Dormant vs eliminated HPV

I got HPV 16 probably in 2005 and it stayed in my cervix for 4 years. When the dysplasia (CIN III) was removed by excision, HPV may be have been removed in toto. In case I will be tested HPV- after the treatment, should I assume that:
1. HPV is eliminated from my body or
2. HPV has become dormant (and where is it located if dysplasia was removed, in healthy epithelium of cervic?)

And if it remains dormant, why will it not become undormant immediately again, because my immune system will be the same that it was when the HPV was active?

I understood previously that if HPV becomes dormant/eliminated it cannot anymore become active. If that is not correct, please refer a link to a scientific study/article that proves that after one has tested negative for HPV, it can become active/undormant again (without new infection).

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Testing negative for HPV does not mean that HPV has been eliminated, that you no longer have it or that it will never come back. HPV tests are based on a viral presence threshold. The current 'cutpoint' for HPV commerical testing is 1 pg/ml. Anything less than 1 pg/ml is considered a 'negative' result. That does not mean that the HPV virus isn't present. It just means that there isn't enough of it present to tip the scale to a positive result. HPV is considered dormant once a person who has tested positive for HPV now has a viral load that reads less than 1 pg/ml. This means that a patient's immune system has fought the virus enough to reduce the viral load.

As to your question about why the HPV wouldn't become immediately active again, there are a few explanations. You should be doing everything you can to help your immune system fight the virus. Sleeping enough, exercising, eating well. Look into DIM to promote cervical health. I personally take supplements, including green tea for which there is currently a clinical trial. Your immune system is very sensitive and can be affected by all of these things. I am careful not to be around those with colds or the flu. Fighting HPV is enough of a job for my immune system thank you very much, you may keep your germs. Also, doctors will tell you that following a procedure such as an excision, your immune system 'revs up' to treat the 'injured' part of your body. So your immune system is not a static thing, it is constantly changing, so take care of it the best you can.

I'm hoping all of this is relatively comprehensible, if not, I can give it another go, but I am sure some of the others can weigh in here too.

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Hi Pirkar -- Here's a link to an abstract (research paper summary) entitled "Rate of human papillomavirus clearance after treatment of cervical intraepithelial neoplasia." The abstract concludes, "Surgical treatment of CIN usually results in clearance of HPV infection within 3 months"

I would highly suggest finding the full text of this article. If you google the title, sometimes you can find the full paper from a source where you don't have to pay. Otherwise, the cost is usually about $30.

I'm pretty sure I found this paper and read the whole thing at one point, but I can't find it any longer. The researchers in this (and other) studies have found that excisional procedures usually result in clearance of HPV. One researcher speculated that it's because the HPV is simply removed along with the dysplasia. They quoted another paper where researchers dissected the tissue outside the excisional area and found that HPV in normal appearing tissue was rare. But I read another paper that said that HPV outside the excisional area was not uncommon.

In two papers I read, researchers speculated that recurrence of dysplasia resulted from:
1. Not all the HPV or dysplasia was removed via the procedure.
2. HPV migrated back up to the cervix from other spots in the genital area (such as vagina, vulva, etc, if the infection was still active there) or
3. Reinfection from an infected partner.

http://www.ncbi.nlm.nih.gov/pubmed/12423862

So Pirkar -- we don't really know whether an excisional procedure removes all the HPV or whether it remains in other spots throughout the genital area. If it did remain, it would be in the basal layer of one or more cells. But, a procdudre reduces viral load enough that women usually test negative for HPV within 3 months -- in research labs where I believe the testing is more sensitive than commercial tests (but I don't know that for sure).

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Hi GormCanor and corellin!

Thank you so very much! This issue became much clearer for me.

I do have one more question :-):
- if HPV will be not detected by HPV DNA test after the surgery, does it make sense to vaccinate? How many of you have been vaccinated after the treatment? It is rather expensive (and may have side-effects), so it makes sense to establish the likelyhood that these shots will protect you from: 1. infection by new type,
2. reinfection with the same type/recurrence by the same type. Do you have any clue in this? Have there been any studies on this?

