4. Evolution of a lineage that we didn't detect until now because it wasn't common.
We need to stop making the assumption that our surveillance systems are comprehensive. They're pretty bad, actually -- and they're generally incredibly biased in what they're looking at. Even if we were doing unbiased random sampling and sequencing, we'd have to do huge volumes of it to reliably detect rare strains.
(aside: and if we did do that, we'd be in non-stop panic mode, because we'd be finding a new strain every day.)
Define "huge". There are about ~30 mutations on the spike protein from the closest known relative, and there's a fairly strong selective pressure against the wild type (both from vaccine and natural infection). I think it's quite probable that we missed a few months of evolution of a strain circulating in a single-digit percentage of people.
This is particularly true when you consider that this strain has S-gene dropout (Delta does not), and was probably dismissed as Beta and never targeted for sequencing by most labs. That's why I meant by my original comment that we're biased about what we look at.
We're panicking and closing borders and doing untold damage because...we continue to overestimate our ability to see what nature is doing in an unbiased way.
Like, a continuous mixing and mashing feedback loop.
If nothing else, the variants occurring in real time right before our very eyes should make the idea of evolution a lot easier for some in various communities to finally grasp.
I don't think the issue of evolution has ever been a question of people grasping the science. The issue has and continues to be the resolution of its conflict with their faith. Some have found a way through that mental obstacle course, but most have not.
So yes, it is a question of people grasping the science, not of this specifically, but as a whole. They are not on-board, they never fully confront any contradictions that they encounter or spew. Logic is not their friend, they are not inquisitive, getting to the bottom of something is not in their nature. You might think that in general people are reasonable, but margins are not that high and informed-ness is very surface-level.
It’s reasonable to dislike GMOs (or some subset of them) because of who’s selling them and why, unrelated to the science. It’s reasonable to argue against fluoridated water even while accepting it’s good for dental health, because you disagree with mass medication. It’s reasonable to buy organic food if you know it to be free of certain chemicals which, knowing their scientific characteristics, you would rather avoid.
I think this is a pithy description of human beings. :)
Of course, it's a habit we'd all do well to do out best to develop.
In case of GMO it is a play with the unknown (health, stability), it is a risk against a somewhat cheaper food. In case of vaccine it is still a play with unknown, but there the risk is against another risk not just money. If the virus would be less deadly much less people would have taken it. And the other way around as well, would be more deadly people would queue up instantly.
It is not as black and white as you describe. stupid vs smart people as you say it.
And by the way, this is called common smartness. Everybody is susceptible for different thing everybody is resistant to different things so the whole word is hard to take on.
This baffles me. I believe most Christian religions(definitely Catholics and most Protestants) embraced the evolution decades ago. So who is debating it and why?
In programming terms, evolution is like tweaking a program a few lines at a time, with the requirement that the program has to still run and be useful after each tweak. You can evolve a C program this way to get a faster, or smaller, or more memory efficient, or more featured C program, but you are not going to be able to evolve a C program into an APL or Haskel or LISP program that way.
That macro evolution is possible is quite amazing and astounding when you stop and really think about the constraints. It is not at all obvious that micro evolution implies the possibility of macro evolution.
It's really something that is best approached from the opposite direction. We see evidence of macro evolution, and then use micro evolution as part of the explanation of how this is happening.
I struggle with the speciation aspect of Evolution. Not hard to empirically verify in-species adaptations, but I'm still waiting to see coronavirus turn into influenza (etc)
Covid won't change into the flu, that's like assuming a chicken might evolve into it's ancestors species or humans will evolve into apes. Evolution goes forward, not (or rarely) backwards.
It's a completely new species that, up until 2019, did not exist in the human population.
This sort of evolution happens frequently when people are in close contact with animals. Hence the reason European disease wiped out native populations but not the reverse. Also, a direct example of human evolution.
I think this is where we differ. That obnoxious spiky little ball we all now know as coronavirus(es) existed in both humans and bats long before making the "jump". Ignoring the possibility that humans are directly responsible for the new host capabilities, it's not like we watched influenza slowly morph into a coronavirus and cause a new form of havoc. All we saw was an existing "species" that had mutations inside the bounds of its genetic code that enabled it to survive elsewhere.
