December 30, 2009 by admin · Comments Off
Information on HPV and Genital Warts
What is a genital HPV infection?
Genital human papillomavirus (also called HPV) is the most common sexually transmitted infection (STI). There are more than 40 HPV types that can infect the genital areas of males and females. These HPV types can also infect the mouth and throat. Most people who become infected with HPV do not even know they have it.
HPV is not the same as herpes or HIV (the virus that causes AIDS). These are all viruses that can be passed on during sex, but they cause different symptoms and health problems.
What are the signs, symptoms and potential health problems of HPV?
Most people with HPV do not develop symptoms or health problems from it. In 90% of cases, the body’s immune system clears HPV naturally within two years.
But sometimes, certain types of HPV can cause Genital Warts in males and females. Rarely, these types can also cause warts in the throat — a condition called recurrent respiratory papillomatosis or RRP.
Other HPV types can cause cervical cancer. These types can also cause other, less common but serious cancers, including cancers of the vulva, vagina, penis, anus, and head and neck (tongue, tonsils and throat).
The types of HPV that can cause Genital Warts are not the same as the types that can cause cancer. There is no way to know which people who get HPV will go on to develop cancer or other health problems.
Signs and symptoms of HPV-related problems:
Genital warts usually appear as a small bump or groups of bumps in the genital area. They can be small or large, raised or flat, or shaped like a cauliflower. Health care providers can diagnose warts by looking at the genital area during an office visit. Warts can appear within weeks or months after sexual contact with an infected partner—even if the infected partner has no signs of genital warts. If left untreated, genital warts might go away, remain unchanged, or increase in size or number. They will not turn into cancer.
Cervical cancer usually does not have symptoms until it is quite advanced. For this reason, it is important for women to get regular screening for cervical cancer. Screening tests can find early signs of disease so that problems can be treated early, before they ever turn into cancer.
Other HPV-related cancers might not have signs or symptoms until they are advanced and hard to treat. These include cancers of the vulva, vagina, penis, anus, and head and neck. For signs and symptoms of these cancers, see www.cancer.gov.
RRP causes warts to grow in the throat. It can sometimes block the airway, causing a hoarse voice or troubled breathing.
How do people get HPV?
HPV is passed on through genital contact, most often during vaginal and anal sex. HPV may also be passed on during oral sex and genital-to-genital contact. HPV can be passed on between straight and same-sex partners—even when the infected partner has no signs or symptoms.
A person can have HPV even if years have passed since he or she had sexual contact with an infected person. Most infected persons do not realize they are infected or that they are passing the virus on to a sex partner. It is also possible to get more than one type of HPV.
Very rarely, a pregnant woman with genital HPV can pass HPV to her baby during delivery. In these cases, the child can develop RRP.
How does HPV cause genital warts and cancer?
HPV can cause normal cells on infected skin to turn abnormal. Most of the time, you cannot see or feel these cell changes. In most cases, the body fights off HPV naturally and the infected cells then go back to normal. But in cases when the body does not fight off HPV, HPV can cause visible changes in the form of genital warts or cancer. Warts can appear within weeks or months after getting HPV. Cancer often takes years to develop after getting HPV.
How common are HPV and related diseases?
HPV (the virus). Approximately 20 million Americans are currently infected with HPV. Another 6 million people become newly infected each year. HPV is so common that at least 50% of sexually active men and women get it at some point in their lives.
Genital warts. About 1% of sexually active adults in the U.S. have genital warts at any one time.
Cervical cancer. Each year, about 12,000 women get cervical cancer in the U.S.
Other cancers that can be caused by HPV are less common than cervical cancer. Each year in the U.S., there are about:
- 3,700 women who get vulvar cancer
- 1,000 women who get vaginal cancer
- 1,000 men who get penile cancer
- 2,700 women and 1,700 men who get anal cancer
- 2,300 women and 9,000 men who get head and neck cancers. [Note: although HPV is associated with some of head and neck cancers, most of these cancers are related to smoking and heavy drinking.]
- Certain populations are at higher risk for some HPV-related health problems. This includes gay and bisexual men, and people with weak immune systems (including those who have HIV/AIDS).
