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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Pupil size in sleep reveals how memories are processed!
Researchers have found that the pupil is key to understanding how, and when, the brain forms strong, long-lasting memories. 1/
By studying mice equipped w/ brain electrodes & tiny eye-tracking cameras, researchers find that new memories are being replayed & consolidated when pupil is contracted during a substage of non-REM sleep. When the pupil is dilated, the process repeats for older memories. 2/
The brain's ability to separate these two substages of sleep with a previously unknown micro-structure is what prevents "catastrophic forgetting" in which the consolidation of one memory wipes out another one. 3/
Impact of COVID-19 on accelerating of immunosenescence & brain aging
The pandemic has highlighted a complex interplay between viral infection, immune aging & brain health, that can potentially accelerate neuroimmune aging & contribute to persistence of long COVID condition 1/
By inducing chronic inflammation, immunosenescence, and neuroinflammation, COVID-19 may exacerbate the processes of neuroimmune aging, leading to increased risks of cognitive decline, neurodegenerative diseases, and impaired immune function. 2/
Both aging & COVID-19 can induce neuroinflammation through the accumulation of senescent cells, persistent microglia and astrocytes’ activation, and increased pro-inflammatory cytokine production, such as IL-1β, IL-6, and TNF-α. 3/
A NEW study shows the onset of autism in COVID exposed babies at 28 months. Researchers found 23 of 211 children (11%), screened positive for autism spectrum disorder, compared with an expected prevalence of 1-2% at that age 1/
When researchers analyzed videos of children lying on their backs in what’s called General Movement Assessment, 14% of infants showed signs of developmental problems. The test evaluates early motor functions & is often used to assess the risk of neurodevelopmental disorders 2/
Later, the findings proved equally troubling. At 6-8 months old, 13 of 109 infants born to infected mothers — almost 12% — had failed to reach developmental milestones. In stark contrast, all infants in a control group born before the pandemic showed normal development. 3/
Researchers have identified interleukin-23 receptor (IL-23R) as a significant biomarker of cellular senescence and aging. Experiments show that IL-23R levels in the bloodstream increase with age and can decrease, reflecting senescent cell clearing, with senolytic therapies. 1/
Cellular senescence occurs when cells stop dividing but do not trigger apoptosis mechanisms that would allow them to die naturally. 2/
Instead, they are stuck in a zombie-like state, where they still have the urge to feed and carry out metabolic activities, but with increasingly incoherent cell signaling and increased pro-inflammatory cytokine secretions. 3/
Coupling antigens from multiple subtypes of influenza can broaden antibody and T cell responses!
A novel vaccine platform that improved protection against diverse influenza subtypes when tested in animal models and human organoids. 1/
The seasonal influenza vaccine contains strains of viruses from distinct subtypes that are grown independently and then combined.
However, most individuals exhibit a more robust response to one of these strains and thus are vulnerable to infection by others. 2/
By studying a monozygotic twin cohort, the researchers found that although prior exposure was a factor, host genetics were a stronger driver of subtype bias to influenza viral strains. 3/
Clinical evidence suggests that SARS-CoV-2 directly disrupts vascular homeostasis, with perfusion abnormalities observed in various tissues. The pancreatic islet, a key endocrine mini-organ reliant on its microvasculature for optimal function, may be particularly vulnerable. 1/
Studies have proposed a link between SARS-CoV-2 infection and islet dysfunction, but the mechanisms remain unclear.
Here, researchers investigated how SARS-CoV-2 spike S1 protein affects human islet microvascular function. 2/
Using confocal microscopy and living pancreas slices from non-diabetic organ donors, they show that a SARS-CoV-2 spike S1 recombinant protein activates pericytes — key regulators of islet capillary diameter and beta cell function—and induces capillary constriction. 3/