-extreme growth advantage over similar strains
-'profound immune evasion'
-unusual mutations in spike
-high affinity to bind to receptors
The researchers examined the XBB116 strain to see why it had become dominant so quickly in India:
They found that the strain has a number of advantages for viral fitness and infectivity relative to current competing similar strains in the XBB family (SARS3 STRAINS)
As we have previously LONG AGO established the new strains are so diverse from the original Sars2 that they are basically a new Sars: they are as different from Sars2 as Sars1 is from Sars2:
As can be seen here, from a previous study looking at the extreme drop in neutralization from antibodies to past infections and boosters with old strains, there's barely any neutralization in the XBB GENERATION:
The present study looked at XBB116 to see why it has the insane growth advantage it does: they found the strain has mutations in key parts of the virus:
Inside spike protein (S) they found 2 key mutations: one on the N terminal domain (mutations here can effect how well..
..well existing antibodies are able to nuetralise and recognise the virus.
The second mutation of note is inside the recptor binding domain (RBD) through which the virus attaches to recptors for cell entry and replication (infection)
Further, there was a significant drop in neutralization from infection to other recent strains: 18X decrease in neutralization of BA2 AND 37X decrease to BA5:
'neutralization assays demonstrated the robust resistance of XBB.1.16 to breakthrough infection sera of BA.2 (18-fold versus B.1.1) and BA.5 (37-fold versus B.1.1).'
They note that:
'The increased fitness of XBB.1.16 may be due to (1) different antigenicity than XBB.1.5; and/or (2) the mutations in the non-S viral protein(s) that may contribute to increased viral growth efficiency.'
Seen here is XBB116's increase in binding affinity to ACE2 receptors through which the virus infects cells: the higher the binding the more infectious to simplify: there's a 2.4x increase in binding ability vs Xbb15...
'XBB.1.16 RBD to the human ACE2 receptor is significantly (2.4-fold) higher than that of XBB.1.5 RBD, while the KD of XBB.1.16 RBD is significantly (1.8-fold) lower than that of XBB.1 RBD (Figure S1D). These results suggest the binding affinity of XBB.1.16 RBD to ACE2..
..s higher than that of XBB.1 RBD and lower than that of XBB.1.5 RBD. Pseudovirus experiments showed higher infectivity of XBB.1.5 compared to the parental XBB.1, which is consistent with our previous study'
Next they looked at infectivity:
'Pseudovirus experiments showed higher infectivity of XBB.1.5 compared to the parental XBB.1, which is consistent with our previous study'
The XBB116 strain was found to be extremely infectious on other receptors as well, not just ACE2:
'The S:T478R substitution significantly increased infectivity, while the S:E180V substitution significantly decreased infectivity (Figure S1E). The acquisition of two combination mutations in the S protein, one that evades antiviral immunity and attenuates infectivity..
..(e.g., F486V, G446S, Y144del), and another that increases infectivity (e.g., L452R, N460K, V83A) is a strategy of Omicron evolution previously observed in BA.54, BA.2.755, and XBB.1.6 Our findings suggest that XBB.1.16 possibly..
...follows the evolutionary pattern of previous Omicron variants.'
Next, they looked at nuetralisation from previous infections to other old strains: BA2 antibodies showed an 18x decrease in nuetralisation relative to Alpa (b.1.1.
Once again showing the back boosting effect that everyone will pretend isn't happening forever for some reason: anyway.
BA5 infects had an even more significant drop of 37x:
There's really nothing like Covid blood : it does your head it.
If they had XBB1 antibodies then they could generate some modest neutralization to XBB116: nothing impressive though: that's the immune imprinting for you: RIGHT THERE AGAIN
'Finally, antigenic cartography based on our results 88 (Figures S1F-H) showed that the antigenicity of XBB.1.16 is different from that 89 of XBB.1.5, and rather relatively close to that of XBB.1'
This shows how different the XBB strains are antigenically from b.1..1 (ALPHA)
And BA2 AND BA5: and somehow all of these still get considered the same virus?
So, as we can see: huge reductions in neutralizing antibodies, higher affinity for binding to receptors which allow for infectivity, and new mutations that are advantageous to the virus have made
It is fitter and thus much more infectious and able to evade immunity better than any other strain so far: each new dominant 'omicron' has an increased ability to evade 'immunity' so essentially you have less neutralisation against it each time:
Therefore, it becomes more severe as there's less resistance against it:
A bunch of complete idiots who don't know anything about this virus think all Omicrons are the same 🤣😩
It's so stupid what they think doesn't even warrant even basic attention: anyway here's today's new paper: enjoy biorxiv.org/content/10.110…
As there's less and less neutralisation it means that the virus is met with less and less resistance and so by default: even if it had the much lauded 'mildness' of BA1 but with this level of immune escape it would be pretty severe none the less still.
They haven't included BA1 here because even in this study which is from September 2022 BA1 was already well out of date and not even worth studying: so BA2 they used which can use to estimate BA1 neutralisation against XBB family:
So going by that very clearly we see that even if you had the 'mildness' of BA1 you wouldn't have anywhere near the level of nuetralisation: making it by default more infectious and more severe
We'll just add this to this ever growing pile of evidence on this new strain and it's beocming increasingly clear why Modi implemeted his 5 fold strategy to tackle it:
in summary they say it's predicted to become the next global strain due to these multiple advantages: and that would seem extremely likely to me: good luck.
one final point: the reason you see all this eye stuff even more with these strains is due to the higher binding affinity with the receptors: and the eyes have loads of ace2 all over them so there you go: that's that
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that's right. And they say in this study a 28 year old with no co-morbid suddenly go t it from asymptomatic Covid: and is happening A LOT. Often going undiagnosed.
My thoughts are that a lot of what's called LC: with the shortness of breath and coughing and so on is fibrosis: but because it happens to young people they refuse to diagnose it correctly.
'Alarming' asymptomatic 'silent' & 'mild' Covid found to cause severe progressive lung scarring (fibrosis:) that unlike other lung fibrosis that 'usually occurs in the elderly, post-COVID fibrosis is seen irrespective of age and other co-morbidities', shows new study.
Many cases seen in young people with no underlying conditions.
A new study has been released documenting what has long been known by many, but is only now making it into the study literature: that asymptomatic..
...Covid is causing severe progressive lung disease: pulmonary fibrosis: scarring in the lungs which essentially leads to hardened and dying lungs:
New National Institutes of Health (NIH) #Longcovid study shows 'MILD' COVID CAUSES LOW levels of CD4 AND CD8 T cells in LC in yet another striking parallel with HIV/AIDS:
'Most participants had mild symptoms during their acute infection...The results showed that people with Long COVID had lower levels of CD4+ and CD8+ T cells—immune cells involved in coordinating the immune system’s response to viruses—compared to healthy controls'… twitter.com/i/web/status/1…
Singer Lizzo struck down by virus after performing a few days ago at the Met gala and now has to cancel shows: her account has been put on lockdown since going public about her illness after super spreader show:
Not a finding I would expect to be honest based on the known imprinting of the virus, and I'm not entirely sure this will hold true as it goes against the previous research:
The problem with this idea is that you're just trying to swap one for of imprinting for another: so what happens when you imprint for XBB strains? and replace WT for that? all is doing is creating the same problem later down the line