My gyn (who seems not particularly updated or competent in HPV related issues) said that two weeks after surgery I shall vaccinate myself. However, my gyn/onc (who did the surgery) said it is too early - that first cervix shall heal (about 6 weeks or more), and it seemed to me that he did not believe vaccination would prove particularly beneficial. I was thinking that gynecologists may make some money or get other bonuses from medical companies if they are able to sell the vaccine so they are eager to propagate it even if there is no proof it would help?

PS I came across an abstract from Gyn Oncology journal that says that in addition to immunesuppresion and other risks (smoking, herpes etc), there are other risk factors like hormones etc. Thus, some of these risk factors we do have some control over (like smoking or immune system); on others probably not (like hormones). what do you think?

"It is not clearly understood why HPV infections resolve in certain individuals and result in cervical intraepithelial neoplasias in others, but several factors are thought to play a role; including individual susceptibility, immune status and nutrition, endogenous and exogenous hormones, tobacco smoking, parity, co-infection with other sexually transmitted agents such as HIV, herpes simplex virus type 2 and Chlamydia trachomatis as well as viral characteristics such as HPV type, concomitant infection with other types, viral load, HPV variant and viral integration."

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WG6-4PWF3M2-2&_u ser=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version= 1&_urlVersion=0&_userid=10&md5=15d337b1da2b99cf5b6413acd8e732a7

Thanks a lot for sharing your knowledge and all the best for now!
Pirkar

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Hi Pirkar -- I've always eaten tons of vegetables and have had a great immune system (and it seems to me that HPV progresses just as often in people with average/normal immune systems), so I tend to think that the progression of HPV depends on the virus type and degree of initial exposure more than anything -- plus the general susceptibility of your cervical/vaginal tissues. If the tissues are compromised in any way -- for example, dry, unlubricated sex, there's likely to be more tearing and more opportunities for the virus to implant in the basal cell layer. People who use tampons have less chance of clearing HPV and douching/over-bathing mess with the vaginal/cervical fluids that help clear out infections -- so, it's just really important to keep the cervical/vaginal tissues resiliant and healthy by not messing with the vagina. Hormonal birth controls such as the pill or progesterone producing IUD's can also affect the course of HPV. I don't believe that doctors ever mention those factors to women when we have dysplasia/HPV. My own doctor gave me nothing to do except wait, and the dysplasia progressed rapidly in 11 months. I also think that continued exposure to someone who has an active HPV infection before you've developed immunity to the virus can result in additional spots of infection throughout the genital area, so a person's partner's HPV status (whether they can clear the virus or not) may determine the outcome in some cases.

I have been reluctant to get the Gardasil vaccine, because I don't think there are any good studies about how it might affect an existing infection. I'm hoping there will be more data. Theoretically, it should protect from infection with types you haven't had. It can't clear an existing infection, but could it prevent an additional HPV16 exposure, for example -- especially if that exposure is a different variant? I don't know... I spoke with a researcher and she said there's no evidence that the vaccine could protect someone who has had HPV16 from an additional HPV16 exposure with the same or a different variant, but that doesn't theoretically make sense to me. I also wrote Gardasil and asked them and they couldn't answer that question. Theoretically, I would think it would protect against an additional exposure from the same virus, but wouldn't help clear the virus that's already implanted in the basal cell layer (if any exists there).

I hope that as the FDA is looking at possibly approving Gardasil for women over age 26, that they find more data to help us with this decision. The FDA did turn down Gardasil's request to extend approval for women over 26 not too long ago (I think in June of this year), but they didn't give details as to why approval was denied. Was it for health concerns or because they felt it wasn't cost effective?

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The thing you should know about Gardasil is that it's not a 'live-virus' or even dead virus vaccine like many others. What this means is that it does not contain the HPV virus and therefore one cannot become infected with HPV from the vaccine.

The studies that I have read are pretty conclusive on its effect against an existing infection. It has none. Very large study, and the results have been replicated.

I've not yet decided whether to get the vaccine once fully healed. I'm not currently sexually active so it's sort of a moot point for me. But, knowing that I could protect myself against other strains of HPV is a big sell on my end.

The real problem here is that the jury is still out on whether removing affected tissue is just removing affected tissue, or if it's removing all the virus. My intuition says no, given what I know about virology.

