Molecular mimicry between SARS-CoV-2 and the female reproductive system.

PMID: 

Am J Reprod Immunol. 2021 Aug 18. Epub 2021 Aug 18. PMID: 34407240

Abstract Title: 

Molecular mimicry between SARS-CoV-2 and the female reproductive system.

Abstract: 

Oogenesis, the process of egg production by the ovary, involves a complex differentiation program leading to the production of functional oocytes. This process comprises a sequential pathway of steps that are finely regulated. Genetic predisposition and abnormal immune responses are some of the numerous possible causes of female infertility. The question related to SARS-CoV-2 infection and fertility has been evoked for several reasons, including the high expression of ACE2 in the female reproductive tissues, the entry receptor for SARS-CoV-2, and the potential damage to germline (oocytes) due to the dysfunction of autophagy in COVID-19. In addition, molecular mimicry may contribute to female infertility by leading to the generation of deleterious autoantibodies, which could also participate to the onset of an autoimmune disease in infected patients. We carried out a systematic study to improve our understanding of the possible effects of SARS-CoV-2 infection on female fertility using the angle of molecular mimicry as a starting point. Results show a number of rather long linear sequences shared by the SARS-CoV-2 proteins and oogenesis-related proteins that might play a role in the production of possibly pathogenic crossreactive autoantibodies. SARS-CoV-2 spike glycoprotein was found to share 41 minimal immune determinants, i.e., pentapeptides, with 27 human proteins that relate to oogenesis, uterine receptivity, decidualization, and placentation. All the shared pentapeptides that we identified, with the exception of four, are also present in SARS-CoV-2 spike glycoprotein-derived epitopes that have been experimentally validated as immunoreactive. This article is protected by copyright. All rights reserved.

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