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Med Hypotheses . Mitochondrial hijacking: a potential mechanism for SARS-CoV-2 to impair female fertility

tetano

Editor, Senior Moderator
Med Hypotheses


. 2022 Jan 25;110778.
doi: 10.1016/j.mehy.2022.110778. Online ahead of print.
Mitochondrial hijacking: a potential mechanism for SARS-CoV-2 to impair female fertility


Jun Sun[SUP] 1 [/SUP], Qiong Liu[SUP] 1 [/SUP], Xinling Zhang[SUP] 1 [/SUP], Shu Dun[SUP] 1 [/SUP], Li Liu[SUP] 2 [/SUP]



Affiliations

Abstract

As well as causing respiratory lesions, the multi-organ complications caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are also well known. Combined with the epidemiological characteristics of SARS-CoV-2 with high transmission rate and low lethality, the impact of complications caused by its infection on infected individuals seems to be of greater concern. There has been evidence that viral infection is complicated by female reproductive impairment, but the mechanism by which SARS-CoV-2 impairs female fertility is unclear. In addition, RNA-GPS technology has revealed that the SARS-CoV-2 genome resides in mitochondria of the host cells and affects mitochondrial function. Considering the close relationship between mitochondria and female fertility, this paper takes mitochondrial hijacking as an entry point to elucidate the possible mechanisms by which SARS-CoV-2 affects female fertility through the mitochondrial hijacking pathway, which will be important for timely preventive measures and identification of therapeutic targets for infected women with reproductive needs, especially those with asymptomatic infection.

Keywords: ACE2; Fertility; Mitochondria; Oocytes; SARS-CoV-2.
 
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