Have we reached to the peak of 2nd #Covid wave in India? May be, yes! Its already 2.5 months in to it. Most badly affected countries peaked within 1.5-3 months of onset of a new surge. Is it too early to comment? 1/
More interesting would be to see which way our curve goes: the UK/Israel or the US way! While both UK/Israel took 1.5-2 months to flatten their curves w/ strict lockdowns & aggressive vaccination, US had a long plateau (>3.5 months) 2/
However, there is heterogeneity in caseloads: While states like MH, UP, CG, PB, DL are showing ⬇️ in case load, some southern & eastern states (KA, KL, AP, TN, WB, ) still reporting cases in high numbers! What is driving Covid in these states? 3/ indiatoday.in/coronavirus-ou…
Different variants (VOC) are circulating in diff states of India. While it is #B1617 is in MS & neighboring states, #B117 in PB, DL & northern states, Delhi & #B1618 in WB & eastern states outbreak.info/situation-repo… 4/
Now, a new variant having #N440K spike substitution is believed to be behind the sudden rise of cases in southern India, particularly in KA, KL, AL & Telangana. Some believe it is believed to be 15 times more lethal than the earlier ones 5/ biorxiv.org/content/10.110…
So, what lies in store for #India? The few key factors that may extend India's suffering for a prolonged period:
1-lack of strict #lockdowns: having halfway yo-yo lockdowns are not the answer!
2-sluggish #inoculation drive: still only 2% of the population received 2-doses! 6/
3-rampant circulation of #variants: not sure which one is the main driver!
4-limited #sequencing: only 1% of isolates sequenced!
5-modestly efficacious #vaccines: unlike the other 3 countries
6-lack of #effectiveness data on currently employed vaccines: so, driving blindly! 7/
What could be the saving grace? Hoping the rapid descent follows the explosive ascent! And the virus, mutating at a staggering pace, might be heading for an evolutionary cliff all on its own. Amen! 8/ bbc.com/future/article…
One interesting thing to note: All the three countries had 3 waves, the last surge the severest!
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When antibodies from people w/ longCOVID were injected into healthy mice, the animals appeared to experience pain & fatigue — two of the hallmarks of long COVID. 1/
The finding — now from two studies — suggests that the antibodies are the cause of the long COVID symptoms.
Antibodies isolated from people with long COVID increase pain sensitivity and reduce movement in mice when transferred to the animals, research shows. 2/
The findings suggest that antibodies might drive some symptoms of longCOVID — although how that process works is unclear, and the results will need to be replicated in larger studies. 3/
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/