I have done some research in this areas, hopefully to be published shortly but we didnt noticed a difference in our methylation genes and HPV 16 and HPV 18. But there may be in other genes.

When you consider HPV is just the initiator of the release of DNMT through E6 and E7 upregulation all the hrHPV types have an effect on host methylation to some degree.

Hi Stephen!

So, interesting that you have done some reaserch. I have actually done some findings that confirme methyation in the E2BS in episomal HR HPV. But, it is interesting that you have other findings. Im happy to hear that also other people are intersted in this reaserch. I would love to read your reaserch when you publish.

Stephen Reynolds But I'm agree that the methylation difference is not that huge between HPV16 and 18. Because of the ability HPV 18 has to integrate 100% in cervical cancer, methylation plays no central role in carcinogenesis. Since methylation affects episomal HPV.

I was looking at host methylation rather than HPV methylation. I think the HPV methylation has a roll like with the S5 classifier but if there are mutations in the episome over time it may not hold up, the human genome is a bit more stable.

There may indeed be a difference in episomal methylation in HPV types though, HPV 16 also has the ability to bind E7 and allow a form of semi targeted methylation which is fascinating too

Stephen Reynolds Wow i did not know about the semi targeted methylation! Do you have any litterature i can read?

Yea, there may be some preferential binding depending on DNA sequence but it hasnt been fleshed out but would be a reason why there is a somewhat conserved nature in host methylation in HPV infection and not just a random methylation pattern.

A quote from my thesis 'There is some evidence to suggest that viral components can also influence DNMT activity such as E1a in adenovirus and HPV’s E7. DNMT1/E7 complexes seem to increase inheritance DNA methylation in the cell. This may be occurring as DNMT1/E7 may be promoting DNA binding and AdoMet recruitment allowing for more efficient methylation. The question of specificity and whether the DNMT1/E7 complex has other complexes involved is still unanswered (Burgers et al., 2007; Hervouet et al., 2018).'

Burgers, W. A. et al. (2007) ‘Viral oncoproteins target the DNA methyltransferases’, Oncogene, 26(11), pp. 1650–1655. doi: 10.1038/sj.onc.1209950.

Hervouet, E. et al. (2018) ‘Specific or not specific recruitment of DNMTs for DNA methylation, an epigenetic dilemma’, Clinical Epigenetics. Clinical Epigenetics, 10(1), p. 17. doi: 10.1186/s13148-018-0450-y.