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The virus is in the basal layer of cells, so if the basal layer is removed during the procedure, then the virus is simply "cut out" (at that spot). But HPV can affect various sites throughout the epithelium, so removing it from one spot doesn't necessarily mean it doesn't remain somewhere else.

I understand that a person cannot become infected with HPV from the vaccine, but I don't know how the development of antibodies when a person already has that HPV type might affect the body's immune response to the virus. I don't know because I don't have a background in immunology and I haven't read any information that would explain to me how that would work.

And, yes, I understand that the vaccine wouldn't remove an existing infection, but we don't know that it wouldn't prevent an additional infection from the same virus type. There are many variants of HPV16 and a person can be infected with more than one of them, so why wouldn't the vaccine prevent an additional HPV16 infection. And... if natural immunity is not strong enough to prevent additional infection with the same virus type, then why wouldn't the vaccine prevent a person from being reinfected with HPV16 if they had cleared their initial infection.

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Thanks a lot! I guess as long as there remain more questions about the benefit of the vaccine for someone who is over 26 and has had HPV infection than straight answers are found, we should "wait and see." :-)

Many crucial questions remain as Corellin pointed out, like "how the development of antibodies when a person already has that HPV type might affect the body's immune response to the virus". Vaccine does not remove infection, but has it any effect on existing infection - does it help the immune system clearning it up or vice versa, perhaps it inhibits the process? Or may be there are no effects at all.

If there would be enough evidence, that it does not have negative effect on the existing infection and it will protect women over 26 from other strains of HPV, it would still be useful to vaccinate.

Corellin, I did not know that HPV 16 has many types!? Most leaflets and other general information sources tell us about different strains of high risk and low risk HVP.
How are these subtypes of HPV 16 distinguished?

My test said HPV 16 positive.
Should I request my doctor to specify also which type of HPV 16 and the viral load? I assume Gardasil protects from all HPV 16 types. Are some types of HPV 16 more aggressive (faster) than the others and do they know which are?

It is getting very complicated for someone without special education in biology, so I do not wonder that most gynecologist I spoke to were so ignorant about the details of HPV :-)

Thanks a lot for your input in making sense of this!

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Hi Pirkar,
I don't think your doctor would be able to tell you the variant or the viral load, but those two additional pieces of information would be incredibly valuable, since higher viral load usually indicates a higher risk of progression. (They have the capability to determine variant/viral load in a research lab, but I'm guessing not commercially.) And, yes, some variants of HPV16 are thought to be more aggressive than others, but it may depend on a person's ethnicity. Some studies have indicated that some ethnic groups are more susceptible to certain variants of the virus. I'm late for work and need to run, but you could google HPV16 variants and pull up all sorts of research studies that give probabilities related to the different sub-types. Also, I think there's a difference between sub-type and variant, but I'm not sure what the definition is -- maybe someone could find that out. And... there's even a way to distinguish a particular infection with HPV16, which gets down to even more detail than sub-type or variant, so you could conceivably figure out whether an infection is a recurrence or a new infection from an additional exposure if we were tested at that level of detail. Personally, I think if we had as much information as possible about our infection, we could pretty quickly unravel the infection/progression patterns of this virus, because we know the details of our personal lives/sexual history better than anyone. Lots of times I think research studies are a bit of a shot in the dark because they make a lot of assumptions based on limited information. But... it could be really prohibitively expensive to give that level of detail in testing. But, I don't know, because there hasn't been an emphasis on determining whether someone has HPV -- the emphasis is on determining whether someone has lesions that need to be treated. That's why, as GormCanor said above, they set the detection level higher, such that lower viral load results in a "negative" result, even though a person might still have HPV, and maybe even have it at a level that's contagious or might still progress. Sometimes I feel like researchers/regulators/ clinicians are dangling important information just out of our reach because they don't feel it's relevant because the emphasis is on treatment, not prevention. It's just very frustrating! I better end this before I start to rant!!

