On Nimbus, Stratus and… TACTful misinterpretation (misinformation?).
Has anyone by any chance read this Substack?:
Yes, as they claim, T.A.C.T. has consistently been ahead of the curve… but just in completely the wrong direction! TACT prides itself on being able not only to assess the epidemiological situation and its clinical consequences correctly, but also to predict them. In this Substack, TACT describes in detail the differences between Nimbus (NB 1.8.1) and Stratus (XFG) and their descendants or subvariants, explaining how—according to them—a delicate balance between mutations responsible for infectivity on the one hand and immune evasion on the other endows each variant with properties that determine how and why their spread, growth advantage, prevalence and clinical symptoms are shaped by various temporal-spatial conditions and individual vulnerabilities, respectively.
Everything is therefore explained in detail… or is it? No, it is not, because these smart alecks understand everything except the real immunological dynamics at play. For example, they still believe that the in vitro virus-neutralizing capacity of antibodies is representative of such antibodies in vivo. They forget that a highly infectious, inflammatory virus can no longer be neutralized in time in vivo, because, once it infects the upper respiratory tract, it is very rapidly adsorbed onto the dendritic cells present there. Although this yields a kind of virus-neutralizing effect, they overlook that it simultaneously puts pressure on the humoral-inflammatory arm of the innate immune system! This is disastrous, because in typical acute self-limiting viral infections it is precisely the innate immunity (as the first line of defense) together with the humoral adaptive immunity that terminates the infection. Because T-cell immunity can never curb transmission of viruses that cause acute self-limiting infections (at best it prevents severe disease with low- or moderately infectious strains), mutations in T-cell epitopes—largely conserved among SARS-CoV-2 variants—offer no competitive advantage. Unlike humoral innate or adaptive immunity, T-cell immunity therefore never exerts meaningful pressure on such viruses. Moreover, the wise guys who claim that T-cell immunity will most probably continue to protect fail to grasp that, once humoral innate or adaptive immunity is undermined, T-cell immunity springs into action far too late (even if previously primed) to rein in the unbridled dissemination of the virus from the upper airways!
Their position—rightly worrying about the rampant amplification and spread of the Nimbus and Stratus variants while simultaneously relying on T-cell immunity to keep an escalation of clinical symptoms into severe disease (possibly caused by highly virulent strains) at bay—is a true contradictio in terminis! (“…these variants pose no greater public health risk than those before” or “NB 1.8.1, XFG, and their sub-lineages cause illness very much in line with Omicron’s usual behavior”).
This misinterpretation nevertheless leads them to keep claiming that the Covid-19 (C-19) vaccination remained beneficial because, besides the humoral response, it also boosted T-cell immunity and thereby prevented severe disease. It truly makes one wonder why they still want to update the vaccines, given that they themselves admit vaccination can never halt transmission (“…breakthrough infections can occur (particularly with XFG)…”). If you cannot become seriously ill anyway, thanks to those T cells, and infection cannot be avoided anyway, why update the vaccines at all? Yet our TACT know-it-alls still have not understood that this will only accelerate the process of immune escape, which has now reached the innate immune system!
Their belief that “high transmissibility often comes with lower or equal virulence” betrays nothing but impressive naïveté and ignorance regarding the adaptive interplay between the virus and the host immune system in highly C-19-vaccinated populations.
The authors do seem to realize that the circulating variants influence other immunological or inflammatory mechanisms, but they fail to articulate this properly:
“There's also growing suspicion that variant-specific immune interaction may be changing how and where inflammation shows up in the body,” or: “While Orf3a mutations don’t directly alter spike-antibody binding, they could influence the virus’s ability to cause inflammation or avoid innate immune responses,” and: “The main difference might be if Orf3a mutations (like W193R in PQ.2) trigger stronger inflammatory responses—some speculate this could potentially influence illness (Orf3a is known to interact with host immune pathways). However, this remains theoretical,” or: “…the virus is exploring new evolutionary space beyond spike. While these haven’t translated to more severe disease yet, such changes could affect transmissibility or host-virus interactions in ways we need to understand.”
This once again proves that scientists can be dangerous—not because the data they collect are incorrect, but because their interpretation is hamstrung by the tunnel vision of their specialization and the dogmas it breeds. Hence, I call them ‘dangerous know-it-alls’: they often think they hold a monopoly on science because they have the most sophisticated analytical and modelling methods, while failing to see the forest for the trees, simply lacking the broader view of biological phenomena—in this case population-level immunology and the mutual adaptation of the immune system and the virus.
The consequences are catastrophic: their short-sightedness and short-term thinking (“…these variants have not rendered vaccines powerless – vaccines continue to keep people out of the hospital, which is their primary purpose”) lead them to keep advocating the harmful C-19 vaccination!
Owing to their lack of insight, these smart-alecks indeed keep asserting (believing?) that the temporary protection against disastrous outcomes of breakthrough infections is due to the still partial protection provided by the vaccines (“…many people still get only mild illness thanks to partial immune memory.”).
At least the authors agree with us that “Covid-19 is not over and that the virus is still evolving.” The way they think this story will unfold differs only slightly from my own predictions. Moreover, their forecasts offer no end to this C-19 pandemic. My predictions may be somewhat less rosy, but they certainly do foresee a definitive end to this health crisis…
Well, at least they aren't trying to push the narrative that COVID-19 has become endemic. But their poorly thought out silo thinking in this situation is amazing. (“…these variants have not rendered vaccines powerless – vaccines continue to keep people out of the hospital, which is their primary purpose”).... really? These variants are the black clouds of a coming immune escape hurricane.
"Spike mutations that help SARS-CoV-2 infect the brain discovered"
Expect "better" bioweapon brain targeting in the future.
The Northwestern University and the University of Illinois-Chicago authors of this study were so pleased with themselves when they told the world look at us, look what we have found - "a series of mutations in the SARS-CoV-2 spike protein (the outer part of the virus that helps it penetrate cells) that enhanced the virus’ ability to infect the brains of mice." study name "Spike mutations that help SARS-CoV-2 infect the brain discovered"