other organs, presence of specific receptor angiotensin‐converting enzyme (ACE2) and corresponding proteases such as transmembrane serine protease 2, basigin and cysteine protease cathepsin L make follicular somatic cells as well as oocyte as potential targets for SARS‐CoV‐2 infection. The SARS‐CoV‐2 causes inflammation and hypoxia that generate reactive oxygen species (ROS) in critically ill patients. In addition, a large number of casualties and insecurity of life due to repeated waves of SARS‐CoV‐2 infection generate psychological stress and cortisol resulting in the further generation of ROS. The excess levels of ROS under physiological range cause meiotic instability, while high levels result in oxidative stress that trigger various death pathways and affect number as well as quality of follicular oocytes. Although, emerging evidence suggests that the SARS‐CoV‐2 utilises cellular machinery of ovarian follicular cells, generates ROS and impairs quality of follicular oocytes, the underlying mechanism of viral entry into host cell and its negative impact on the follicular oocyte remains poorly understood. Therefore, this review summarises emerging evidence on the presence of cellular machinery for SARS‐CoV‐2 in ovarian follicles and the potential negative impact of viral infection on the follicular oocytes that affect ovarian functions in critically ill and stressed women.