You might find that pondering the existence of "ring species" proves enlightening. It turns out that "species" isn't even a well defined concept when you look closely enough.
https://en.wikipedia.org/wiki/Ring_species
(Also, you needn't capitalize "evolution". It's not a god :))
Only if the members of those communities are receptive to re-evaluating their ideas and changing their minds.
I've heard people say that hurricanes and natural disasters were God punishing us, I can easily see the same logic applied to COVID. No need to rely on science for answers when a vengeful god suffices.
We basically guess what the US flu will be by what is “popular” in Asia or Southern Hemisphere, we figure in about 6 months or so it’ll be in the US. I have no idea how Europe or Rest Of World makes flu vaccine guesses.
Guess what though? They do the same. What is “popular” in the west MAY be popular in Asia in a few months.
The flu game is constantly a best guess of what others saw months ago.
https://www.cdc.gov/flu/vaccines-work/past-seasons-estimates...
https://twitter.com/MaxCRoser/status/1465970246934749188/pho...
If this had been circulating in Europe, North America, or South America before Africa, we'd know. If it came from Asia or the Middle East, it'd be quite odd that it didn't get exported to Europe but just to Asia. It's overwhelmingly likely that it originated somewhere in Southern Africa, though the exact country will be anybody's guess right now.
I think it is telling that it was South Africa, probably one of the few SSA nations with the infrastructure to do this testing of a representative sample of their population, where this was found first.
Omicron also causes s-dropout: https://www.bbc.com/news/health-59460252
I speculated about this in another post recently. Might as well try putting it up for consideration here again:
If it's in co-infection with HIV, then it isn't only the immune status that's abnormal in the physiology, and it might not even be the most significant circumstance with respect to what's happened here.
They're not particularly closely related, but both coronaviruses and retroviruses apparently pack their genome as positive-sense, single-stranded RNA, so it doesn't seem wildly implausible to me that HIV's modifications to nucleic acid metabolism would operate on coronavirus RNA, and HIV is infamous for generating plenty of variability for itself. It copying sloppily and doing it on purpose, insofar as that can be ascribed to an organism like this.
I never got particularly deep into viruses, so there may be certainly be known aspects about this I'm missing, but so far I haven't been able to find anyone to tell me a compelling reason why it wouldn't work.
What are the markers that suggest evolution in a human? I'd be interested to see a reference.
The shared cytoplasm condition is perfectly reasonable requirement, certainly, but it's also not a terribly high bar to clear. HIV does indeed prominently infect CD4+ T lymphocytes, but that is by no means the only cell type it infects.
At the very least, both species have been described to infect macrophages (and both may display tendencies to promote cell fusion, in which case I would expect many normal categorizations of what a cell type is, are off).
As for the polymerases being roughly equivalent, I have a hard time believing that. As I've understood it, coronavirus RNA polymerase does perform proofreading, and over the course of the pandemic there has been plenty of media statements of relief and optimism about SARS-CoV-2 evolution not being such a big problem because the genome seems to be relatively stable as RNA viruses go. Many of the people making those statements may have had more hopes than facts to back that up, by all means, but simply grabbing a few highly ranked search result on mutation rates (I don't have time to do a more proper review now, sorry) does seem to suggest SARS-CoV-2 was estimated to have a low mutation rate (https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7387429/) at least early after the introduction to human. Admittedly, it's also reported that mutations which should be suspected to reduce the proofreading effectiveness appeared early (https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8134885/).
But on the other hand, HIV is change virtuoso, and one of the first things you hit with a search engine on that topic currently (https://journals.plos.org/plosbiology/article?id=10.1371/jou...) has the following very interesting piece in the abstract:
"extremely high mutation rate of (4.1 ± 1.7) × 10^{−3} per base per cell, the highest reported for any biological entity. Sequencing of plasma-derived sequences yielded a mutation frequency 44 times lower, indicating that a large fraction of viral genomes are lethally mutated and fail to reach plasma. We show that the HIV-1 reverse transcriptase contributes only 2% of mutations, whereas 98% result from editing by host cytidine deaminases of the A3 family."
