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. 2021 Mar 31;12:614451. doi: 10.3389/fpsyg.2021.614451

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Copyright © 2021 Reyes-Lagos, Abarca-Castro, Echeverría, Mendieta-Zerón, Vargas-Caraveo and Pacheco-López.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A gestational infection triggered by SARS-CoV-2 may produce a maternal immune activation (MIA) and cytokine storm syndrome (CSS). The activation of the maternal and/or fetal cholinergic anti-inflammatory pathway (CAP) via the efferent vagus nerve and transplacental interactions could downregulate such CSS. The analysis of maternal and fetal heart rate variability (mHRV and fHRV) might be considered for assessing maternal and fetal CAP activation. Also, a gestational infection by SARS-CoV-2 may produce fetal neuroinflammation and microglial activation, increasing the risks of several neurodevelopmental disorders in the offspring and even an altered long-term cognitive function in adulthood: (1) neuronal migration; (2) axonal and dendritic growth; (3) programmed cell death; (4) synaptogenesis; (5) myelination; and (6) process modeling/synaptic refinement. ASD, autism spectrum disorder; SCZ, schizophrenia; AD, anxiety disorders; MD, mood disorders; ICD, impulse-control disorders.