Post Reply - Corona/CoViD-news

tern
@1goodtern
·
10h
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Well it's another study that comes like a kick in the gut.

Covid infection in pregnant mothers disrupts immune balance, alters fetal brain cells and increases offspring's risk of neurodevelopmental disorders.

link; https://www.nature.com/articles/s41380-024-02822-z or https://www.nature.com/articles/s41380-024-02822-z ;

Maternal COVID-19 infection increases the incidence of neurodevelopmental disorders (NDDs) in offspring, although the underlying mechanisms have not been elucidated. 

This study demonstrated that COVID-19 infection during pregnancy disrupted the balance of maternal and fetal immune environments, driving alterations in astrocytes, endothelial cells, and excitatory neurons. 

A risk score was established using 47 unique genes in the single-cell transcriptome of gestational mothers. 

The high risk score in CD4 proliferating T cell level served as an indicator for increased risk of offspring NDDs. 

Summary-based Mendelian randomization and phenome-wide association study analyses were conducted to identify the causal association of the transcriptional changes with the increased risk of offspring NDDs. 

Additionally, 10 drugs were identified as potential therapeutic candidates. 

Our findings support a model where the maternal COVID-19 infection changed the levels of CD4 proliferating T cells, leading to the alterations of astrocytes, endothelial cells, and excitatory neurons in offspring, contributing to the increased risk of NDDs in these individuals.

DJ-T-cell damage...
Jane Johnson 〓〓
@JaneJohnsonBakr
·
10h
Replying to @1goodtern
Or indeed leads to stillbirth, as happened to my poor niece.

DJ, "living with the virus" is getting killed by the virus...on the long run. 

https://www.thailandmedical.news/news/how-autoimmune-responses-in-the-brain-could-explain-long-covid-symptoms or https://www.thailandmedical.news/news/how-autoimmune-responses-in-the-brain-could-explain-long-covid-symptoms  with a link to;

https://www.sciencedirect.com/science/article/pii/S2090123224005307 or https://www.sciencedirect.com/science/article/pii/S2090123224005307 ;
Conclusions
The current study provides the first evidence indicating that autoimmune responses directed at neuronal proteins play a key role in Long COVID disease. Brain reactive autoantibodies directed at MBP, MOG, tubulin, CP2, and synapsin are elevated in patients with Long COVID disease indicating a neuro-autoimmune pathophysiology of this condition. The severity of the physio-affective phenome (CFS, depressive and anxiety dimensions), which represents a major dimension of Long COVID, is significantly predicted by increased IgM/IgA-synapsin, IgA/IgG-MBP, IgG-MOG, and CRP and AOPP levels. The current study is a proof of concept and mechanism study that autoimmune, inflammatory, and oxidative responses play a significant role in the pathophysiology of Long COVID disease, and in the CFS and affective symptoms (the physio-affective phenome) due to Long COVID.
Our findings highlight the pivotal role of immune-inflammatory responses in LC and align with evidence-based psychiatry's focus on integrating biological markers for guiding diagnosis and treatment [78]. By addressing the fundamental pathways that connect immunological dysregulation to psychiatric disorders, such integration enhances clinical practice.
DJ, Disease often is the result of immunity system fighting an infection....Sometimes the virus/bacteria NEEDS a strong immune reaction. However over-reaction/ immunity going on after the disease is gone or damage by the immune reaction itself can be a problem. 