A new study from Germany found that intravenous administration of the SARS-CoV-2 spike protein in mice led to neuroinflammation and accumulation of alpha-synuclein in brain regions associated with Parkinson’s disease. 1/
Authors also discovered “sex-dependent alterations in astrocyte reactivity and parvalbumin-positive interneurons.” 2/
These findings suggest that exposure to the spike protein alone, without full viral infection, may contribute to neurodegenerative processes linked to Parkinson's, thus highlighting potential long-term neurological risks following COVID infection. 3/
ACE2 and Neuropilin-1 receptor expression altered following S1-protein exposure.
Most pronounced effects occur in brain regions associated with Parkinson’s disease pathology. 4/
The above mentioned study builds upon Ali Erturk’s lab report from December 2024 which showed that persistence of spike protein at the skull-meninges-brain axis induced neurological damage in mice. 5/
Vaccination reduced but did not eliminate spike protein accumulation after infection in mice. These findings suggest persistent spike protein at the brain borders may contribute to lasting neurological sequelae of COVID-19. 6/6
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Researchers found that people with LongCOVID fatigue have damaged gut barriers & signs of immune activation.
Preexisting gastrointestinal symptoms before COVID infection predisposed people to developing LongCOVID fatigue. 1/
LongCOVID patients were found to have an increased LBP/sCD14 ratio & lower IL-33 levels, which indicates altered immune activation & a reduced intestinal barrier. In addition, there were increased IL-6 levels, which are considered a marker for systemic inflammation. 2/
LBP/sCD14 is the ratio of lipopolysaccharide binding protein to soluble CD14.
This study emphasizes the impact of SARS-CoV-2 infection on the gut, which might be associated with the onset of Fatigue seen in LongCovid patients. 3/
A significant discovery in the fight against #LongCovid!
➡️ Researchers have identified the epipharynx, a part of the pharynx, as a key site for chronic inflammation driven by residual SARS-CoV-2 RNA. 1/
Using a next-generation molecular mapping technology called Visium HD spatial transcriptomics, researchers from Japan provided the world's first high-resolution spatial gene expression analysis of the epipharynx in patients with longCOVID. 2/
According to the study, the viral RNA from SARS-CoV-2 can persist in the epipharynx for more than six months post-infection, and here they activate local immune signals in specialized cells like B cells, plasmacytoid dendritic cells, and ciliated epithelial cells. 3/
A new article on #LongCOVID shows that millions of Americans continue to suffer from LongCOVID which is a very complex and heterogeneous disease, with no diagnostic tests and no approved treatments. 1/
New clinical trials will target specific biological pathways including immune dysfunction and autoimmunity, viral persistence, and microclots rather than treating LongCOVID as a single disease. 2/
Trials include REVERSE-LC, which will use the immune-modulating drug baricitinib, and ADDRESS-LC, which will test bezisterim, a novel anti-inflammatory that can cross the blood-brain barrier. 3/
A study new finds that neutrophils—the most abundant white blood cells in humans—may be altered by SARS-CoV-2 virus to cease their normal function of destroying pathogens in the body and, instead, significantly inhibit other immune cells critical for fighting the virus. 1/
The study finds that in some COVID infections, SARS-CoV-2 may dramatically impair the immune response by reprogramming neutrophils—front-line immune cells central to fighting infections—into a cell type called polymorphonuclear myeloid derived suppressor cells (PMN-MDSCs) 2/
Polymorphonuclear myeloid derived suppressor cells (PMN-MDSCs) are known to suppress virus-fighting T cells & it is believed that the reprogramming that creates them could provide a mechanism by which severe COVID, a more dangerous form of the disease, may arise. 3/
COVID-19 carries neurological and psychological risks. Alternative polyadenylation (APA) is ubiquitous in human genes, resulting in mRNA variation, and has been shown to play a key role in the starting and progression of many diseases, including viral infections. 1/
Here, researchers analyzed the APA usage across different cell types in frontal cortex cells from non-viral control group and COVID-19 patients, and identified functionally related APA events in COVID-19. 2/
According to this study, the poly(A) site (PAS) usage is different among cell types and following SARS-COV-2 infection. 3/
A NEW study reports that 68 individuals with LongCOVID had unusually active CD8+ T cells and elevated IL-3 levels, which may drive inflammation and symptom severity up to 18 months after acute COVID infection. 1/
A pronounced T cell hypo-reactivity and reduced expression of IL-3 was found in patients with severe acute SARS-CoV-2 infection. Interestingly, the opposite was the case as researchers detected a marked hyper-reactivity of T cells in LongCOVID. 2/
Hyper-activation was evident by a higher percentage of CD8+ T cells expressing the activation marker CD25, a stronger upregulation of CD25 after polyclonal stimulation, a stronger release of cytokines especially IL-3 and a higher fraction of memory T cells. 3/