Around 10 years ago, I was told that there was presence of HPV. Since then, I got regular checkups, however, the virus seemed to either shed itself or disappear because my paps always came back with no HPV.
Since I had been diagnosed, I never had any outward signs of HPV--i.e., warts. However, about two days ago, I got checked up because I had growths around my rectum and anus. Initially, I thought they were hemorrhoids because the growth was right by my opening. But more appeared and when I went to the doctor, she said that it was warts. I was so surprised because this has never happened before.
Has any one had this happen--have you ever had been diagnosed with HPV, not have any signs for many years--even been told that the virus may have shedded itself--and now, you have warts?
Also, how rare is it to get more than one strain of HPV? There are more than 100 different strains of HPV, but only a few cause warts. Typically within a few years of contracting HPV, the body essentially immunes itself to it or corrects the problem. What has most likely happened is that you have picked up another form of HPV recently and that has caused the outbreak. The form you contracted 10 years ago may not have been the wart causing type. I have done lots of research on STD's due to working in the preventive medicine clinic for the military, and I have discovered that HPV has been found on people's hands. At a minumum, 65% of Americans have at least one strain of HPV and don't even realize it. I hope this helps you out a little bit. I have Hpv for about 5 years ..1 break out. They said its when your body get worn down you can have an out break. The flu, pregnancy etc. Just be care full. Surgery is PAIN-FULL, but effective. Stay calm, refrain from sex. Because during a break out you can transmit it and pass it along. The creams never worked for me, but may work for you. Sometimes they go away on there own! There is no cure for HPV however in most cases a person builds immunity to their HPV type or types.
Our Pap smear looks for abnormal cells of the cervix. An HPV test may not be run if no abnormal cell changes are found.
The FDA approved HPV test screens for 13 high risk HPV types no low risk HPV types are included in this screening. Our HPV test does not tell us what specific HPV type or types we carry. A new partner can introduce a new HPV type. They are 30+ HPV low and high risk HPV types that affect the genital area. The HPV test is only a sampling of our cervical tissue. It does not include vulva or anal cells. There is no standard screening for these areas.
INTENDED USE
The hc2 High-Risk HPV DNA Test飩€?DNAwithPap鈩?* using Hybrid Capture飩€? (hc2) technology is an In Vitro
nucleic acid hybridization assay with signal amplification using microplate chemiluminescence for the qualitative
detection of thirteen high-risk types of human papillomavirus (HPV) DNA in cervical specimens. The HPV types
detected by the assay are the high-risk HPV types 16/18/31/33/35/39/45/51/52/56/58/59/68. The hc2 High-Risk
HPV DNA Test cannot determine the specific HPV type present.
http://www.digene.com/pdf/L2290-P.I,%20h...
HPV type 6 or 11 causes most all visible genital warts.
At this moment your HPV infection is of the anal area. If you have engaged in anal sex then it may be a good idea to see a proctologist to see if the virus is also located in the anal canal.
Many of us have more than one HPV type.
Genital warts
Condylomata bearing HPV-6 or -11 have identical clinical
manifestations and histology [2]. Recent studies have shown that about
100% of GWs are caused by either HPV-6 or -11 but that 20鈥?0% of
lesions also contain co-infections with HR HPV types [3] and [4]. GWs
do not usually result in major morbidity or mortality, but cause
significant psychological morbidity and very substantial healthcare
costs. Occasionally GWs persist for long periods of time and, rarely,
such long-standing lesions may progress to malignancy. GWs are highly
infectious, with a transmission rate of about 65% within sexual
partnerships from an infected to a susceptible sexual partner, and an
incubation period of between 3 weeks and 8 months, with the majority
developing warts at around 2鈥? months [3]. Once GWs have developed,
they may show minimal change over time, become more numerous or
larger, or regress spontaneously. The majority of placebo-controlled
GW therapy trials show low rates of regression (around 5% complete
clearance) in the short term, although in one study over 16 weeks 20%
of women and 5% of men using placebo completely cleared their warts,
and 38% of women and 22% of men using placebo cleared over 50% of
their baseline warts [3]. Regressing warts contain significantly more
CD4 positive T cells, both within the stroma underlying the lesions
and the condylomata themselves, and greater expression of activation
markers [3]. There is no report of the rate of spontaneous regression
that may occur in the longer term. Following GW clearance with
therapy, recurrence is common and is often seen within 3 months in 25%
of cases, although rates of up to 67% have been observed [3]. In
clinical practice recurrences are often seen at sites of previous
lesions, and in these cases HPV infection in stem cells or
slow-turnover cells at the site of previous clearance has persisted
and then reactivated. The proportion of HPV-6/11 infections that are
either completely cleared or persist in a latent form after clinical
resolution is unknown, and, indeed, animal models suggest that both
outcomes can occur [3].
HPV-6/11 as a cause of cervical neoplasia
HPV-6 and -11 are frequently associated with LSIL. A recent
meta-analysis of 55 studies reported HPV-6 to be present in 8.1% of
HPV-positive LSIL cases and HPV-11 in 3.2% of cases [25]. However, it
remains unclear in what proportion of these HPV-6/11-positive LSIL
cases there is concomitant co-infection with a HR type, and whether
such HR co-infections would be "minority passenger" infections as
described in GWs, or represent true multiple-morphology cervical lesions.