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i so agree with the frustration with the ability - or inability - to prevent hpv infection from developing into dysplasia. i'm going to post more on that in a moment....i've been feeling lots of frustration! and, corellin, i've read several of your postings which indicate that the excision process can remove not only the dysplasia but also the hpv, but what's going on if there is dysplasia and the hpv test shows negative? i understand that the virus can be elsewhere which is why there can be a recurrance of the dysplasia, but what about when it's not even showing with the current dysplasia? thanks in advance for enlightenment on this sort of situation.

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Flowershoplady -- that's a difficult question and one I've thought about and don't completely know the answer.

The HPV test could be a false negative, because the virus is at a more advanced stage and is not as productive -- or it could be a virus type not covered by the digene test. Also, there's a lag time between when the active HPV infection ends and dysplasia clears (I've read about 3 months) -- so it could be that the HPV has cleared and that the dysplasia will eventually regress as well. A researcher also told me that it's possible to develop immunity to HPV, but your body hasn't been able to clear a spot of dysplasia, such that once the dysplasia is surgically removed, you're not necessarily going to continue to develop more problems. In that instance, I wonder whether you will test positive for HPV. I'm pretty sure that if you biopsied the dsyplasia itself -- it would test positive for HPV -- particularly at higher grades of dysplasia. But maybe the virus is not shedding enough to be detectable -- except that it seems you would pick up some HPV when you scraped the dysplasia, uness the HPV is further down in lower cells.

It's also common to test positive for one HPV type but for the dysplasia to contain a completely different HPV type -- because the dysplasia corresponds to an earlier infection and the measurable HPV to a more recent, active infection.

Also, I was reading about HPV testing and found a bunch of research abstracts that compared the various tests. I since can't find my way back there, which is so frustrating!!! One of the abstracts was comparing the digene test to another test by another company and said that the digene test is only 67% sensitive for detecting HPV. So... when they say the digene test is 96% sensitive, they don't mean 96% sensitive in detecting any HPV -- they mean it's 96% sensitive when used in combination with the pap smear in detecting abormalities at a certain level.

HPV is also intermittently detectable and can fluctuate with our hormones and other things, so I think it's important to test negative twice in a row -- and usually that's what's required in research studies to confirm that HPV is more likely to be negative -- and research studies are using more senstive testing.

Those are some thoughts, but I don't think that's the full story. I think that's a good question for the research community, and maybe I'll ask that at the conference if there's an opportunity.

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thanks for that info, corellin. and, i think it's great that you're going to the conference....it would be so valuable to have someone very knowledgeable about hpv to attend and ask questions. at last year's conference, i had a basic knowledge of hpv, but have learned much more over the last year. (and your info you just posted fits some of what i probably experienced.). but....doesn't it seem like some of these questions really don't have answers because this &#@(O* virus doesn't behave in a consistent manner? i wonder what the hpv researchers think is the best way to handle hpv infection....yes, prevention would be best, but there's no sure way to currently do that. so, is the 'ideal' a way in which to treat the current hpv infections? or to somehow identify who will get dysplasia from their hpv infection? are we to accept that most people have hpv and target the 'cure' to those who develop hpv related disease, or are we to find a way to truly prevent the transmission and somehow detect who has it and when it can be transmitted. will that approach work, or is there too much room for error?
and, like you, i've got a strong immune system, have always eaten well, and yet my gyn immune system (ok, my immune system in all things between waist and knees!) is evidently not so strong. i think there needs to be a many branched approach to dealing with the whole issue of hpv related disease. how do we make sure that we won't get another hpv infection, or a rcurrence of our hpv infection, and if we do, what do we do? and, now i'm starting to vent...and to show my frustration. i understand that there is a goal to prevent cancer, but there also needs to be a goal to prevent dysplasia development. i look at my own history, and some of the women here, and we've been through years and years, even decades of having hpv related disease and treatments and surgeries. heck, even my hernia is indirectly related to hpv because i wouldn't have had two hernias if it weren't for the hysterectomy, and i wouldn't have had the hysterectomy if it weren't for the dysplasia, which bottomline all comes from the hpv infections. so, ok, i'll stop for now, and say thanks.

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Thanks once more, flowershoplady and corellin!

