[pitpatagain]

That's because other strains weren't covered by the original vaccines: Strains 16 and 18 were the high risk strains covered in the 2008 roll-out, the roll-out to young girls of the broader vaccine covering other high risk strains didn't start until 2017.

“In 2017, one of the first birth cohorts of women in Denmark who were HPV-vaccinated as teenage girls in 2008 reached the screening age of 23 years,” Nonboe explained."

It will take several more years to see the effects on other strains. It seems to have been wildly successful so far.

[ars]

The other strains were not covered because they were not common.

Now they are.

Which means some new strain will become common. Is there any data on how quickly/easily new strains show up? I assume it's not as fast as cold/flu, but if it is people will need a vaccine yearly, and that's not realistic.

[pitpatagain]

Also after some research about rate of change: It's extremely slow.

HPV is a double-stranded DNA virus with very high replication fidelity. The emergence of types like 16 and 18 happened hundreds of thousands of years ago.

I did know it was quite slow but not just how slow. Very long term vaccine efficacy is expected.

[wzdd]

Not anti-vax by any means, but it's not too conclusive to use past mutation rate here because the presence of a vaccine targeting successful strains introduces a strong evolutionary pressure for the more rapid emergence of novel strains in the future.

[pitpatagain]

It's not just the past empirical observed rate, it's the type of virus it is/other things that we know about it.

On top of being structurally a dsDNA virus which doesn't change much, HPV is subject to "purifying selection": because of the way it is built and the mechanism it uses to interact with host cells, it is very difficult for it to have productive mutations that don't immediately die out. It's highly constrained in a way that eg influenza, COVID, HIV, are not.

Some pathogens are just easier to deal with than others:

We have been curing syphilis since 1943 with just penicillin. It doesn't develop resistance because it doesn't have horizontal gene transfer and the mechanism it has that penicillin targets is too critical and conserved, it just can't mutate away from it.

Polio mutates quickly, but is extremely constrained, almost all mutations are defective, and the capsid structure is highly conserved. That vaccine has been in use since 1955 without losing effectiveness or introducing new variants.

The biology of HPV says it will be more like those cases, and since the introduction of the vaccine in 2006, that's what studies have been finding empirically.

To emphasize the difference in meaning of "strain" for HPV: There are 200+ HPV genotypes that have been numbered this way, but they are all of ancient origin. There are observed shifts in prevalence of different genotypes, but not newly evolved genotypes.

We also only care about targeting oncogenic strains. If we open up selective pressure for non-oncogenic strains to be more relatively successful and take over, great.

[pitpatagain]

The total prevalence of all high-risk cases went down in the study, from 46% in the pre-vaccine era to 32% post vaccine.

16/18 were chosen because they are highly carcinogenic and cause the most cancer, they are the two most aggressive high risk types. They cause 70% of all the cancer but are much less than 70% of the cases of high risk strains.

It takes real mental gymnastics to downplay how positive this vaccine is.