Published by the University of Chicago Press
______________________________________...
Title Concurrent and Sequential Acquisition of Different Genital Human Papillomavirus Types
Author(s) Katherine K. Thomas, James P. Hughes, Jane M. Kuypers, Nancy B. Kiviat, Shu-Kuang Lee, Diane E. Adam, and Laura A. Koutsky
Identifiers The Journal of Infectious Diseases, volume 182 (2000), pages 1097鈥?102
DOI: 10.1086/315805
PubMed ID: 10979905
Availability This site: PS | HTML | PDF (78.8k)
Copyright 漏 2000, the Infectious Diseases Society of America.
Abstract Coinfection with multiple types of genital human papillomavirus (HPV) has been reported, but how frequently it occurs and whether prior infection with specific HPV types inhibits subsequent infection by related types are not known. To address this, 518 women were followed for an average of 2.9 years, and behavioral information and cervical and vulvovaginal swabs for HPV DNA assay were obtained at 4-month intervals. A polymerase chain reaction based method was used to detect types frequently found in cervical cancers (HPV 16, 18, 31, and 45) and in genital warts (HPV 6 and 11). Concurrent acquisition of multiple types occurred more often than expected by chance. However, no 2 types were more or less likely to be acquired concurrently than any other 2 types. When considering sequential acquisition of HPV types, we found that risk of acquiring a new HPV type was not decreased among those with prior infection by a phylogenetically related or unrelated type (hazard ratio [95% confidence interval], 1.0 [0.4 3.0] and 1.3 [0.8 2.1], respectively).
Chapter 5: Updating the natural history of HPV and anogenital cancer
Anna-Barbara Moscickia, , , Mark Schiffmanb, Susanne Kjaerc and Luisa L. Villad
aDepartment of Pediatrics, Division of Adolescent Medicine, University of California, San Francisco, 3333 California Ave Suite 245, San Francisco, CA, USA
bHormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA
cInstitute of Cancer Epidemiology, Copenhagen, Denmark
dDepartment of Virology, Ludwig Institute for Cancer Research, Sao Paulo, Brazil
Received 1 March 2006; accepted 6 June 2006. Available online 23 June 2006.
Abstract
The major steps in cervical carcinogenesis include infection of the metaplastic epithelium of the cervical transformation zone with one or more of the 12鈥?8 carcinogenic types of human papillomavirus (HPV) infection, viral persistence, clonal progression of the persistently-infected epithelium to cervical precancer, and invasion. Although these fundamental steps are established, several new epidemiologic studies have shed light on the factors that influence each of these transitions. The importance of the transformation zone in cervical cancer has been extended to other HPV-induced cancers such as anal or tonsillar cancers. Natural history studies show that HPV with normal cervical cytology and cervical intraepithelial neoplasia (CIN) grade 1 behave similarly, with the majority of both showing regression. Although these studies have demonstrated the importance of HPV persistence in the development of precancer CIN-3, the timing from infection to evidence of CIN-3 varies from 1 to 10 years. Whether equivalent lesions diagnosed later differ in their natural history remains unknown. Several factors have been implicated in enhancing persistence and/or progression. However, none are consistently associated with both except age: young women are less likely to show persistence and older women with persistence are more likely to be at risk of invasive cancer. Recent studies have also underscored the importance of the host immune response in clearance of established infections. Finally, data on non-cervical HPV infections, such as penile infections are limited to date compared to cervical infections. Several ongoing cohort studies should give us further insight into male infections in the near future.
Keywords: Natural history; HPV; Anogenital cancer
linkinghub.elsevier.com/retrieve/pii/S...
CHAPTER 3 Pathology of HPV infection at the cytologic and histologic levels: Basis for a 2-tiered morphologic classification system
Thomas C. Wright, Jr.
Available online 31 January 2007.
Abstract
Over the last 2 decades the pathogenesis and natural history of cervi-cal cancer has become clearer. As a result, the cytologic and histologic terminol-ogy used to refer to cervical cancer precursors has needed to change. Today we recognize that almost all cervical cancers are due to infection with specific high-risk types of human papillomavirus (HPV). Most women become infected with these viruses within several years of initiating sexual intercourse and a productive HPV in-fection frequently results in characteristic morphologic changes within the infected cervical squamous cells. Cells demonstrating the morphologic changes associated with a productive HPV infection are referred to as low-grade squamous intraepi-thelial lesions (LSIL) when observed in cytologic specimens and low-grade cervical intraepithelial neoplasia (CIN 1) when observed in histologic specimens. In some women, HPV gene expression becomes unlinked to the state of differentiation of the infected epithelial cells and deregulated expression of the early region of the viral genome results in a dramatic increase in expression of two HPV oncoproteins (E6 and E7). This results in loss of normal cell cycle control of the epithelium and genetic instability. When this occurs the epithelium develops characteristic mor-phologic features, with immature 鈥渂asaloid-type鈥?squamous cells and mitotic fig-ures in the upper half of the cervical epithelium. Such lesions are felt to represent 鈥渢rue鈥?neoplasia and are referred to as high-grade squamous intraepithelial lesions (HSIL) when observed in cytologic specimens and high-grade cervical intraepithelial neoplasia (CIN 2,3) when observed in histologic specimens.
KEYWORDS: Squamous intraepithelial lesion (SIL); Cervical intraepithelial neoplasia (CIN); Cervix; Cancer precursors; Human papillomavirus (HPV |
