How did #India fare? The graphic tells the whole story:
➡️Brutal onslaught by #B16172: having the highest transmissibility & most immune evader of all VOCs with higher virulence?
➡️No support from Vaccination (negligible coverage & high breakthrough, but reinfections rare) 1/
➡️ Social mitigation measures worked! Or the virus ran out of steam? Or still too early to conclude?
➡️ India struggled (significant mortality/health infrastructure collapsed) but survived!! 2/
New study on immune escape potential of #B16172 in comparison to #B1351 w/ #BNT162b2 vaccine: More immune evader than even B1351 VOC! Significant loss of antibody neutralisation vs live B16172 (-5.8x, akin to B.1.351) @TheLancet 3/ thelancet.com/journals/lance…
Increased age & time since 2nd dose correlated with reduced virus neutralisation across all strains. Not unusual, but given low starting titres vs #B16172, more of a concern to see neutralisation “dropping off”, significantly. Boosters may be needed!! 4/
…………starting from a lower titre (#B16172) means small changes in NAbs titre now likely to have larger effect on vaccine efficacy! 5/
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/