genital warts

Factors involved in clearance of genital warts

admin — Sat, 13 Mar 2010 17:39:22 +0000

Consecutive patients with first presentation of external anogenital warts had the location, duration at presentation, number of warts and wart area, age, smoking and sun bed use, and presence of coexistent sexually transmitted infections (STIs) recorded. The number of treatment episodes, and number of weeks, to clear the warts were documented. Number of warts and wart area at presentation were associated with time and number of treatments to clear. Those with 1-3 warts required significantly fewer treatment episodes and less time to clear than those with 11-41 warts, as did those with warts area 2-19 mm(2) compared with wart area 100-1038 mm(2). Using survival analysis, the number of warts was significant for the number of treatments and weeks to clear. The hazard ratio for clearance with double the number of warts after 4 treatments was 0.53 (95% confidence interval [CI] 0.37-0.76), and at 4 weeks was 0.70 (0.45-0.86). The clearance rates in non-smokers compared with smokers were higher, but not significantly different. Wart burden at presentation is an indicator of time to clearance. The number of warts is the best predictor – fewer warts results in earlier clearance.

Topical treatment of genital warts in men To evaluate the clinical efficacy of a 0.15% and a...
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Topical treatment of genital warts in men

admin — Sat, 13 Mar 2010 17:37:37 +0000

To evaluate the clinical efficacy of a 0.15% and a 0.3% cream formulation of podophyllotoxin in comparison with the 0.5% solution in the treatment of condylomata acuminata and to compare the treatment modalities regarding side effects. DESIGN–The study was designed as an open randomised trial. Ninety male patients with signs of penile HPV infection, with either acuminate or papular lesions, were randomised into three parallel treatment groups. The study medication comprised 0.15% and 0.3% cream and 0.5% solution of podophyllotoxin. The patients treated themselves twice daily for three consecutive days and if total regression of the warts was not achieved after this first treatment cycle, further treatment cycles at 7-day intervals were to be repeated up to a maximum of four treatments. SETTING–The study was carried out in three outpatient clinics: two STD clinics, Department of Dermatology and Venereology, University Hospital (45 patients) and Institut Antoine Fournier, Paris (30 patients), and one military hospital, S1/FO 47/48, Sjukhusenheten, Enköping (15 patients). RESULTS–Statistical evaluation of the treatment effect was based on a “Response rate” calculation at each visit. The number of completely responding patients after the first, second, third and fourth cycle were 40 (44%), 61 (68%), 67 (74%) and 70 (78%), respectively. There was no statistically significant difference between the three treatments after four treatment cycles. However, the 0.15% cream had a significantly slower onset of efficacy as compared with the 0.3% cream and 0.5% solution. Adverse effects were less severe and less frequent with the 0.15% cream than with the other treatment modalities. Severe adverse effects were reported by 12 patients, of whom two were treated with 0.15% cream, five with 0.3% cream and five with 0.5% solution. Thirty-one patients were completely free from adverse effects. CONCLUSION–In this open randomised study with three parallel treatment groups, two cream formulations of 0.15% and 0.3% podophyllotoxin and a 0.5% solution of the same drug all showed an equally good response rate after four treatment cycles. Reported adverse effects were few and mild. The convenience of having different formulations to offer when prescribing treatment for condylomata must be considered.

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THE MECHANISMS OF HUMAN PAPILLOMAVIRUS PATHOGENICITY

admin — Sat, 13 Mar 2010 17:26:37 +0000

Human papillomaviruses (HPV) cause benign and malignant hyperproliferative disease. A woman infected with HPV 16 (a high risk HPV)

