I've read that BOT and tonsils are lymph tissue and, because of that, traps bacteria and viruses. Most tonsillitis is due to some bacterial or viral infection that causes the inflammation.
I think that there needs to be some clarification of the saying that most
HPV infections are transient. High risk
HPV infections generally fall into three camps: residential, episomal, and integrated. Only a few percentage of these infections become integrated, and once they do, they are part of the host DNA. It becomes a part of the host like HIV or herpes would--although, it is now known that it is possible to get rid of HIV using bone marrow transplation, and radiation. When HPV16 becomes integrated, that's when the real damage begins as it begins to produce E6 and E7 proteins. I believe, based on the biology, recurrence is likely.
Here is an excerpt from The
HPV Handbook "Human Papillomavirus and Cervical Cancer", edited by Professor Walter Prendiville and Dr Philip Davies, which supports detection of oncogenic activity vs. DNA or PCR detection (page 75 and 76):
"Testing for
HPV oncogenic activity, rather than for the presence of
HPV DNA, may therefore be a more relevant clinical indicator of the development of cervical cancer. The detection of
HPV E6/E7 mRNA indicates
HPV oncogenic activity and may be used as a clinically predicitive marker to identify women at risk of developing high-grade cervical dysplastic lesions and cervical carcinoma."
The
HPV Handbook further elaborates on the subject
HPV protein and DNA testing:
"Several methods exist for the detection, typing and quantitation of
HPV. Commercially available
HPV antibodies can be employed for the detection of
HPV proteins using techniques such as immunohistochemistry, western blotting and immunoprecipitation. However, it is difficult to detect the
HPV oncoproteins themselves, firstly because of insufficiently sensitive and specific monoclonal antibodies and, secondly, because of the very short half-life and turnover rate of E6 and E7 gene products. Consequently, the standard practical methods for the diagnosis of
HPV infection are based on the detection of
HPV DNA.
The incorporation of
HPV DNA testing into primary screening remains controversial, however. The great majority of
HPV infections are transient and clinically non-significant, although they frequently produce temporary cytologic changes. Only 10-20% of
HPV infections become persistent and contribute to the development of high-grade precancerous lesions or cervical cancer. This is particularly relevant to women in their teens and 20s. It is possible that widespread use of
HPV DNA testing will result in the identification of large numbers of women at risk, even though their infections are likely to be transient. Such misclassification would result in over-treatment of lesions, unnecessary expenditure and considerable anxiety for patients."