Evidently those cytidine deaminases act on viral DNA sequences as a host defense mechanism, so that source of mutations at least, would be distinguishing for an RNA dependent DNA polymerase such as HIV reverse transcriptase (which, by the way, apparently really doesn't do any proofreading), as compared to a coronavirus RNA dependent RNA polymerase. Now I'd be curious to see if B.1.1.529 mutations appear preferentially at positions which would have cytidine after reverse transcription. I guess that would be the guanosines in RNA original?
I was under the mistaken belief that SARS-CoV-2 lacked RNA Pol proof-reading, so that is my bad there and responsible for my equivocation between it and HIV.
I completely accept that not only is it likely that there will be the viruses sharing the same cytoplasms on occasion, in large enough numbers, on long enough infections, etc etc - because one thing we know about biology is how slippery and stochastic things become, but the fact they dont generally share the same host does make this more of an interesting edge case I would imagine.
Thanks for your interesting links and thoughtful reply!
The article speculates that the animal reservoir could be rodents. If so, it's not sewer rats, at least not in one of the many countries that samples sewage to monitor outbreaks. https://journals.asm.org/doi/10.1128/mBio.02703-20
By the way the transmissability of delta doesn't pose a hurdle for omicron. They are not competing, except in the sense that the severity of the delta wave makes people isolate and mask up.
Chronic infection produced many mutations, it also did that across many HIV infected individuals in South Africa.
Those infections mutated via natural selection to avoid in-host immune responses and actually transmit poorly in the population.
One of these chronically infected individuals recently came into contact with someone else that was recently infected with circulating virus.
The doubly infected individual allowed Omicron to mutate via recombination and pick up mutations that allow it to spread better and so it took off.
This is also more or less how animal spillback would happen as well. The animal type should be better animal-adapted and not better human-adapted. You probably need a recombination event to spill it back effectively.
They basically tried a wide range of possible mutations and tested the effect on vaccine/infection antibodies:
https://www.bloomberg.com/news/articles/2021-11-30/china-bas...
https://time.com/6124937/omicron-china-covid-borders/
https://fortune.com/2021/11/30/omicron-covid-variant-china-e...
https://www.washingtonpost.com/world/asia_pacific/china-omic...
You get the idea. If the world stage is relative, even if the net impact is bad...it's still a positive outcome if you fare substantially better than everyone else.
Mask adherence was already a thing in China before this pandemic, so I don't find it hard to believe compliance is very high and China doesn't have major problems with the pandemic.
There is also zero chance that, had Omicron been first detected in China, instead of South Africa, that they would have done the responsible thing and disclosed it to the world.
https://nextstrain.org/ncov/gisaid/global
with Delta being the large green and blue parts at the top, and Omicron being a few red dots a little up from the bottom. If you trace back, you'll see that its nearest relative is wildtype from the spring of 2020. That's pretty weird, and there are really only three ways I can think of that it could happen:
1. human manipulation in a lab using early wildtype samples. This seems unlikely, because what would be the point and how did they let it escape?
2. chronic infection in a single immunosuppressed patient. We've seen this before (see, for example, this: https://www.nejm.org/doi/full/10.1056/NEJMc2031364 ) and southern africa has a lot of immunosuppressed people thanks to HIV. Additionally, there are some genetic markers that suggest evolution in a human.
3. spillover of wildtype in spring 2020 to some animal, evolution in that population for about 17 months, then spillback last month into humans.
I'm with the article, in that I favor 3 even though there's some evidence for 2 just because i can't quite understand how the omicron patient might have gone all that time without infecting anybody else with a proto-omicron version of the virus (which would then spread and be picked up on that chart). It's possible, I guess, that omicron got increased transmissability in a mutation in the recent past, and it could have lived in the patient with bad transmissability for a long time previous. And since delta is so amazingly transmissable, any proto-omicron could have infected a couple of people and then died out undetected. But still.