has a 200-fold increased risk for the development of cervical cancer while one infected with HPV 6 (a low risk HPV) has a 10-fold increased risk. Notably, HPV 6 is the causative agent of the most prevalent viral sexually transmitted disease, benign hyperproliferative genital warts. Over a million new cases of this disease are diagnosed annually and almost four billion dollars in US health care costs are spent annually. HPVs replicate in the differentiated compartment of the epithelium. The viruses must, therefore, have the ability to either abrogate growth arrest that occurs when the infected cells differentiate or induce differentiated cells to re-enter the cell cycle. While an examination of the high risk viruses has been emphasized, it is imperative that we understand the mechanism of pathogenicity of the low risk viruses, clinically significant pathogens in their own right. Therefore, our focus is to define the interactions between HPV 6 and a differentiating epithelium that dictate the outcome of infection. Because of the interaction of E7 with pivotal cell cycle control proteins, E7 is likely to play a critical role in altering the intracellular environment in such a way as to promote the virus life cycle. For this reason, we have chosen to concentrate on this gene product. In Specific Aim 1 of the proposal we will establish the role of E7 in the HPV 6 life cycle. We will use the intact HPV 6 genome, with a translation termination linker in the E7 gene, to determine the necessity of 6E7 for a) episomal maintenance in primary undifferentiated keratinocytes during the non-productive stage of the life cycle, and b) the HPV-mediated aberrant cellular DNA synthesis in the suprabasal cell layer of organotypic raft cultures during the productive stage of the life cycle. We will also use the raft culture to determine the sufficiency of 6E7 in altering epithelial cell growth. In Specific Aim 2 we will conduct a structure/function analysis of the 6E7 protein to identify regions of E7 pertinent to the virus life cycle. We will analyze the mutants in the context of the intact genome for their necessity in episomal maintenance in undifferentiated cells and for reprogramming suprabasal cells to enter S phase. In Specific Aim 3 we will determine the cellular targets of 6E7 relevant to the life cycle of the virus, with emphasis on the pRb family:E2F-mediated pathways. The effect of 6E7, in the context of the entire genome, on cellular gene expression during the non-productive and productive stages of the life cycle, will be determined. By conducting these experiments under physiological conditions that mimic a natural infection, we expect to make novel contributions on the activities of this important protein.

CELLULAR TARGETS FOR PAPILLOMAVIRUS E6 ONCOPROTEINS The human papillomaviruses (HPVs) are associated with specific human cancers,...
HUMAN PAPILLOMAVIRUS T AND B CELL RESPONSES Genital human papillomavirus (HPV) infections represent the most common viral...
Human Papillomavirus – HPV Human papillomavirus (HPV) infection Human papillomavirus (HPV) infection is the most...

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STRATEGIES AGAINST HPV RELATED GENITAL DISEASES IN WOMEN

admin — Tue, 09 Mar 2010 16:04:43 +0000

The human papillomavirus (HPV) is a significant etiologic agent in lower female genital tract neoplasia. Novel interactions with other co-carcinogens and/or immuno-deficiency lead to tumorigenesis and cancer progression. However, both the lack of adequate animal models and prospective clinical trials are impediments to the development of effective anti-HPV therapies and prevent a thorough understanding of human interactions with this virus. The objective of this proposal is to support the career development of Bradley J. Monk, M.D. Under the direction of Dr. Luis P. Villarreal, Ph.D., Dr. Monk will evaluate co-carcinogens and anti-viral agents in a recently described severe combined immunodeficiency mouse model using implanted human HPV infected epithelium, cervical intraepithelial neoplasia (CIN). Dr. Monk proposes to study the neoplastic transformation as well as the progression or regression of these cervical tissue implants. The influence of specific promoters or genotoxic compounds (e.g. hormones, nicotine) as well as novel anti-HPV agents (e.g. stimulated immune cells, anti-sense oncogenes) and nutritional supplements (e.g. indole 3-carbinol or I3C) will be studied. In addition, under the direction of Philip J. DiSaia, M.D., a Gynecologic Oncologist; Frank L. Meyskens, M.D., a Medical Oncologist with expertise in Chemoprevention; and Jeffrey S. Weber, M.D., Ph.D., a Medical Oncologist with expertise in Immunology, Dr. Monk will conduct two prospective clinical trials of novel HPV therapies. First, I3C, a compound found in cruciferous vegetables and effective in HPV related laryngeal papillomatosis, will be evaluated in patients with HPV induced genital warts in a randomized phase II trial. Second, a phase I and II study of a DNA plasmid vaccine encoding an immunogenic portion of the HPV type 16 E7 protein is planned among women with CIN. Dr. Monk will focus his career on translational research in the area of anti-HPVmodalities specifically related to female lower genital
tract neoplasia. Mentors in Virology, Chemoprevention, Immunology and Gynecologic Oncology will allow Dr. Monk to investigate unique anti-viral agents both in the laboratory and in clinical settings with an emphasis on HPV immunity. This path will develop Dr. Monk into an independent investigator able to study anti-HPV therapies first in animals then in human chemoprevention trials. It is expected that Dr. Monk will have obtained extramural funding for both his laboratory and clinical studies by the end of the period of support requested.

