Which arm is crucial for viral clearance & protection against #SARSCoV2? 1/
Early on in the #pandemic questions arose regarding how #SARSCoV2 is cleared during acute/primary infection & what aspects of the #adaptive immune were necessary and sufficient for protection from repeat infection 2/
Using mouse models of SARSCoV2,@BenIsraelow Rt al demonstrate that both humoral and cellular adaptive immunity contributes to viral clearance in the setting of primary infection 3/
Either convalescent mice, or mice that receive #mRNA vaccination are protected from both homologous infection & infection with a VOC, B.1.351 4/
Additionally, they conclude that protection is largely mediated by antibody response and not cellular immunity, and highlight the in vivo protective capacity of antibodies generated to both vaccine & natural infection @VirusesImmunity@SaadOmer3 5/
Another study on Rhesus #Macaques finds that T cells play a role in the recovery from acute #SARSCoV2 infections, their depletion does not induce severe disease, & T cells do not account for the natural resistance of rhesus macaques to severe #COVID19@fitterhappierAJ 6/
Neither primed CD4+ or CD8+ T cells appeared critical for immunoglobulin class switching, the development of immunological memory or protection from a second infection 7/
CD4, CD8, & CD4/8 depletion in Macaques prior and during infection did not affect disease course and only mildy attenuated viral clearance! 8/
The debate continues.....Difficult to write-off the importance of T-cells. This virus is weird. Need more studies before we dump cellular arm. What we know, a harmony between the two is needed for a successful immune response! 9/
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In a small trial, researchers have found that a drug designed to treat celiac disease supported a more rapid return to normal activities for patients following COVID. The researchers found the oral drug #larazotide—an experimental drug originally designed to treat celiac disease—was both safe and effective in treating children with MIS-C. 1/
Current MIS-C treatments are limited. Some patients receive general anti-inflammatory drugs, but many experience a rebound of symptoms after completing a course. Such drugs are not designed to target the sticky SARS-CoV-2 viral particles that may persist in the gut. 2/
Enter larazotide, an orally administered drug that does target the gut. Larazotide strengthens intestinal barriers to limit the number of materials—like SARS-CoV-2 viral particles—that exit the intestines and enter circulation. 3/
Researchers have discovered that gut bacteria produce a molecule that not only induces but also causes atherosclerosis, the accumulation of fat and cholesterol in the arteries that can lead to heart attacks and strokes.
This unexpected link between microbes and cardiovascular disease — the leading cause of death in humanity — is a paradigm shift. 1/
The new results show that some gut bacteria, in certain states, produce imidazole propionate, a simple molecule with six carbon atoms, eight hydrogen atoms, two nitrogen atoms, and two oxygen atoms (C₆H₈N₂O₂). This compound enters the blood, interacts with immature white blood cells, and triggers an inflammatory reaction in the arteries, which promotes the buildup of fatty plaques. Imidazole propionate induces atherosclerosis on its own. There’s a causal relationship. 2/
Furthermore, scientists observed elevated levels of imidazole propionate in one out of every five volunteers with active atherosclerosis, the type in which fatty plaques are more likely to rupture and form the blood clots that cause heart attacks and strokes. The new results demonstrate that atherosclerosis is not only a disease caused by fat, but that it also has an inflammatory and autoimmune component. 3/
An exceptional study from Stanford found that lymphocytes from ME/CFS & #LongCOVID patients show elevated oxidative stress, disrupted redox balance, and mitochondrial damage.
These abnormalities lead to excess energy use by immune cells, which may contribute to severe fatigue and other symptoms. 1/
The researchers identified increased lipid peroxidation and glutathione metabolism changes, indicating shared metabolic dysfunction in ME/CFS and LongCOVID.
Females show higher mitochondrial ROS levels and insufficient antioxidant levels (GSH), while males show mitochondrial lipid oxidative damage. These findings suggest that the pathophysiology for ME/CFS and LC are distinct between sexes. 2/
The group also tested ROS-targeting therapies. Metforminshowed some benefit on CD4 T cell proliferation in vitro, and the findings suggest oxidative stress could be a target for diagnosis and therapy. 3/
New gene discovery may change cancer and autoimmune treatment!
Researchers have identified the #SDR42E1 gene as crucial for absorbing vitamin D from the gut and metabolizing it into the active hormone calcitriol, which is essential for bone health, immune function, and cellular processes.
They used CRISPR/Cas9 gene editing to disable SDR42E1 in HCT116 colorectal cancer cells, resulting in a dramatic 53% reduction in cancer cell viability while leaving healthy cells unharmed. 1/
The gene disruption triggered widespread molecular changes affecting over 4,600 downstream genes involved in sterol metabolism and cancer-related signaling pathways.
A specific mutation in #SDR42E1 on chromosome 16 has been linked to vitamin D deficiency, causing the protein to be cut short and rendered inactive. 2/
This discovery opens potential new avenues for precision medicine, including targeted cancer therapies and treatments for autoimmune diseases where vitamin D plays a regulatory role. 3/
A promising new COVID-19 vaccine candidate developed by researchers at the Centenary Institute and the University of Sydney has shown strong potential to protect against both current and emerging coronavirus variants.
By targeting features shared by a range of coronaviruses, the vaccine is designed to offer broader and longer-lasting protection as the virus continues to evolve. 1/
The new study shows that the vaccine candidate, named #CoVEXS5, protected mice from multiple coronaviruses, including the highly immune-evasive omicron XBB.1.5 variant and SARS-CoV-1, a relative of SARS-CoV-2 that was responsible for the 2002–2004 SARS outbreak. 2/
In laboratory tests, CoVEXS5 reduced virus levels in the lungs of infected mice by approximately 99.9% compared to unvaccinated controls, demonstrating a dramatic protective effect. 3/
A new Yale study has found a promising target for treating the brain fog that can follow COVID-19 and offers new insight into a hypothesis about the origin of Alzheimer's disease.
Researchers obtained viable postmortem human retinal tissue and generated human retinal organoids that contain electrophysiologically active neurons.
They demonstrated that SARS-CoV-2 induced amyloid-β extracellular protein aggregates in human retinal explants and retinal organoids. 1/
While the etiology of Alzheimer’s disease remains unknown, there is growing support for the amyloid-β antimicrobial hypothesis.
Amyloid-β, the main component of amyloid plaques in Alzheimer’s disease, has been shown to be generated in the presence of microbes.
Entrapment of microbes by aggregated amyloid-β may serve as an innate immune response to pathogenic infections. 2/
Lastly, pharmacological inhibition of neuropilin-1 resulted in reduced amyloid-β deposition in human retinal explants treated with SARS-CoV-2 Spike 1 protein.
These results suggest that Spike 1 protein, during infection with SARS-CoV-2, can induce amyloid-β aggregation, which may be associated with the neurological symptoms experienced in COVID-19. 3/