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/
This signaling potentially contributes to the chronic symptoms experienced by patients with long COVID, which include fatigue, persistent cough, dizziness, and cognitive issues continuing for months after the acute phase of infection. 4/
Using advanced technique, the researchers found that the residual viral RNA isn't merely leftover debris; instead, it actively triggers immune responses and inflammation. 5/
The epipharynx is one of the most important sites for SARS-CoV-2 infection, yet its anatomical location makes it difficult to observe w/out endoscopic evaluation. This region will gain more research attention as a potential target in understanding and treating longCOVID 6/
To address the issue, the team explored epipharyngeal abrasive therapy (EAT) as a treatment. EAT is a treatment for chronic epipharyngitis that has been practiced in since the 1960s, involving the swabbing of the epipharynx with a 1% zinc chloride solution. 7/
After three months of weekly EAT treatment, the patients showed a remarkable improvement in symptoms. 8/
On a closer analysis, the researchers observed a significant reduction in the viral RNA and a suppression of inflammatory responses marked by a decrease in expression of signaling molecules like pro-inflammatory cytokines and antibody-related genes. 9/
The spatial gene analysis post-treatment revealed that EAT promotes the removal of damaged ciliated epithelium. Additionally, it also downregulates the overactive immune pathways, underscoring its promising role in immune modulation and tissue repair. 10/
Spatial transcriptomic analysis has enabled a deeper understanding of the biology of longCOVID from a completely different perspective than conventional approaches, including the potential application of a treatment already in clinical use in Japan. 11/
While most existing treatments focus on managing these symptoms, this study goes deeper, identifying the epipharynx as a hidden reservoir of viral RNA and immune disruption, thereby opening new avenues for more targeted therapies. 12/
The study marks a significant leap in medical science, especially in light of estimates showing that 31–69% of recovered COVID-19 patients continue to suffer lingering symptoms. 13/13
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/
A new study, the first to compare inflammation & brain stress in #LongCOVID patients w/ those who have fully recovered shows that those w/continued brain fog & other cognitive issues have a lower ability to adapt to stress & higher levels of inflammation in their brains. 1/
While previous longCOVID studies have shown changes in these markers in mice, this study evaluated the infection's impact on the brain in documented COVID-positive patients. 2/
The pilot study included 17 confirmed COVID patients (10 with longCOVID and seven who were fully recovered with no lingering symptoms). 3/
A new study suggested that COVID-19 may cause lasting damage to the esophageal epithelial barrier, increasing its permeability & provoking an exacerbated inflammatory response. These changes may explain the prevalence of post-infection gastroesophageal symptoms 1/
This prospective study found that 55 hospitalized patients recovering from COVID reported significantly increased symptoms of heartburn and acid reflux 3 to 6 months after hospital discharge. 2/
Biopsies revealed higher esophageal permeability under acidic conditions, increased IL-8 levels, and elevated expression of Claudin-2, a tight junction protein that weakens epithelial barrier function. 3/