Human Papillomavirus – HPV Human papillomavirus (HPV) infection Human papillomavirus (HPV) infection is the most...
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Immunology of Genital Warts HPV infection on the host immune response, include cell-mediated immunity...

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PREVALENCE OF HPV IN THE ORAL CAVITY OF HIV+ INDIVIDUALS

admin — Tue, 09 Mar 2010 16:01:31 +0000

Human immunodeficiency virus (HIV) has infected over 33 million people worldwide leading to immune suppression from the selective depletion of CD4+ T cells. This lack of immunity results in numerous opportunistic infections with over 50% of the HIV-infected individuals developing pathology involving the oral cavity. Among the pathogens responsible for oral disease in HIV+ patients is the mucosatropic human papillomavirus (HPV). Although HPV cannot be routinely cultured, it is the most common viral sexually transmitted disease. HPV is the etiologic agent of oral and genital warts, focal epithelial hyperplasia, and a large proportion of cervical, anogenital, and oral squamous cell carcinomas. HIV co-infection leads to increased rate of HPV genital infection, increased HPV persistence, and increased rates of HPV-related pathology (cervical or anal dysplasia), which is more difficult to treat. Similarly, preliminary studies indicate that HIV co-infection leads to increases in the prevalence of oral HPV and HPV-related oral pathology including oral cancer. Surprisingly, treatment of HIV with highly active anti-retroviral therapy (HAART) has led to increases in apparent HPV-related oral warts. These warts have been large, painful, and difficult to treat. Continued use of HAART for the HIV+ patient may lead to substantial increases in the incidence of oral warts and other HPV-related oral pathology such as squamous cell carcinomas. The studies to date have been limited by the lack of or the restrictive scope of the molecular techniques used to detect HPV infection. Thus, little is known about the prevalence, site of infection and natural history of oral HPV infection. A better understanding of oral HPV infection particularly in the HIV+ co-infected individual is of paramount importance in order to prevent HPV-related oral pathology. Preliminary data demonstrates the ability to detect oral HPV infection utilizing consensus PCR primer sets that were developed for detection of genital HPV. These techniques can be extended to detect oral HPV types. We hypothesize that a high throughput PCR-based method for detecting oral HPV types can be developed and utilized to determine the prevalence and site of oral HPV infection in a cohort of HIV+ individuals

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HUMAN PAPILLOMAVIRUS T AND B CELL RESPONSES

admin — Tue, 09 Mar 2010 16:00:25 +0000

Genital human papillomavirus (HPV) infections represent the most common viral sexually transmitted disease in the United States. These functions cause conditions that include anogenital warts and cervical dysplasias. These diseases can spontaneously regress but the immunologic mechanisms that contribute to the regression are poorly characterized. The experiments in animal models strongly suggest that papillomavirus-associated diseases can be prevented by immunization with virus-like particles (VLP) derived from the major capsid protein of HPV. The present proposal will focus on clinical samples from two unique patient populations. The first is comprised of human volunteers vaccinated with the first HPV type 11 VLP vaccine. This trial is completed and lymphocytes and sera are available. A second group with clinically evident anogenital warts will be treated with autogenous vaccination to induce clinical regression. Sera, peripheral blood mononuclear cells, and most importantly, wart infiltrating lymphocytes will be available for study. These samples will be utilized to study the antigen specificity of the B and T cell populations involved in HPV- specific vaccine responses and anogenital wart regression. Specifically, the peripheral T cells responses to structural and non-structural HPV-6 and -11 proteins will be identified, and the fine specificity for the reactive proteins will be further determined. The frequency of these HPV-6 and-11 specific CD4 and CD 8 T cells will be measured in peripheral blood. Using these results as a guide, the antigenic specificity and frequency of infiltrating T lymphocytes in anogenital warts will be determined. The specific relationship between disease regression and T cell populations will be investigated. For the B cells, the capsid protein conformational and linear epitopes that are recognized by the subjects will be determined, and whether any of the linear epitopes are neutralizing will be established.