RRP is very rare. It is estimated that less than 2,000 children get RRP every year in the U.S.
How can people prevent HPV?
There are several ways that people can lower their chances of getting HPV:
Vaccines can protect males and females against some of the most common types of HPV. These vaccines are given in three shots. It is important to get all three doses to get the best protection. The vaccines are most effective when given before a person’s first sexual contact, when he or she could be exposed to HPV.
Girls and women: Two vaccines (Cervarix and Gardasil) are available to protect females against the types of HPV that cause most cervical cancers. One of these vaccines (Gardasil) also protects against most genital warts. Both vaccines are recommended for 11 and 12 year-old girls, and for females 13 through 26 years of age, who did not get any or all of the shots when they were younger. These vaccines can also be given to girls as young as 9 years of age. It is recommended that females get the same vaccine brand for all three doses, whenever possible.
Boys and men: One available vaccine (Gardasil) protects males against most genital warts. This vaccine is available for boys and men, 9 through 26 years of age.
For those who choose to be sexually active, condoms may lower the risk of HPV. To be most effective, they should be used with every sex act, from start to finish. Condoms may also lower the risk of developing HPV-related diseases, such as genital warts and cervical cancer. But HPV can infect areas that are not covered by a condom – so condoms may not fully protect against HPV.
People can also lower their chances of getting HPV by being in a faithful relationship with one partner; limiting their number of sex partners; and choosing a partner who has had no or few prior sex partners. But even people with only one lifetime sex partner can get HPV. And it may not be possible to determine if a partner who has been sexually active in the past is currently infected. That’s why the only sure way to prevent HPV is to avoid all sexual activity.
HUMAN PAPILLOMA VIRUS â?? A REVIEW
Sameera Mohotti (BSc, MSc, MD(MA))
HPV is one of the most common sexually transmitted viral diseases. It is
difficult to estimate the overall prevalence of HPV infection, it is estimated that the prevalence could be as high as 20 million (Revzina 2005). The total health care cost associated with the screening and treatment of cervical cancer in the U.S. is estimated to be $6 billion per year (Koutsky 1997). A US sero prevalence study performed by Revizina et al revealed that the highest prevalence of
HPV is among college students and women attending STD clinics Data from clinics in Australia indicate a prevalence of 4- 13% among STD clinic attendants Following initial infection, HPV establishes latent infection, from which symptomatic recurrences may develop periodically (Revzina 2005),(Armstrong 1986).
The main aim of this review was to evaluate the current literature regarding the types of HPV, symptoms and its pathogenesis.
SPECTRUM OF HPV INFECTION
Over 200 types of HPV have been classified on the basis of their DNA sequence homology. 85 HPV genotypes are well characterized.
HPV can be grouped as high risk HPV and low risk HPV based on their association with cancer and precursor lesions. High risk HPVâ??s have a high oncogenic potentials. This group includes serotypes 16,18,31,33, 34, 35,39,45,51,52,56,58,59,66,68. Low risk HPVâ??s have less oncogenic potentials and usually results in the formation of low grade precancerous lesions. This group includes
serotypes 6, 11, 42, 43, 44. This difference in the capacity to induce malignant transformation is due to the functional difference seen in E6 and E7 proteins of the two groups (Burd 2003; Longworth and Laimins 2004).
Although many HPV infections are sub clinical, symptomatic HPV infection typically results in lesions. Each HPV serotype infects certain parts of the body and responsible for different types of lesions. According to the current classification system (Bethesda system) of HPV lesions, there are three main groups. They are anoGenital Warts, low grade squamous intraepithelial lesions (cervical / anal intraepithelial neoplasia and mild dysplasia) and high grade squamous intraepithelial lesions (moderate and severe dysplasia).Cervical/anal/vulvar/penile carcinomas usually develop from high grade squamous intraepithelial lesions (University 2001).
Genital Warts (proliferative foci of epithelial keratinocytes infected with HPV) appear as bumps or abnormal growths in the genital area. This is one of the commonest clinically recognized disease manifestations of genital HPV. These are usually found in vulva, urethra, anus, and vagina and on the cervix. Warts are extremely contagious and they occasionally lead to cancer of the cervix in
women or cancer of the penis in men (Lacey 2005).
