Part I of this exclusive report details what we know about the new SARS-CoV-2 ‘variant of concern’.
News of this new variant absolutely smashed across the world stage on Wednesday/Thursday of the US Thanksgiving holiday week.
The wall of coverage was intense and saturating. Every major print and news video outlet in every western nation covered this new variant in-depth and in urgent, if not overtly fearful tones. Even ‘weather.com’ managed to sneak out an “everything you need to know” article in just a few hours.
On Thursday (Thanksgiving) night stock futures began to tumble and on the shortened trading day of Friday (11/26/21) US equities were hammered for big losses. The US Dow lost over 1100 points when the brief (15 min) aftermarket futures session is included:
Oil was utterly smashed. Down more than 13% oil sent a huge, huge message:
These messages, in total, scream: “LOCKDOWNS COMING! ECONOMY AND TRAVEL TO BE CRUSHED!!”
Is this warranted? Did a scary new variant suddenly emerge that warrants this level of coverage, concern, handwringing and even outright panic?
No, not even close. More carefully, I should say, “no, there’s simply not enough information to ascertain at this point if this new variant is of greater, lesser, or no additional concern at all.”
In Part II I will let you know what I suspect is really at work here, and why, but since those are my speculations, opinions, and ‘best guesses’ they have to remain behind our member paywall for now. I wish I could still operate in the complete open, but I’ve learned that people like me who care about evidence and letting the data form our conclusions (rather than the other way around) are allowed zero errors. People holding the center mass view, who are often and routinely not just wrong, but spectacularly wrong, are never held to account and rarely even questioned about their horribly deficient and misleading track records.
This new variant, initially identified in samples taken in Botswana on November 11th and named “Nu” was quickly renamed “Omicron” by the W.H.O. By the end of the day on Friday, Nov. 26th, the W.H.O. had declared it a “variant of concern.” It was initially detected in 4 diplomats who had traveled to Botswana (from where I don’t know). It has since been detected in Hong Kong within a traveler in quarantine, and then within samples in Gauteng, South Africa.
It’s a weird beast with a lot of genetic changes and it absolutely deserves deeper inquiry into its exact mutations in order to gain an understanding of why it has freaked so many people out. But we have zero clinical or outcome data to suggest if it’s better, worse, or neutral as far as its health impacts.
As a reminder, a live virus particle consists of a string of nucleic (or genetic) material – the instructions – packaged inside a carefully constructed capsule made up of many different individual proteins stuck to the outside of, or sometimes protruding through, a lipid membrane capsule. In the case of SARS-CoV-2 there are ~30 different proteins encoded by the instructions.
It’s those viral proteins that are the focus here. Each protein is assembled out of a series of molecular building blocks, which are themselves called amino acids. There are 20 amino acids in all used by nature out of which the entire fascinating, magnificent universe of proteins are assembled.
One way to think of amino acids is like those necklace beads that pop together and then back apart again, but with each amino acid being a plastic bead of a different color and shape from all the rest. Kind of like these:
A ‘protein’ then is a specific necklace made up of a very specific pattern of colors and shapes. Because of that unique assembly, every protein has entirely different shapes and functions from all the others.
You’re read a lot about the spike protein – that is an ~1286 long amino acid chain. Because of its precise ‘string of beads’ it binds extremely well to human ACE2 receptors (and several others, unfortunately) but far less so to other species. Were the string of beads any different at all, it would either lose or gain some of its many functions that allow it to bind to and enter humans cells.
With that background, we can discuss “variants.” Each variant is a faithful copy of a virus that was rather unfaithfully copied. Mistakes were made during the reproduction of the genetic (or nucleic) instructions. Because of those instructional errors, the new genetic code does not code for the original virus particle with its very precise protein strings, but instead has one or more of those amino acid ‘beads’ replaced by another.
If the original colors of the necklace were:
Now they might be:
Every variant has a unique ‘fingerprint’ at least one or usually many of these exchanged amino acids. The wonkish details include the way these things are talked about using scientific shorthand, which you’ve certainly encountered by now. Every amino acid used by the virus is numbered beginning with the first amino acid in the first protein and ending with he last one in the last protein. Further, each amino acid is represented by a single letter of the alphabet. So if we saw P681 that would mean there was the amino acid named Proline in the 681 position. If we saw P681R, that would be shorthand for a mutation that saw the P swapped our for an “R” or Arginine (A was already taken, so R it is!).
And that’s a mutation right there! One amino acid swapped out for another. One colored shaped bead in a chain swapped out for another. A red apple for a yellow banana. New shape, new color and a brand new function.
That specific mutation, P681R, was one of the more critical ones that made Delta what it was. That specific location was the P in the PRRA which was, infamously, the inserted furin cleavage site so fondly used by gain of function researchers in labs, but that’s another story for another day.
99.999% of the time mutational changes are so deleterious to the viral lifecycle that the affected virus cannot reproduce and the lineage dies on the spot. Boom! Gone. Done-in-one.