CELLULAR TARGETS FOR PAPILLOMAVIRUS E6 ONCOPROTEINS The human papillomaviruses (HPVs) are associated with specific human cancers,...
THE MECHANISMS OF HUMAN PAPILLOMAVIRUS PATHOGENICITY Human papillomaviruses (HPV) cause benign and malignant hyperproliferative disease. A...
Immunology of Genital Warts HPV infection on the host immune response, include cell-mediated immunity...

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CELLULAR TARGETS FOR PAPILLOMAVIRUS E6 ONCOPROTEINS

admin — Tue, 09 Mar 2010 15:58:25 +0000

The human papillomaviruses (HPVs) are associated with specific human cancers, most notably human cervical cancer. More than 70 different HPVs have now been described and approximately 25 of these are associated with lesions of the anogenital tract. These anogenital associated HPVs can be further subdivided into two groups on the basis of the clinical lesions with which they are associated. The “low risk” HPVs (e.g. HPV-6 and HPVI l) are associated with benign genital warts or condyloma acuminata that only very rarely progress to cancers, whereas the “high risk” HPVs (e.g. HPVI6 and HPVI8) are associated with intraepithelial neoplasias that can progress to cancer. Approximately 85-90% of human cervical cancers contain and viral DNA from a “high risk” HPV type and express the HPV E6 and E7 genes. This along with independent biochemical evidence, suggests strongly that the proteins encoded by the E6 and E7 genes of the “high risk” HPVs contribute directly to carcinogenic progression in the HPV positive cancers. The E7 proteins functions in cellular transformation, at least in part. through interactions with the product of the retinoblastoma susceptibility gene, pRB, and the other pRB related “pocket proteins”. The major target of the E6 oncoprotein encoded by the genital tract, cancer associated human papillomaviruses is the p53 tumor suppressor protein. However, several lines of evidence indicate that the E6 protein of the cancer associated HPVs has additional cellular targets. Furthermore, the strongly oncogenic E6 protein encoded by the bovine papillomavirus does not cause transformation by a p53 dependent pathway. The specific aims of this grant proposal are designed to examine additional targets of the papillomavirtts E6 proteins that may be important to the transformation functions of the virus and to determine how the E6 interaction may affect the function of these cellular targets. We will determine the physiologic consequence of the interaction of E6 with the focal adhesion/LIM domain proteins paxillin and hic5. We will determine the consequences of the binding of HPV16 E6 to Interferon Regulatory Factor (IRF-3). Also we will determine the relevance of the binding of E6 to specific cellular targets to its transformation and tumorigenic functions.

THE MECHANISMS OF HUMAN PAPILLOMAVIRUS PATHOGENICITY Human papillomaviruses (HPV) cause benign and malignant hyperproliferative disease. A...
HUMAN PAPILLOMAVIRUS T AND B CELL RESPONSES Genital human papillomavirus (HPV) infections represent the most common viral...
Genital Warts – Human Papillomavirus (HPV) Genital Warts – Human Papilloma Virus (HPV) Genital warts are...