The presence of abnormal cells on the surface of the skin is called dysplasia.
Dysplasia is not a cancer and mild dysplasia is likely to self resolve. However, mild, moderate and severe dysplasia could be progressed in to a cancer, if not detected and treated at its early stage. Studies indicate that even adolescents with low grade squamous intraepithelial lesions and high grade squamous intraepithelial lesions are also at high risk for progression to high-grade cervical abnormalities (Wright, Pinto et al. 2004).
HPV is a nonenveloped, double stranded circular DNA virus with a diameter of 5.5 nm. The genome is approximately 8 Kb in size and encased in an icosahedral capsid which is composed of 72 capsomeres. Capsid comprises of an outer protein coat which consists of two capsid proteins, L1 (major) and L2 (minor) (Sapp, Volpers et al. 1995).
HPV genome is functionally divided in to 3 regions .They are the upstream regulatory region, early region and the late region. The upstream regulatory region involves in viral replication and also controls the transcription of some sequences in the early region. The early region of the genome encompasses 6 open reading frames (ORFâ??s) named E1, E2, E4, E5, E6 and E7. These encode proteins involved in viral replication, transcription and cellular transformation. E6 and E7 regions are responsible for the oncogenic properties of HPV. The late region encompasses two ORFâ??s and these encode L1 and L2 structural proteins which is necessary for capsid production (Sapp, Volpers et
PRODUCTIVE HPV INFECTION
HPV gain entry into the host cells through the basal layer of the epithelium. In initial infection HPV is present as an episome. It has been proposed that HPV-6 attaches to the host cells via ?6-intergrin in the epithelium cells; where as, HPV16 and HPV 33 attach to host cells via cell surface heparin sulphate. The papilloma viral gene expressions are linked with the differentiation stages of the epithelium and virus multiplies as it progresses through the natural epithelial cell maturation (Giroglou, Florin et al. 2001).
During viral replication, the E1 gene product (E1 protein) binds to the viral origin of replication and this result in the extra chromosomal replication of the viral genome. The E2 gene product (E2 protein) down-regulates the E6 and E7 regions to allow the normal differentiation process of the cell. The capsid genes L1 and L2 synthesize the capsid protein and envelopes each episomal DNA in a protein capsid. The E4 gene product (E4 protein) is associated with the maturation and release of papilloma virus particles(Burd 2003),(Longworth and Laimins 2004).
The productive viral stage results in flat or papillary lesions. Since the papilloma virus replication goes hand in hand with the epithelial cell differentiations, as the lesions are formed the superficial and intermediate epithelial layers would contain a large amount of viral DNA. The accumulations of viral particles in the superficial epithelial layers provoke the cells to the koilocytosis cytopathic effect. This gives rise to koilocytes, in which the cellular nucleus is displaced to the side with a ‘hollow’ appearance of the cytoplasm. The virus particles are released as dying koilocytes are shed (zur Hausen 1991; Longworth and Laimins 2004).
PATHOGENESIS OF ONCOGENIC HPV
When a person gets infected with high-risk HPV, it may take up to 20 years for the
cancer changes to appear. This persistency of HPV infection is necessary for the malignant transformation of the cells. In HPV associated benign lesions, the HPV DNA is usually located extra chromosomal where as in HPV associated cancers , the HPV DNA is usually found integrated in to host genome. Integration of high risk HPV DNA in to the host cell disrupts the E2 region. This results in the loss of normal E2 down-regulation of E6 and E7 which leads to the up-regulation of the two HPV viral oncogenes; E6 and E7.These E6 and E7 gene products has the ability to destabilize the cell growth regulatory and modify the cellular environment in which it replicates (Jan M. M. Walboomers 1999; Yoshinouchi, Hongo et al. 1999; Burd 2003).
pRB and pRb related proteins are critical components of the cell cycle as they seize the
transcription factor E2F which is necessary for the functions of the cell cycle. When E7 proteins bind to the pRB, pRB-E2F complex gets disrupted and this results in the E2F liberation. This disruption affects the normal functions of the cell. E6 viral gene product, the E6 protein, targets the immunosuppressor protein p53 (low risk HPV typeâ??s bind p53 in decreased affinity). The p53 protein prevents cells from completing the cell cycle and up-regulates genes involved in DNA repair, if it comes across any DNA damage. Another important function of the p53 protein is to instruct a cell with DNA damage to commit suicide. If the p53 function is inactivated then these damaged cells would continue to divide and accumulate mutations which would eventually lead to the formation of a tumor.
