SARS-CoV-2 still has one strain. The current vaccines are hyper-targeted at "variants", something much smaller than a strain.
Think of "influenza" like "dog", "strain" like "chihuahua" vs "golden retriever", and "variant" like "chihuahua with blue eyes" vs "chihuahua with brown eyes".
The distinction can get a bit muddied at the border* but I don't think we've reached that point yet.
We're not seeing much in the way of mutation in the SARS-CoV-2 structural proteins. And for other coroanviruses where we've developed vaccines, for dogs and pigs, we haven't had the same sort of problems with having to produce new vaccines that we do with the fast mutating flue.
Now, resistance does fade and to keep your dog protected you need to give it a booster shot every year or two and it might very well be the same with humans and SARS-2. But at least we wouldn't have to play the game of guessing which strain would be dominant in an upcoming season.
Do these variants mean something? The UK has some of the best genomic testing in the world. I'm guessing most countries have their own variants floating around with no clue.
And we should remember that flu is much more deadly when nobody has existing immunity. Even when the virus mutates, humans create a broad spectrum of antibodies against different parts of a virus and usually at least some will still bind to variants, but maybe not as well. Once a significant portion of the population is vaccinated COVID may become as or less deadly than flu.
This is why the only flu variants scientists freak out about are zoonotic strains. They're different enough that existing antibodies don't work.
Zoonosis is unlikely to produce more coronavirus pandemic strains like flu because flu infects our livestock and birds, and these SARS-like coronaviruses seems to only exist in bats. Humans have very little interaction with bats.
I find it likely that COVID vaccine will become a one-and-done vaccine given to children, given its low zoonotic hybridization potential and slowish mutation rate.
It’s not like the flu. The strains aren’t functionally different, with the possible exception to the one that spilled back over from infected mink which was slightly less responsive to human antibodies in lab experiments. Unless there’s more significant change the vaccine should work for all the different variants.
EDIT- Be careful reading too far into statements like “XYZ mutation makes it easier to bond to ACE2 therefore it’s more contagious” Infection is more than just binding to a receptor, even if lower quality preprints jump the gun in their conclusions
As mentioned elsewhere in this thread, this is a variant, not a strain.
This variant does not have any genetic differences in the spike protein targeted by the vaccines. It is unlikely the vaccines will be differently effective.
Interesting. That's not a vaccine anymore that's a strain of SARS-CoV-2 that's never produces symptoms, but is still similar enough to the original to prime the immune system. Presumably it would out compete the original in a Darwinian sense, because people who caught it would never get sick and stay home.
Risky, though, because if it turns out to be less benign than we thought - or mutates in such a way as to become lethal - we've just started a second pandemic.
Current vaccines aren't optimized for the currently dominant Covid strains, they're optimized for the Covid strains that were around a year and a half ago.
That's conjecture. A conclusion from this study[1] is that vaccines correlate with dominance of fitter variants. That suggests that it's possible that vaccines allow them to propagate.
"the decline in lineage diversity was indeed correlated with increased rates of mass vaccination. Furthermore, the decline in lineage diversity was coupled with increased dominance of the B.1.1.7 (alpha), B.1.1.617 (delta) and P.1 (gamma) variants of concern, suggesting that these variants may be “fitter” SARS-CoV-2 lineages.”
I'm starting to suspect this isn't because the vaccines are inherently particularly good, though. They're incredibly effective against one particular strain of Covid-19, and for a while that was pretty much the only thing in circulation, but as soon as more came along their effectiveness against those started to drop. Viruses less novel than Covid-19 presumably have a lot more genetic diversity, so being incredibly effective at one specific variant with one specific genome would achieve a lot less.
Honestly, I'm seriously starting to doubt whether it's even remotely feasible to achieve herd immunity with the current vaccines - the Delta variant is looking really worrying on that front.