But very rarely, every so often, one of them magically makes the virus even more transmissive and then that lineage is off to the races. Because it reproduces faster, better, easier it also gains “market share” very rapidly from the existing strains and before you know it, it’s the dominant strain.
In the graphic above we see the epsilon strain first losing ‘market share’ to the alpha strain which itself then lost market share to the delta strain. That happened because each successive strain was simply better at transmitting than the prior strain(s). That’s how nature works. This ‘selective pressure’ is simply a statement about how something that can reproduce faster and/or better evade defenses, will have an easier time of spreading within and between afflicted individuals.
What makes this variant so different and of such a concern? Simply put, the sheer number of mutations and (gasp!) even an inserted brand-new sequence coding for three brand new colored necklace beads (amino acids).
Which means it is taking over fast in terms of “market share” or prevalence:
That blue wedge at the end is nearly vertical. However, let’s remember that this is “sequenced genomes” and we cannot know how many that is as a proportion of the overall population, whether there was sampling bias or other dynamics such as measuring a large blip within a tiny shrinking pool.
After all, 80% of one hundred is just 80, while 80% of a million is 800,000. So always keep such ‘percentage charts’ at an emotional distance because they can be (and often are meant to be) emotionally misleading.
The first part of the above example is pretty much what I understand the situation to be. Here’s the state of what was known on November 25th:
That’s right, there were just 82 total known sequenced examples (cases?) of B.1.1.529 in the whole world at that point. How many deaths? None that I have yet heard of (here on Nov 26th at 8 pm EST). How many hospitalizations? Not one.
So, the tally so far:
• 82 total cases
• Zero hospitalizations
• Zero deaths
• One entire world freaking out
Now why the freakout?
Well, probably because the family tree for this variant makes zero evolutionary sense. At least to me. So far every subsequent mutation that has led to a new variant, or to a new family of variants (called a ‘clade’) has an easily tracked family history. Each new mutation is built upon the prior mutations.
If you plot these out with dots and line the resulting graph looks like a sideways shrub. Not with Omicron, or B.1.1.529. It sticks out like a whole different thing all on its own. I get concerned on a variety of levels when I see something so unusual, and I guess other people do too (but probably for very different reasons):
The way I read this ‘family tree’ it’s like someone reached all the way back to April 2020, plucked out an existing variant (having only the D614G mutation in common with every other clade & variant) and then somehow, magically, all by itself, came up with not one, not two, not ‘a few,’ but twenty new mutations never before seen in any other variant of concern.
Here’s the complete list from @JeffreyBarett on Twitter:
(Source – Twitter) https://twitter.com/jcbarret/status/1463975708770897923
• Blue and three shades of purple = 19 never before seen amino acid substitutions.
• Red = 9 mutations seen or similar to those seen in other variants of concern. Of note is the P681H which, like the aRginine in P681R sees a basic amino acid hot-swapped into the furin cleavage site possibly (probably) rendering it even more super-charged. In this case the H is histidine, a basic amino acid.
• Green is the ubiquitous D614G which must have been so awesome that every strain/clade/variant saw fit to keep that one in the pool.
• Yellow = 3 brand spanking new, never seen before, changes that could possibly be a problem due to their locations.
Yikes! It’s going to take a while to figure out what that all means
What we don’t know
What bothers me is how much fear and reaction has already gone into this new variant given that we don’t yet have any data at all to suggest that it will have a more dire health consequence. It might, and it’s possible that it might evade current vaccines and even natural immunity, but then again it might not.
That has not stopped the hyperbolic expression of science-free and incautious statements such as these:
Yes, it might be poorly recognized by neutralizing antibodies. Or that might not be an issue. Or it might be that the variant doesn’t cause much harm beyond being transmissive. We simply don’t know yet.
The hyperbole has been off the charts. The science and data-free assertions by a wall of so-called experts about how terrible this variant is going to be has left me practically stunned. And those of you who know me understand that I have a very high degree of tolerance for absorbing hyperbolic BS and not being affected by it.
So far it’s been much ado and hopefully about nothing. We simply don’t yet know enough of anything to state one way or the other if this new weirdly mutated variant will be of greater, lesser, or neutral concern.
We can say that the fear pipes have been blasted on full and well out of proportion to what is actually known so far.
We don’t know how or if those already vaccinated will fare. Better? Worse? We don’t know how the unvaccinated will fare. Better? Worse?
We don’t know how the existing early treatments will perform. Better? Worse?
We don’t know if B..1.1.529 is stable or if it will now spawn an entire new bevy of downstream relations (however, it’s very likely) each with their own attributes, good and bad.
I will be tracking this very closely and doing what I do; informing and educating you as I perform in my role as information scout.
In closing, my own entrant in the naming sweepstakes failed:
I do have my concerns about the reactions and responses and these I will save for Part II for our subscribers. As has been the theme all along in this debacle, things are not as they appear…
Continue to Part II here.