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ACQUISITION & NATURAL HISTORY OF GENITAL HPV INFECTIONS

admin — Tue, 09 Mar 2010 15:57:14 +0000

Human papillomaviruses (primarily HPV 16 and 18) play a central role in the development of in situ and invasive cervical cancer. Based on this observation and the well-recognized shortcomings of Pap smears, several groups have examined the use of HPV DNA testing as an adjunct to cytologic screening and found it to be cost effective. Consequently, a number of laboratories throughout the U.S. have begun offering HPV DNA tests, and in doing so, have left many clinicians and their clients with questions that currently do not have answers. Although the potential consequences of genital HPV infection are well documented, we know relatively little about the long-term implication; of a single or repeatedly positive type-specific HPV DNA test result. Furthermore, it is likely that HPV vaccines will introduced to prevent cervical cancer and, perhaps, genital warts in the future. However, knowledge of the infectivity and natural history of specific HPV types is essential for evaluating the impact and feasibility of vaccines. Much of this required knowledge is currently lacking. Since 1991, we have been studying the short term natural history of HPV in a cohort study of 600 freshman women and are now in a position to build on and extend these studies to gain an understanding of the longer-term natural history of genital HPV infection and of male to female transmission rates. Our specific aims are to l) define the natural history of genital HPV infection over ten years with respect to persistent detection of HPV DNA, SIL, genital warts, and HPV type-specific antibodies, 2) determine the prevalence, seroprevalence, and behavioral predictors of genital HPV infection among a random sample of male undergraduate students, and 3) estimate per partner and per act transmission rates of specific HPV types and define characteristics of partnerships (e.g., courtship behavior, condom use, and frequency of intercourse) and of partners (e.g., age, race, occupation, number of partners, circumcision status, and report of concurrent relationships) that affect transmission. The proposed study is likely to provide important information relevant to the development of effective HPV prevention strategies, including the synthesis of accurate and informative public health messages concerning the transmissibility of HPV and the meaning of a single or repeatedly positive HPV DNA test. Additionally, these data will provide investigators working on HPV vaccine development with information that is needed to guide the selection of appropriate target populations, outcome measures, and immunization strategies.

THE MECHANISMS OF HUMAN PAPILLOMAVIRUS PATHOGENICITY Human papillomaviruses (HPV) cause benign and malignant hyperproliferative disease. A...
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Oral genital warts in Children

admin — Tue, 09 Mar 2010 15:54:47 +0000

The incidence of condylomata acuminata in children seems to be increasing, paralleling a rising incidence reported in adults. This article reviews condylomata acuminata in children. The etiologic agent is the human papillomavirus (HPV), which causes soft, clustered, papillomatous growths of various sizes and shapes seen on moist mucosal surfaces, most frequently around the genital and rectal cases. The authors report a case series of three recent cases of children with condylomata in the oral cavity. For each of the three children described, the following observations were made: examination revealed a healthy child with no findings of warts outside the oral cavity; results of an anogenital examination were unremarkable, without signs of trauma, infection, or genital warts; and serologic tests for syphilis, hepatitis B, and HIV were negative. The authors review the cases presented, including the treatment. They note that the clinical recognition of mucosal HPV infection in a child raises all the unknowns about treatment and prognosis that accompany HPV genital infection in an adult. The additional burden for the pediatric caregiver is the concern that HPV mucosal infections in a child may be a manifestation of child sexual abuse. 5 figures. 28 references.

PREVALENCE OF HPV IN THE ORAL CAVITY OF HIV+ INDIVIDUALS Human immunodeficiency virus (HIV) has infected over 33 million people...
Human Papillomavirus – HPV Human papillomavirus (HPV) infection Human papillomavirus (HPV) infection is the most...
genital warts [caption id="attachment_4" align="alignnone" width="477" caption="SOA-Condylomata-acuminata-female"][/caption] Genital warts (or Condyloma, Condylomata...