When E6 protein binds to p53, E6 associated ubiquitin ligase catalyzes ubiquitin ligase mediated p53 degradation. This destroys the tumor suppressive properties of p53 (Syrjanen 1999; Ha and Califano 2004).
The ability of E6 and E7 gene products to disrupt the cellular p53 and pRB protein functions result in, increase cell proliferation and genomic instability. Eventually the cell accumulates damaged DNA/mutations which may lead to the formation of fully transformed cancerous cells. The low risk HPVâ??s appear to be unable to integrate in to the host genome. But low risk serotypes like HPV 6, 11 may result in chromosomal instability which would lead to the accumulation of mutational events, which in turn may form fully transformed cancerous cells .In addition to the E6 and E7 protein function, methylation of viral DNA, telomere activations, humoral and immunogenic factors also contribute to the cellular transformations (Holowaty, Miller et al. 1999; Burd 2003).
Armstrong, B. K., O. V. Allen, B. A. Brennan, I. A. Fruzynski, N. H. de Klerk, E. D. Waters, J.
Machin, and M. M. Gollow (1986). “Time trends in prevalence of cervical cytological abnormality in
women attending a sexually transmitted diseases clinic and their relationship to trends in sexual
activity and specific infections.” Br J Cancer 54: 669-75.
Burd, E. M. (2003). “Human Papillomavirus and Cervical Cancer.” Clin. Microbiol. Rev. 16: 1-17.
Burd, E. M. (2003). “Human Papillomavirus and Cervical Cancer.” Clin. Microbiol. Rev. 16(1): 1-17.
Giroglou, T., L. Florin, et al. (2001). “Human Papillomavirus Infection Requires Cell Surface Heparan Sulfate.” J. Virol. 75(3): 1565-1570.
Ha, P. K. and J. A. Califano (2004). “The role of Human Papilloma Virus in oral carcinogenesis.” Crit Rev Oral Biol Med 15(4): 188-196.
Holowaty, P., A. B. Miller, et al. (1999). “Natural History of Dysplasia of the Uterine Cervix.” J. Natl. Cancer Inst. 91(3): 252-258.
Jan M. M. Walboomers, M. V. J., M. Michele Manos, F. Xavier Bosch, J. Alain Kummer, Keerti V. Shah,
Peter J. F. Snijders, Julian Peto, Chris J. L. M. Meijer, Nubia MuÃ±oz, (1999). “Human papillomavirus is a necessary cause of invasive cervical cancer worldwide.” The Journal of Pathology 189(1): 12-19.
Koutsky, P., Laura. (1997). “Epidemiology of Genital Human Papillomavirus Infection.” The American Journal of Medicine 102: 3-8.
Lacey, C. J. N. (2005). “Therapy for genital human papillomavirus-related disease.” Journal of
Clinical Virology Supplement: Human Papillomaviruses 32(Supplement 1): 82-90.
Longworth, M. S. and L. A. Laimins (2004). “Pathogenesis of Human Papillomaviruses in Differentiating Epithelia.” Microbiol. Mol. Biol. Rev. 68(2): 362-372.
Revzina, N. V., and R. J. Diclemente (2005). “Prevalence and incidence of human papillomavirus infection in women in the USA: a systematic review.” Int J STD AIDS 16: 528-37.
Sapp, M., C. Volpers, et al. (1995). “Organization of the major and minor capsid proteins in human papillomavirus type 33 virus-like particles.” J Gen Virol 76(9): 2407-2412.
