1) Deficient corticogenesis, brain atrophy, impaired development of the corpus callosum, reduced hippocampal volumes, decreased expression of γ-aminobutyric acid (GABA) are showed by exposing pregnant mam to influenza virus.

The host innate immune Toll-like receptor (TLR) 3 recognizes the viral replicative, intermediate double-stranded RNA (dsRNA). Thus, dsRNA may be critical for the outcome of the infection.

2) PolyI:C is a synthetic analogue of double-stranded RNA and is recognized by TLR3. Upon binding to TLR PolyI:C stimulate the production and release of many pro-inflammatory cytokines, including interleukin (IL)-1b, IL-6, and tumor necrosis factor (TNF)-a. In addition, PolyI:C is a potent inducer of the type I interferons IFN-a and IFN-b.

Administration of PolyI:C mimics the acute phase response to viral infection.

Numerous studies in rats and mice have provided robust evidence for the emergence of a multitude of behavioral, cognitive and pharmacological dysfunctions in adulthood following prenatal exposure to the immune-activating agent PolyI:C (Shi et al., 2003; Zuckerman et al., 2003; Zuckerman and Weiner,2003, 2005; Meyer et al., 2005, 2006a,b,c, 2008a,b,c, in press; Ozawa et al., 2006; Smith et al., 2007; Wolff and Bilkey, 2008).

Importantly, many of the prenatal infection-induced behavioral, cognitive and pharmacological

dysfunctions in adult rats and mice are implicated in some of the most critical phenotypes of schizophrenia and other psychosis related disorders, including abnormalities in sensorimotor gating, selective attention, social interaction, working memory and sensitivity to psychostimulant drugs.

Both COVID-19 and influenza virus have ssRNA

so...

... could maternal COVID-19 infection lead to pathological signs in the offspring’s brains by activating TLR3 with the replicative, intermediate double-stranded RNA (dsRNA)?

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