Some experts suggest Omicron variant may have evolved in an animal host

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.

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?

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.

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.

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?

https://twitter.com/jburnmurdoch/status/1466480120215048199

It might be a bit milder (though we won't know for a while, there's a lot of confounding factors and data lag). It could also be a bit more seriousl. But it seems very unlikely to be an order of magnitude milder.

First, as a practical matter, small molecules like antibiotics are really difficult to develop, the repertoire is limited, and toxicity is often a big problem. The possible repertoire of antibodies against a given antigen is astronomical.

In the case of antibiotic resistance, you’re dealing with an active colony of bacteria continually reproducing within one host. In vaccine immunity, reproduction is nil or extremely limited within the host (simplifying white lie), and it is mostly at the host-population level that immune evasion evolves over time, so the population dynamics are totally different.

Edit: I recommend Lange’s Medical Microbiology and Janeway’s Immunobiology for those who are interested enough in learning more.

This is one reason why vaccine distribution inequity may come back to bite us.

People with a compromised immune system are a good setting for evolving new variante of coronavirus. They stay sick for a long time (meaning more viral replication and more opportunities for mutation) and they apply a weak immune response which while not sufficient to wipe out the disease, provides selective pressure that rewards immune evasion.

There's a common antivaxxer myth that vaccines promote the creation of new variants and that we would be better off without vaccination. I think it's very important to emphasize that is not the case.