Syrjanen, S. M., and K. J. Syrjanen. (1999). “New concepts on the role of human papillomavirus in cell cycle regulation.” Ann Med 31: 175-187.
University, J. s. H. (2001). “HPV-induced Anal Dysplasia: What Do We Know and What Can We Do About It?” (Online)
Wright, J. D., A. B. Pinto, et al. (2004). “Atypical Squamous Cells of Undetermined Significance in Girls and Women .” Obstet Gynecol 103(4): 632-638.
Yoshinouchi, M., A. Hongo, et al. (1999). “Analysis by Multiplex PCR of the Physical Status of Human Papillomavirus Type 16 DNA in Cervical Cancers.” J. Clin. Microbiol. 37(11): 3514-3517.
zur Hausen, H. (1991). â??Human papillomaviruses in the pathogenesis of anogenital cancer.” Virology
If you are sexually active, you must be aware of the wide range of STDs that can affect you. take a look at std guide we have compiled below and explore everything you need to know. There is a wide variety of sexually transmitted infections and sexually transmitted diseases, so take a look at the news, we have given below and learn how to protect yourself against them. Sexually transmitted diseases or sexually transmitted infections are taken through many types of sexual contact, including anal penetration, oral and vaginal sex. There are many sexually transmitted diseases and sexually transmitted infections, although we have provided information on some key below. If you need additional advice, please contact a doctor or nurse in sexual health. Genital Warts are a widespread sexually transmitted infections. they are caused by the virus detection of HPV, which can be transmitted during sexual intercourse with. However, not everyone who suffers from the virus develops Genital Warts. A number of people suffering from discovering the virus will be allowed in the body over time. it is rare for Genital Warts to be the cause of any long-term health problems. HIV is the most serious std. It attacks the body’s immune system, which usually defends the body against infection and disease. HIV infects cells that are called CD4 cells and are responsible for the fight against disease and infection. after being infected by HIV, HIV destroys CD4 cells. what makes someone who is infected with HIV with a high risk of contracting a serious infection or diseases, including cancer. For more help and support on sexually transmitted diseases and sexually transmitted infections, go see your sexual health centre. they will be able to test yourself, and also offer treatment. You can also try pr your visit for advice. do not be nervousabout pr your visit, they often sensitive issues. The only way to be 100% sure of MTS and sexually transmitted infections is refraining from any sexual activity. despite this, if you are sexually active, you can protect your sexual health by having regular testing and std sti, especially if you get a new sexual partner. it goes without saying that condoms are a must. They protect you against pregnancy, and a wide range of MTS and sexually transmitted infections.
The Herpes Simplex Virus (HSV) is highly contagious. Although there are eight different strains, HSV1 and HSV2 are responsible for the majority of herpes infections. Herpes simplex is a viral disease caused by both herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection.
Oral herpes, the visible symptoms of which are colloquially called cold sores, infects the face and mouth. Oral herpes is the most common form of infection. Genital herpes, commonly known simply as herpes, is the second most common form of herpes. Other disorders such as herpetic whitlow, herpes gladiatorum, ocular herpes, cerebral herpes infection encephalitis, Mollaret’s meningitis, neonatal herpes, and possibly Bell’s palsy are all caused by herpes simplex viruses.
Herpes viruses cycle between periods of active disease, followed by a remission period during which the sores disappear. Genital herpes, however, is often asymptomatic, though viral shedding may still occur. After initial infection, the viruses move to sensory nerves, where they reside as life-long, latent viruses. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time, episodes of active disease reduce in frequency and severity.
Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable method of preventing transmission of herpes, but they merely reduce rather than eliminate risk.
Herpes simplex should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is a viral disease caused by varicella zoster virus. There is also a possibility of confusion with “hand, foot and mouth disease” due to apparition of lesions on the skin. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and Genital Herpes are harder to diagnose; laboratory testing is usually required.
Current statistics from the American Social health Associations show that up to 60 million Americans have Genital Herpes with 1 million new diagnoses each year, representing up to 30% of the population being infected. Twenty percent of the U.S. population has antibodies to HSV-2, although not all of them have a history of genital lesions.
