Day: July 4, 2024

In the face of severe adverse outcomes of pandemic Coronavirus disease 2019 (COVID-19) infection, vaccines proved potently immunogenic and safe in humans and are today strongly recommended in pregnancy. This study investigates, in offspring mice, the effect of maternal COVID-19 vaccination on postnatal physical development, behavior and neurogenesis. After inoculation with inactivated COVID-19 vaccine (Vero Cell) at gestational day 14.5, antibodies to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were detected in serum of both dams and pups. At one month of age, pups born to vaccinated dams, but not the offspring of non-vaccinated dams, exhibited greater working memory and more neural cell proliferation, neuroblast formation, neuronal stem cell activity and larger numbers of mature neurons within the dentate gyrus (DG). Luminex multiplex assay revealed elevated levels of hippocampal cytokines/chemokines critical to neurogenesis and memory function, namely interferon-{gamma} [IFN-{gamma}] and CX3C motif chemokine ligand 1 [CX3CL1]. Conditional knockout technology implicated microglial IFN-{gamma} receptor 1 (IFN{gamma}R1) and CX3C motif chemokine receptor 1 (CX3CR1) as crucial intercellular participants in the neuronal developmental process, via regulating microglial activation and chemotaxis, respectively. We propose that, rather than posing risk for neurodevelopmental abnormalities, maternal SARS-CoV-2 vaccination transiently enhances hippocampal neurogenesis and working memory in offspring.

The post SARS-CoV-2 vaccination during pregnancy enhances hippocampal neurogenesis and working memory in offspring via IFN-gamma responsive microglia first appeared on The CoronaVirus Alerts – The News And Times.

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IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

Post author By Mike Nova
Post date July 4, 2024

Treatments available to prevent progression of virus-induced lung diseases, including coronavirus disease 2019 (COVID-19) are of limited benefit once respiratory failure occurs. The efficacy of approved and emerging cytokine signaling-modulating antibodies is variable and is affected by disease course and patient-specific inflammation patterns. Therefore, understanding the role of inflammation on the viral infectious cycle is critical for effective use of cytokine-modulating agents. We investigated the role of the type 2 cytokine IL-13 on SARS-CoV-2 binding/entry, replication, and host response in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 infection in vivo. IL-13 protected airway epithelial cells from SARS-CoV-2 infection in vitro by decreasing the abundance of ACE2- expressing ciliated cells rather than by neutralization in the airway surface liquid or by interferon-mediated antiviral effects. In contrast, IL-13 worsened disease severity in mice; the effects were mediated by eicosanoid signaling and were abolished in mice deficient in the phospholipase A2 enzyme PLA2G2D. We conclude that IL-13-induced inflammation differentially affects multiple steps of COVID-19 pathogenesis. IL-13-induced inflammation may be protective against initial SARS-CoV-2 airway epithelial infection; however, it enhances disease progression in vivo. Blockade of IL-13 and/or eicosanoid signaling may be protective against progression to severe respiratory virus-induced lung disease.

The post IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo first appeared on The CoronaVirus Alerts – The News And Times.