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.
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.