I'm genuinely asking, I'm a simple software dev not a doctor.
And bacteria self-replicate, whereas a virus needs to infect a cell and be reproduced by that cell. Some antiviral mechanisms attack the reproduction proteins that the human cells use, which the virus cannot do without. And the human cells don't have reproductive pressure to replicate viruses, quite the contrary.
2) To further illustrate, some viruses have been nearly eliminated with a single vaccine. Polio didn't manage to adapt before going almost extinct. And a good reason why is:
3) Viruses can only evolve inside contaminated hosts. If you find a cure that stops quickly the virus from multiplying and contaminating, you are also curtailing its ability to adapt. A contaminated host is a giant casino machine, allowing the virus to mutate until it hits a new evolutionary step. A strong enough vaccine or treatment is like throwing out the virus before it has time to play much.
FWIW, I was trained as a bacterial geneticist and routinely used bacteriophage (viruses that infect bacteria) with various resistance mutations.
Viral mutations are not restricted to viruses that infect bacteria.
edit: in fact, fundamental aspects of the genetic code were determined by analyzing and exploiting viral mutations.
https://en.wikipedia.org/wiki/Crick,_Brenner_et_al._experime...
But so what? Anti-pathogen drugs are useful in the period during which resistance hasn't become universal, and if and when it comes a problem, we'll have other drugs.
Besides: sometimes you get lucky and the virus goes extinct before it can develop resistance (e.g. smallpox)
Is it so wrong of me to demand competence of my spammers?
And no, strep throat is not worse than ebola.
There’s some ambiguity in their comment because it isn’t obvious what we’re sort of… averaging over, but I think they clearly don’t mean that there no serious viral infections exist.
The Crick, Brenner et al. paper that I cited above
* studied mutations in a viral gene called "rIIB"
* the authors used those rIIB mutations to determine that the genetic code was a non-overlapping triplet (now called codons) -- a pretty fundamental discovery.
* What's amazing to me is that they still have NO IDEA what the rIIB gene actually _does_, mechanistically.
It's like learning a little bit about God using an enigma machine (sorry, shitty simile).
And even worse, some viruses can swap genes if a host has multiple infections at a given time. Bats in particular are known as "hot pots".
It's an extreme example, but it demonstrates a fundamental constraint that can't be evolved around. Ideally vaccines can find an equivalent in the space of mechanistic interactions that cut off any evolutionary pathway a virus could reach, either exterminating the virus before it has enough time to complete the search, or by genuinely leaving no pathway even with infinite searching.
Contrary to what you may have heard from Jeff Goldblum life does not always find a way.
I think the biggest difference is that bacteria can react to a treatment, while viruses don't have the capacity to react. If you've stopped a virus from replicating, it's essentially dead. A bacterium may have defensive measures it can take. It could form an endospore and try to wait things out. If you've stopped it from reproducing, as it ages it might start accumulating free radicals that increase DNA damage, leading to a higher chance of it mutating to resist the antibiotic. Etc.
And the really, really bad part about abusing natural parts if the immune system to provoke pathogen resistance against them is that the resistance will target part of natural immunity.
Bacteria also swap genes between themselves [0], whereas two viral particles sitting on the same Petri dish are too inert/simple for that. That represents an additional way for adaptive tricks to spread.
Based on my recollections of this paper https://pmc.ncbi.nlm.nih.gov/articles/PMC5499642/
So yeah, I wouldn't be super worried about the virus evolving to become worse in absolute terms as a result of antiviral exposure. Virii are evolving all the time anyways. Antivirals can also reduce evolution speed by fighting an infection: A more severe infection means more virions means greater evolution speed. I believe some new COVID variants were thought to have evolved in the body of someone who was severely infected. (However: Note that it's not necessarily beneficial for fitness for the virus to evolve greater infection severity, especially if that interferes with transmission.)
I think (also without a citation) that this was never properly demonstrated.
And there is nearly nobody left who has no immunity from either infection or injection. We are definitely still seeing quite a few deaths from COVID.
The examples that you gave that I checked were not supportive of your assertions.
Admittedly the method in the present article is probably better than the idiocy of extracting antibacterial peptides from context for use as drug products, since at least this will always be used in the context of a full immune system and they trigger a number of genes which probably regulate a whole subcomponent of measures rather than just one or two mechanisms.
Even so, it lifts up a particular part from the diffuse field of defenses as salient and particularly worthwhile to defeat.
Also, keep in mind that many species of virus have so small genomes they have to overload the readings of parts of the nucleic acid sequences to get a full set of proteins.
Evolve to evade the immune system, certainly. But if you're implying that it will happen in the same ways, at anything like the same rate and to the same extent regardless of what we do, no that's not right.
By your logic, we'd be better off if we gave patients a cocktail containing small amounts of many different antibiotics. By giving a single antibiotic in a large dose, we are "lifting up a particular part of our field of defenses as salient and particularly worthwhile to defeat". Sounds bad.
Willing to bite the bullet and sign on to this kitchen-sink approach, of offering patients a cocktail containing small amounts of many antibiotics?
The problem I see with the cocktail approach is that a pathogen can gradually evolve defenses against everything simultaneously, in parallel. With a cocktail, every element of the cocktail provides a distinct glide path for a virus to increase its contextual fitness. That also sounds bad! The main way I see this situation improving is if two elements of the cocktail happen to act as a sort of clamp, where any virus which begins to defeat one ends up increasing the effectiveness of the other.
There are indeed bacteria which can survive high bleach concentrations. It was a minor nitpick.
But I bet if you weren't worried about etching or skin safety you could find a concentration that would handle those little buggers. It's the sterilization equivalent of "It can't be stuck if it's liquid"