One thing still (among many, actually :-) puzzles me: when they say that HPV infection can progress into severe dysplasia and name the risk factors (immune supression, smoking, othe STDs like genital herpes and chlamydia etc ), they never mentione celluar level or gyn immune system. However, from discussions here I have understood that several women (like you two?) have not had risk factors (have had strong immune system, never smoked, not abused alcochol, always eat well, do not have other STD etc) and STILL HPV infection progressed to high grade dysplasia. (In my case, I know that I had several risk factors (due to stress and luck of sleep my immune system was down, I smoked, got STD (herpes) from my partner). BUT, as I learned from your posts, some women do not have any risk factors, but still develope cervixal dysplasia???

Thus, the general immune system may play little role in some cases of cervical dysplasia? Am I right?

PS Correlin, it would be awesome to read about some of important information that you will learn in the conferece.

With my very best wishes,
Pirkar

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sorry for misspelling, corellin :-)

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Have there been any timelines suggested for HPV to dysplasia/cancer? I had a cervical cancer diagnosis in 1990 and had a hysterectomy.

If it was from an HPV infection, I would have contracted it either 25 years before or just 3 months before.

Since it was 18 years ago and I was given *no* information whatever except that the pathology report came back as "boarderline" for possibility of spreading, I don't know the suspected cause or if there even was one. My mother had cervical cancer when I was 19 so I had just assumed that "like mother, like daughter" and never questioned it before the information on HPV came out.

There are no records for me to refer to as my doctor retired and the hospital says it doesn't keep any records beyond a few years.

I was tested for STD's as a standard test before surgery and the results were negative but did they test for HPV in 1990? Is HPV the only cause of cervical cancer and if not, what might some other factors be? I can find nothing about any other possible cause except HPV and for obvious reasons I'm having my doubts that either of my scenarios fit. Also, my mother says there's no possibility that her cancer was caused by HPV. Suggestions please?

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Hi Pirkar -- A researcher told me once that HPV can evade the immune system -- so your immune system can't fight what it can't see at all.

Here's a link to an article that says something similar, entitled "Study suggests HPV16 can skirt the immune system."

http://www.innovations-report.de/html/berichte/medizin_gesundheit/bericht-1 9954.html

But...what determines whether someone exposed to HPV actually gets the infection in the first place? Here's a link to research exploring why some women repeatedly exposed to HIV aren't infected and I'll bet some of these theories are relevant to HPV also. This article describes the anatomy of the female genital tract. This link is just to the abstract, and I have a printout of part of the article that I want to transcribe, but don't have time right now as I'm again running late for work. This abstract isn't going to be of much value, and I'm not sure where I got the detailed printout to the main article -- maybe I purchased it at one point. I'll try to type what I have after work today or see if I can get the article from the hospital library -- or you can purchase for $29.95. But it's a really interesting description of the genital tract and what affects susceptibility.

http://www3.interscience.wiley.com/journal/117966619/abstract

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lagata, hpv is the causative agent for at least 99.8% of cervical cancers, and some researchers are saying it's for all cervical cancers, even the more rare cervical cancers that they initially excluded. that means that the woman needs to have had an hpv infection at some point in order for cervical cancer to develop. of course, most women with hpv do not get cervical dysplasia nor cancer, so other factors come into play as well. i've read that the progression usually takes at least 10 years from initial hpv infection until cancer development, but i'm not sure how current that data is, particularly with hpv16 which often seems to progress faster than other hpv strains. also, you wouldn't really know when you initially got your hpv infection....it would be most probable in a new relationship, but not necessarily.

and, in 1990 there was no 'digene hpv test' which is done to detect cervical/vaginal hpv infections in women. doctors who were current on their gynecologic knowledge DID know in 1990 about the link between hpv and cervical cancer. i had my first experience with cervical dysplasia right around that time, and i still have the american cancer society booklet about hpv and how it can cause cervical cancer. at that time, without the 'hpv test' the pathology results, including paps, would indicate that a condition was indicative of hpv.

i'm sure that your mother may want to think that she didn't/doesn't have hpv....but we know that hpv is the causative agent of cervical cancer....meaning it's necessary for a woman to have an hpv infection in order to develop cervical cancer. there were never tests for hpv, and many people think there's a stigma associated with the virus, so that may be why she thinks she didn't/doesn't have hpv. remember that the hp virus strains that can cause cervical cancer don't show any symptoms, and unless there are earlier tests (such as paps) to show development of disease, cervical dysplasia/cancer can quietly develop, and once there are symptoms (such as bleeding), the devlopment has already reached a stage of cancer.

another interesting factor to consider is that having a mother or sister with cervical cancer increases one's odds for developing cervical cancer because the women share the genetic ability or inability to fight off the hpv infection. the longer the hpv infection is active, the higher the risk for developing dysplasia/cancer.

i hope all this info is helpful and makes sense for you.

