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Review
. 2022 Aug 12;14(16):3303.
doi: 10.3390/nu14163303.

Fetal Brain Damage during Maternal COVID-19: Emerging Hypothesis, Mechanism, and Possible Mitigation through Maternal-Targeted Nutritional Supplementation

Affiliations
Review

Fetal Brain Damage during Maternal COVID-19: Emerging Hypothesis, Mechanism, and Possible Mitigation through Maternal-Targeted Nutritional Supplementation

Chiara Germano et al. Nutrients. .

Abstract

The recent outbreak of the novel Coronavirus (SARS-CoV-2 or CoV-2) pandemic in 2019 and the risk of CoV-2 infection during pregnancy led the scientific community to investigate the potential negative effects of Coronavirus infection on pregnancy outcomes and fetal development. In particular, as CoV-2 neurotropism has been demonstrated in adults, recent studies suggested a possible risk of fetal brain damage and fetal brain development impairment, with consequent psychiatric manifestations in offspring of mothers affected by COronaVIrus Disease (COVID) during pregnancy. Through the understanding of CoV-2's pathogenesis and the pathways responsible for cell damage, along with the available data about neurotropic virus attitudes, different strategies have been suggested to lower the risk of neurologic disease in newborns. In this regard, the role of nutrition in mitigating fetal damages related to oxidative stress and the inflammatory environment during viral infection has been investigated, and arginine, n3PUFA, vitamins B1 and B9, choline, and flavonoids were found to be promising in and out of pregnancy. The aim of this review is to provide an overview of the current knowledge on the mechanism of fetal brain damage and the impact of nutrition in reducing inflammation related to worse neurological outcomes in the context of CoV-2 infections during pregnancy.

Keywords: COVID-19; fetal brain damage; nutrition; pregnancy; prevention; supplementation in pregnancy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
SARS-CoV-2 entry pathways. The cell surface entry pathway requires Spike viral protein to bind ACE2 bolstered by TMPRSS2, which promotes the fusion of the viral capsid with the host cell. If the cell expresses insufficient TMPRSS2 or if the virus–ACE2 complex does not face TMPRSS2, the virus–ACE2 complex is internalized via clathrin-mediated endocytosis. ACE2, angiotensin-2 converting enzyme; TMPRSS2, transmembrane protease serine 2.
Figure 2
Figure 2
SARS-CoV-2 direct CNS damage mechanism. CNS, central nervous system; ACE2, angiotensin-2 converting enzyme; TMPRSS2, transmembrane protease serine 2.
Figure 3
Figure 3
SARS-CoV-2 indirect CNS damage mechanism. CNS, central nervous system. ↓: increase ↑: decrease.

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