This is a follow up post to a previous post on mine on how we might look for a natural attenuated (mild) strain of SARS-CoV-2 by genome sequencing [0]. While the COG-UK has not been looking directly for such a strain, their data does show that strains with the right type of mutations do exists.
While it might be possible to use a natural attenuated strain as a vaccine directly, the real value of having such a strain may be in using it as a safer test strain in a human challenge trial of a conventional vaccine. This could shave many months off us getting an effective vaccine for COVID-19 [1].
first issue here is the differences in terminology regarding strains, vs variants.
strains are signifigantly different from each other, variants are a nuance on the same theme.
the virus strain that infects small mammals is separate from the trans specific strain that spilled over to humans.
the virus with small changes to the spike sequence altering spike structure or function is a variant.
under emergency conditions a 3phase trial is not mandatory , and would likely be a quick deliberation under normal conditions for small adjustments to the sequence, similar to seasonal influenza vaccines.
> Over time, as more mutations occur, the vaccine may need to be altered. This happens with seasonal flu, which mutates every year, and the vaccine is adjusted accordingly. The SARS-CoV-2 virus doesn’t mutate as quickly as the flu virus, and the vaccines that have so far proved effective in trials are types that can easily be tweaked if necessary.
Coronaviruses like SARS-COV-2 mutate relatively slowly and minimally compared to others. So mutation isn't expected to be a huge concern, unlike say influenza which mutates relatively rapidly and requires an annual tweak to the vaccines.
What's more, any new strains we do see spreading more widely will do so because their mutations confer a competitive advantage. In practice that usually means more drift towards higher infectiousness but less severe symptoms - the same mechanisms that have left us with 4 other endemic but mild common cold coroanviruses.
The new SARS-COV-2 vaccines may be a useful tool to get us over this hump where the virus is still novel to a large proportion of the population, but are unlikely to be required indefinitely.
We are observing mutations, and there’s a number of preprints out there describing mutations along the spike protein. I’m not sure which of the 100 vaccine candidates would continue to work if that were the case, but perhaps it will become like the flu where we need a different vaccine per strain and that sometimes the vaccine only provides partial protection
Flu vaccines are effective — but the government has to try to predict which specific strains of flu will be active that season. If they mispredict, you might get the flu despite having the vaccine since you got a different strain.
For COVID-19, there is a known set of strains that hopefully won't change. So a vaccine targeted towards that set should work, at least temporarily.
The following is just me speculating: from what I have heard, coronaviruses are called such because of distinctive proteins on the outside of the cell that are hard for the virus to change. If a vaccine elicited an immune response to target such a protein, then it should be effective for all the strains.
The plural ‘variants’ in the title is a bit misleading. Only one of the four viruses they tested is one we are actually concerned about at this time. The first is the original virus, which was displaced by the second early in the pandemic and against which vaccines are already known to be effective. The third one is the UK variant, which is of interest and the fourth is an artificial virus with a single mutation of interest, which doesn’t circulate in nature. This is all good but the study doesn’t add anything that wasn’t already known. It appears that better funded groups at the NIH, UTMB, Fred Hutch and Columbia beat them to the goal and to publication in the even more prestigious publications like NEJM and Nature. In any case, reproducing important research is a laudable and underrated goal. However, I would suggest a more modest title - ‘Study adds to data for vaccines’ effectiveness against the UK variant of SARS-COV-2’.
There are other variants - Brazilian, South African, Californian, New York, etc - which need to be studied in more detail. There are already data from the aforementioned research groups for at least some of these variants that suggest that vaccines will continue to be at least partially effective.
Think of "influenza" like "dog", "strain" like "chihuahua" vs "golden retriever", and "variant" like "chihuahua with blue eyes" vs "chihuahua with brown eyes".
The distinction can get a bit muddied at the border* but I don't think we've reached that point yet.
*Like these dog breeds: https://www.countryliving.com/uk/wildlife/dog-breeds/a345060...
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