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Hi Corellin!

Thanks a lot for the links! Wow - it is good to know that HPV16 may dodge the immune sytem! This information has not been available in leaflets nor internet sites on HPV/ cervical dysplasia. In opposite, they stress that dysplasia results in part of poor immune system (among other factors). But is its very important to know that strong general immune system may not save one from dysplasia/cervical cancer if one has got HPV16 :-)

Indeed, it would be good to know more about the whole female genital tract. I understand that there is a general immune system that helps to fight common colds etc, but there are also humoral and cellular immune responses that protect LOCALLY from infections and fight them off once already infected. So although my immune system is strong, I my lack adequate cellular response? And I have no control over that local level of immune response? I may eat well, exercise and lead a very healthy lifestyle, and still develop dysplasia for reasons unknown for the researchers.

With best wishes always,
Pirkar

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Pirkar -- I was able to obtain the research paper from the hospital library and will be glad to forward it to you or anyone who wants a copy. You can send me a friend request with your e-mail. It's an amazing paper that goes into detail about various types of immune responses and I think is completely relevant to HPV even though the focus is HIV.

Here are some basic points:
1. Can you believe that in Africa, women account for 60% of HIV-1 infected individuals and in young people 15-24, women account for 75% of all HIV-1 infected people in that region? More than 90% of infections resulted from heterosexual sex. The high rate of infection in women is thought to be because of social inequalities and the high degree of nonconsensual sex and because women are particularly vulnerable to infection due to biology -- "the substantial mucosal exposure of the female genital tract to seminal fluids."
2. We know that the area particularly vulnerable to HPV is the "transformation zone", so here is some information on that. I'm going to cut and paste an entire section -- sorry about the weird spacing... The main point is that the vulnerability of the vagina/cervix changes throughout a woman's life based on child bearing, monthly cycle, etc. -- so that if we're infected at a vulnerable time, I think we'd be more likely to get an infection that could cause harm.

"The area where
the tough squamous epithelium gives away to the fragile
single layer of columnar cells is called the transformation
zone. Throughout the reproductive life the
transformation zone lies at variable distances below
the external cervical os. In a healthy woman of childbearing
age, the cervix is well protected from abrasions
during intercourse by the tougher squamous
epithelium which covers the outside of the cervix.
However, during a condition called cervical ectopy,
the external cervical os is instead lined by a single
layer of columnar cells. This condition mostly occurs
in adolescence, during pregnancy or postpartum and
is associated with susceptibility to infections that can
more easily penetrate this type of epithelia. When
intact, the epithelial layers and the covering mucus of
the vagina and cervix constitute natural barriers to
HIV-1 infection. However, if the vaginal mucosa is
disrupted due to high-risk sexual behaviours, sexually
transmitted diseases or cervical ectopy, micro ulcerations
and breaks in the epithelium may occur. It is
important to mention that micro ulcerations may occur
during ‘normal’ coital acts as well. When studying
the female genital tract mucosa several factors of relevance
for HIV-1 transmission have to be taken into
consideration. The status of the epithelia and mucosal
secretions is influenced by differences in hormonal
levels due to stage of menstrual cycle, pregnancy, age
or use of oral contraceptives or intrauterine devices.
Also, during ovulation and menstruation the cervical
mucus plug which functions as a physical barrier to
invading pathogens is absent. Studies have shown that
being seropositive for herpes simplex type 2 (HSV-2)
may increase the risk of HIV-1 acquisition amongst
high-risk HIV-1-negative people exposed to HIV-1.
Likewise, the infectiousness of individuals co-infected
with HIV-1 and HSV-2 may increase during periods
of HSV-2 reactivation. In fact, it has been stated that
prevalent HSV-2 infection is associated with a threefold
increased risk of HIV-1 acquisition amongst the
general population, thus, in areas of high HSV-2 prevalence
a high proportion of HIV-1 may be attributable
to HSV-2 [2]."
3. Some women are exposed repeatedly to HIV and are never infected. Some even develop certain types of antibodies. It's thought that perhaps they are exposed continuously at very low levels (levels below the threshold of infectiousness) -- but just enough to cause an immune response. Could this also be true for HPV -- and what is enough exposure to cause infection versus to trigger an immune response?
4. It's thought that HIV is most infectious at the early stages -- here's a direct quote and I think this is definitely relevant to HPV -- except that HPV is more highly transmissable than HIV -- but maybe not all transmissions are problem infections that can't clear.