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HPV Genital Warts

admin — Sun, 07 Mar 2010 12:40:53 +0000

Human Papilloma Virus (HPV) is the most common sexually transmitteddisease in the United States. It is also harder to understand thanother STDs. It is actually a group of common viruses which cause wartson different parts of the body. There are particular strains of thatcause genital warts and some are linked cervical cancer. The medicalterm for warts in the genital area is condyloma acuminatum. It isusually spread by genital to genital contact. This can include penilepenetration, but skin to skin contact is all that is necessary. It canalso spread within the genital area after contact; anal lesions aresometimes found in women and men who have had no anal intercourse.Infection after oral sex is rare but has been reported (in some caseslesions were found on vocal cords). Warts on the hand or foot are adifferent strain of and are not transmissible to someone’s genitals.Symptoms: The incubation period is one month to many years. Palpable lump or irregularity of the skin surface (feels rough)

Soft, moist, pink or red swellings, raised or flat a sometimes cauliflower-like

Painful intercourse if the lesions are rubbedNO SYMPTOMS: The virus is often asymptomatic, especially women becausethe warts can be located within the vagina and on the cervix. This iswhy annual Pap smears for sexually active women are so importantGenital warts on the penis and the vulva are usually diagnosed byvisual inspection. is harder to diagnose on the vagina and cervix.Biopsies (tissue samples) and/or magnification with a specialinstrument called a colposcope are sometimes used. Acetic acid(vinegar) may be applied to lesions because this will make them turnwhite so they are easier to identify. For women, can be detected with aPap smear, and often this is the only way that the diagnosis can bemade. Newer Pap smears such as “Thin Prep” are wet smears, and can beused to determine which strains of a person has. Often people wonderwhy there is no blood test for . A blood test looking for antibodies isavailable, but it is expensive and the information it provides is notparticularly useful. is so common that many people will have theantibodies, and then it would be back to a visual exam to decide thenext course of action. Regular Pap smears would be important, but theyare already recommended once a year for all women regardless ofdiagnosis.At present, there is no cure for . For cosmetic purposes, the lesionscan be treated by applying Podophyllin (done by a health carepractitioner). This treatment must be reapplied over several visits toa clinic, and cannot be used on some lesions. Liquid nitrogen,electrocautery, and lasers can also be used to destroy the warts.Recurrence is common and often related to stress.HPV has been strongly linked to cervical cancer in women. All types ofcan cause mild Pap smear abnormalities that do not have seriousconsequences, but 15 of the 30-40 identified genital types can lead tothe development of cervical cancer. Three of these strains areconsidered high risk. Cervical cancer is detected through the Papsmear, and is the most compelling reason for women to receive an annualpelvic exam which includes a Pap smear. When caught and treated,cervical cancer, or often pre-cancerous cells of the cervix do not leadto further health complications. Persistent infection with is the keyrisk for cervical cancer (most women with do not have persistentinfections after the first two years).Since HPV can be transmitted skin to skin and because it is the most common STD around, prevention is particularly difficult. Barrier methods (condoms, dental dams) always help, but are not totally effective due to skin contact beyond the barrier.

Regular testing, especially testing within a monogamous relationshipcan be effective, though symptoms are not always obvious, and testingfor is more complex than just peeing in a cup or getting a blood test.

The virus can be present and transmissible even if not apparent, so barrier methods are still a good idea

Women should have yearly Pap smears to screen for cervical cancer and other precancerous conditions.

Avoid sexual contact with people who have visible symptoms of an STDSince is treatable, but not curable, people with should communicatewith their partners about prevention. Risk of transmission can bereduced by avoiding sexual contact when lesions are present.Additional Info: The most common type of in the US is type 16, which handily enough isalso one of the two strains most likely to cause cancer. (The otheris 18). Currently a vaccine for type 16 is in the later stages ofdevelopment.

At this point, the best way to prevent cervical cancer is to test forthe group of high-cancer-risk strains. This is why Thin Prep or otherwet smears are so coolathey can tell you exactly which strain(s) youhave and thus approximately how much you should worry.

Multiple infection (one or more strains is common) and that almosteveryone will get of some kind in their lifetime. Cervical cancer isdangerous. Worldwide, half the women diagnosed will die. In the US, athird die. Fortunately cervical cancer is extremely slow growing.

The average abnormality takes 10 years to develop into cancer (though afew strains can cause cancer in as little as one year inimmuno-compromised individuals), but if treated early is usually notdeadly.

Vaden has decided to start offering a “wet-preparation” Pap smear. They’re doing the final logistical checks now.

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