The painful clusters of blisters reappear, usually in the same area, with agonizing regularity. Once the disease has been contracted, the patient is infected for life. However, after several years, some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Vaccines are in clinical trials but have not demonstrated effectiveness.
Although the blisters often occur in the genital area, they may also be found on the thighs and buttocks. This genital disease remains dormant in the lower spinal column, ready to migrate down the sensory nerves to the skin during lower immunity, and any herpes treatment must address this as well. Treatments can reduce viral reproduction and shedding, prevent the virus from entering the skin, and alleviate the severity of symptomatic episodes.
Current solutions for herpes simplex treatment such as Acyclovir have a wide variety of side effects, including a metal-like after taste, dry mouth, and constipation. The undeniable and profound pharmacological effects of our OutbreakBalm-Rx treatment for herpes support its therapeutic use. The effectiveness of this line of herpes treatments represents real hope.
OutbreakBalm-Rx is composed of naturally occurring high intensity antiviral extracts which have a lethal effect against herpes simplex viruses 1 and 2 upon exposure. This treatment provides maximum and rapid penetration of antiviral agents into cell membranes without damaging human cells.
Very recent advances in the scientific understanding of medicinal plants suggest a much broader use in the treatment for herpes infections than science thought possible just ten years ago. It therefore comes as no surprise that application of this product during prodrome, the tingling before an outbreak, can prevent herpes blisters forming, aborting the pending flare up altogether.
The anti HSV properties in OutbreakBalm-Rx are highly pronounced and well documented. They quantifiably destroy the herpes virus, thus characterizing OutbreakBalm-Rx as a potent anti herpes agent. To learn more, please go to http://www.naturespharma.org.
Cervical cancer treatment in India is provided at state of the art hospitals by some of the best doctors in the world. Cervical cancer is malignant neoplasm of the cervix uteri or cervical area. It may present with vaginal bleeding but symptoms may be absent until the cancer is in its advanced stages. Treatment consists of surgery in early stages and chemotherapy and radiotherapy in advanced stages of the disease. Cervical cancer treatment in India benefits from a large staff of world class experts and the ultra-competitive cost advantage it offers.
The early stages of cervical cancer may be completely asymptomatic. Vaginal bleeding, contact bleeding or (rarely) a vaginal mass may indicate the presence of malignancy. Also, moderate pain during sexual intercourse and vaginal discharge are symptoms of cervical cancer. In advanced disease, metastases may be present in the abdomen, lungs or elsewhere. Symptoms of advanced cervical cancer may include: loss of appetite, weight loss, fatigue, pelvic pain, back pain, leg pain, single swollen leg, heavy bleeding from the vagina, leaking of urine or faeces from the vagina, and bone fractures.
The most important risk factor in the development of cervical cancer is infection with a high-risk strain of human papillomavirus. The virus cancer link works by triggering alterations in the cells of the cervix, which can lead to the development of cervical intraepithelial neoplasia, which can lead to cancer.
The American Cancer Society provides the following list of risk factors for cervical cancer: human papillomavirus (HPV) infection, smoking, HIV infection, chlamydia infection, dietary factors, hormonal contraception, multiple pregnancies, exposure to the hormonal drug diethylstilbestrol (DES) and a family history of cervical cancer. There is a possible genetic risk associated with HLA-B7.
Treatment of cervical cancer is directed at preventing precancerous cells from becoming cancerous cells.
Indian Medical tourism is fulfilling the growing demands of International Patients for their medical treatments in India that combined the advantages of high quality medical care and absence of waiting lists for most of the medical treatment procedures. International Patients approaching Cervical cancer treatment in India are able to draw on the pool of expertise and skills of board certified doctors / consultants / surgeons who work as a team for the best of care and treatment. In addition to the access to specialist skills, the patients also have the quality assurance that the medical services are peer reviewed and medically audited. For more information on Cervical cancer treatment in India visit us at http://www.forerunnershealthcare.com or mail your queries at firstname.lastname@example.org or you can call at +91-9371136499, +91-9860755000, + 1-415-599-2537 (USA) / +44-20-8133-2571 (UK).