"Although the probability of transmission for each sexual
encounter with HIV-1 is believed to be quite small
(approximately 1 : 200–1 : 2000, male-to-female) [23,
24], new data convincingly indicate that these rates
vary greatly depending on the phase of the infection.
In a study on rates of transmission in an Ugandan
HIV-1-discordant couple’s cohort (i.e. one partner is
HIV-1-infected and the other not), the HIV-1-positive
partner’s stage of infection was highly associated with
the rate of transmission to the HIV-1-negative partner
[25]. Wawer et al. conclude that the transmission of
HIV-1 is the highest during the early-stage of infection
and that the cut off for this direct link between
viral load and transmission seems to be at 1500
HIV-1 RNA copies mL)1 of blood."
5. There's lots of information on different types of immune responses, including mucosal, cell-mediated, etc., but way beyond the ability of my brain to comprehend, so I think you need to read it for yourself -- but very, very interesting, and I'm wondering whether some people with antibodies to HPV never actually acquired the type of infection that was bad enough to cause a problem -- but maybe were at low levels of exposure.
6. I wish people would stop blaming our immune responses. That severely pisses me off!!

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flowershoplady -- back to something you said in a much earlier post about how you "wonder what the hpv researchers think is the best way to handle hpv infection...." -- I actually asked a lead researcher that question a few years ago and she thinks the current protocols which involve screening, LEEP procedures, etc. are just fine. She also told me she'd be more concerned about getting the flu than an HPV infection. When I related my experience with HPV to a urologist and told him I wanted a male test so I could avoid getting HPV in the first place, he suggested counseling for women who have had a bad outomce due to HPV. And, when I talked to the head epidemiologist at my hospital (who's responsible for infection control), he told me that I needed to live my life and not worry about getting an additional infection, because what were the odds that it would cause a problem? This is someone who's part of a handwashing campaign to reduce the spread of germs with the ultimate goal to "save lives." What a double standard we have between HPV, allowed to freely pass from person to person, and all other infectious diseases where there's some attempt at basic infection control!!

Thing is, we're not measuring the cost of our current protocol so regulators, researchers & clinicians all think it's OK just the way it is because we've reduced rates of cancer. I think a place to start is actually tracking the numbers. I'd like to know what's a woman's life-time risk of having an HPV-related procedure, what are those procedures and what are the outcomes of those procedures. Then if we shifted our goal to reducing procedures, rather than cancer, I think protocols would change as well to attain that goal. Currently, the focus is only on cancer prevention and cancer statistics are the only metric for measuring success.

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Now I have established that:
1. I got herpes simplex infection in Febrary 2005 from my current partner four years ago (don't know if type 1 or 2) and
2. because epithelia of my cervix was weakened due to herpes, it was more vulnreable to HPV16, and I got infected with the latter also (from the same partner) probably shortly after that
3. I am lucky that he does/did not have HIV, as according to the extract from the article on HIV, I would probably have got that infection too
4. I am pissed off because it seems that doctors were ignorant of my HPV infection/ASCUS, while after it had developed into CIN III, they became very interested in the surgegy. It made me think that doctors deliberately let my case to progress in order to be able to perform the surgery. This may be too paranoic, but indeed doctors DO seem so ignorant about the HPV infection unless the surgey is needed.

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