Adaptor protein MyD88 confers the susceptibility to stress via amplifying immune danger signals

Exploring the immunogenic properties of SARS-CoV-2 structural proteins: PAMP:TLR signaling in the mediation of the neuroinflammatory and neurologic sequelae of COVID-19

“…These effects were largely mediated by TLR4 and NF-κB signaling ( Olajide et al, 2021a ). Using BV-2 cells, Yao et al found that the receptor binding domain (RBD) of the S protein increased protein levels of CD68, Iba-1, pro-IL-1β and IL-6 ( Yao et al, 2022 ). We found that the S1 subunit produced a proinflammatory cytokine response in primary whole brain microglia isolated from adult rats.…”

“…Inhibition of MyD88 signaling blocked these effects of the S protein. Interestingly, stress exposure (social defeat) potentiated the neuroinflammatory and behavioral effects of the S protein, which were also blocked by a MyD88 inhibitor ( Yao et al, 2022 ). A recent study by Fontes-Dantas and colleagues demonstrated that the S protein injected ICV produces cognitive deficits mediated by TLR4 ( Fontes-Dantas et al, 2023 ).…”

Viral persistence in children infected with SARS-CoV-2: current evidence and future research strategies

“…This situation continues, despite increasing evidence supporting the pathogenic role of neuroinflammation, which might be triggered by viral infections, in psychiatric diseases. 71 Hopefully, long COVID will serve as a model to understand many of the currently unexplained chronic post-viral conditions.…”