It has been a month when @siamosolocani 1st flagged this variant. Later, I started tracking it. We are still amid an ongoing surge, it’s time to take a stock of the situation: what we do know, what we don’t 1/
1-XBB.1.16 has succeeded in creating a new, significant surge in India after a gap of >6 months. A feat that even BA.5, BQ.1 & XBB.1.5 failed to achieve! 2/
2-XBB.1.16 definitely has got a growth advantage & more fitter than other circulating XBBs & has even replaced some other similar sublineages like XBB.1.5 & XBB.1.9 3/ @vinodscaria
3-XBB.1.16 is definitely not a more pathogenic variant than other Omicron’s progenies
4-This variant is still evolving, adding few more mutations. But not all new mutations are beneficial to the virus (i.e. E180V). 4/
5-The chances of XBB.1.16 leading a new, significant wave (i.e. the 4th wave) akin to Jan’ 22 BA.2 wave are remote 5/ @JPWeiland
6-The new surge in cases is yet to peak in India. According to @JPWeiland India is more than 2 weeks from peak cases. 6/
And, now let’s see what we still don’t know:
1-How big this new surge would be?
2-What are the key factors responsible for making XBB.1.16 a more fitter variant than its contemporaries? Higher immune evasion?
Higher infectiousness, i.e. higher ACE2 binding? 7/
We know XBB.1.5 & XBB.1.16 have almost similar Spike barring a few Spike mutations. However, above study suggests that mutations in the non-Spike region may be responsible for increased viral growth of XBB.1.16 10/
The above mentioned study & some early work done by @StuartTruvile in NSW, Australia points that XBB.1.16 is not more immune evasive than XBB.1.5. @StuartTurville calls it “super similar to XBB.1.5 in neut evasion”. 11/
Now, If it's not immune evasion, is the growth advantage is because of stronger ACE2 binding then?
No, in fact, the entry into cells is similar as with Omicrons including XBB.1.5. @StuartTurville has shown this 👇 12/
Most evolutionary biologists now agree to believe that the increased fitness is mainly due to changes at non-Spike region of this variant.
Acc to @LongDesertTrain ORF1a:L3829F is probably the key mute responsible for its advantage over XBB.1.9 13/
As per @SolidEvidence mutation in NSP6 of ORF1ab may be behind this higher fitness 14/
Now, most experts believe the extra mutations at ORF9b & ORF1a are responsible to give “teeth” to this variant.
ORF9b is thought to be involved with suppressing interferon response, so they might make the virus slightly fitter by counteracting the innate immune system. 15/
We still don’t know whether XBB.1.16 will become a global thing replacing the existing dominant variant XBB.1.5. However, all the indications point it will. This is the current projection by @JPWeiland for the US (an update on the CDC graph) 16/
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Fibrinoloid (amyloid-containing) microclots are resistant to degradation and are found in a variety of diseases including #LongCOVID, ME/CFS, and sepsis. A NEW review looks at the use of laser speckle imaging (LSI) and laser Doppler imaging (LDI) to assess how fibrinaloid microclots can disrupt the microcirculation. 1/
The microcirculation typically refers to those capillaries less than 100 mm in diameter. Having shown that blood can clot into an anomalous amyloid form that is rather resistant to fibrinolysis, researchers have previously developed the idea that endothelial dysfunction can both lead to and be caused by the fibrinaloid microclots so formed, such that this can slow or block entirely parts of the microcirculation. 2/
The microclots might be thought of as a ‘structural’ manifestation. This impairment of the microcirculation is referred to as ‘blood stasis’. It is thus desirable to have ‘functional’ methods that can measure these effects on the microcirculation directly. 3/
A NEW study finds that infection with SARS-CoV-2 during the first year of the pandemic was associated with three to five times higher odds of cognitive impairment 2 years after infection. 1/
Survivors of the disease may require special attention from clinical doctors to diagnose and treat cognitive impairment, namely, those who were hospitalized for more than 15 days, in intermediate or intensive care units, and presented disorientation, changes in vision, gait or balance, during infection. 2/
Conversely, although cognitive impairment was less frequent and severe in COVID-19 cases who had been followed in the community during infection, this population is younger. Causality between SARS-CoV-2 infection and cognitive impairment could not be inferred from the present study. 3/
A NEW study finds that anti-SARS-CoV-2 antibodies play a protective role against vital organ-related #LongCovid (LC) symptoms, especially cardiovascular symptoms, but are insufficient in preventing or limiting other highly prevalent LC symptoms, such as neurological, psychiatric and pulmonary. 1/
These data underscore the complexity of the potential involvement of anti-SARS-CoV-2 immune responses in either protecting against or contributing to the development of different #LongCovid phenotypes. 2/
The disturbed immunological profile supports the idea of some sort of silent longCOVID, that may eventually manifest as critical clinical events, such as acute myocardial infarction or cerebral vascular accidents. 3/
A meta-analysis from Egypt of 125 studies involving over 4 million COVID survivors shows that months to years after infection, fatigue was the most common symptom at 43%. Around 27% of people experience cognitive impairment after COVID infection. 1/
Further, 28% experienced memory issues, 24% sleep disorders, 20% headaches, 16% dizziness, 14% depression, and 13% anxiety, with significant variability depending on follow‑up time, disease severity, sex, and BMI. 2/
Neurological symptoms are common & persistent in COVID survivors. This study highlights significant burden these symptoms place on individuals, emphasizing the need for well-resourced multidisciplinary healthcare services to support post-COVID recovery. 3/3
A new review on neuroimmune pathophysiology of #LongCOVID explores how SARS-CoV-2 can cause lasting neurological symptoms through a combination of direct infection, immune dysregulation, and persistent inflammation. 1/
Key mechanisms include viral antigen persistence, autoimmunity, blood–brain barrier disruption, neurotransmitter imbalances, and glial cell dysfunction. The authors link these processes to cognitive impairment, fatigue, dysautonomia, and other Long COVID symptoms. 2/
Despite the perception that COVID-19 is now a mild disease, there is overwhelming evidence indicating that SARS-CoV-2 infection is capable of producing widespread post-acute sequelae in a significant percentage of infections. 3/
As people get older, a growing population of cells starts to consume more energy — perhaps because the cells accumulate damage that leads them to rev up processes such as inflammation. 1/
An emerging hypothesis suggests that the brain accommodates these energy-hogging ‘senescent cells’ by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass. 2/
It’s one example of a growing understanding of how our brains control ageing and how psychological stress can accelerate the process at a molecular level. 3/