Is it true that high risk HPV does not live on skin aside for the opening of the penis or inside the vulva? -

I heard that supposedly high risk strains live only near or in the mucosal gland of the penis or inside the vulva, but not on the outside, where the skin is dry. Supposedly only low risk hpv can survive on the exterior skin. Is this true. I want to know if it s possible for me to have any high risk hpv on the shaft of my penis.

HPV most commonly lives on the inside, but can live on the outside exterior whether it be high risk or low risk. Just make sure you always practice safe sex by wearing a condom to lower your chance of exposure.

i have hpv on the outside of the vulva. the guy that gave it to me had it mostly on the head of his penis but had a few warts down the shaft.

http://en.wikipedia.org/wiki/HPV Note that incidence decreases with age. This is most likely due to the fact that HPV infection can clear with time, or at least sink to harmless and undetectable levels while still present in the body. The concern about life-long recurrences may be based on a misconception rather than a myth. It is true that at present there is no cure for genital human papillomavirus. It will probably remain in the infected person s cells for an indefinite time--most often in a latent state, but occasionally producing symptoms or disease.[citation needed] Recent studies from the Albert Einstein College of Medicine and from the University of Washington suggest that HPV may eventually be cleared, or rooted out altogether, in most people with well functioning immune systems. It appears that in some cases the virus does remain in the body indefinitely, producing symptoms if the immune system weakens.[citation needed] It was estimated that in the year 2000, there were approximately 6.2 million new HPV infections among Americans aged 15-44; of these, an estimated 74% occurred to people between ages 15-24.[11] Of the STDs studied, genital HPV was the most commonly acquired.[11] Genital HPV is the most common sexually transmitted infection. Most sexually active men and women will probably acquire genital HPV infection at some point in their lives.[12] The American Social Health Association reported estimates that about 75-80% of sexually active Americans will be infected with HPV at some point in their lifetime.[13][14] According to the Centers for Disease Control (CDC), by the age of 50 more than 80% of American women will have contracted at least one strain of genital HPV.[15] HPV testing in males Although it is possible to test for HPV DNA in men,[36] there are no FDA-approved tests for general screening in the United States[22] or tests approved by the Canadian government[37], since the testing is inconclusive and considered medically unnecessary.[38] Genital warts are the only visible sign of low-risk HPV in men, and can be identified with a visual check of the genital area. These visible growths, however, are the result of non-carcinogenic HPV types. 5% acetic acid (vinegar) is used to identify both warts and squamous intraepithelial neoplasia (SIL) lesions with limited success[22] by causing abnormal tissue to appear white, but most doctors have found this technique helpful only in moist areas, such as the female genital tract.[22] HPV lifecycle The HPV lifecycle strictly follows the differentiation program of the host keratinocyte. It is thought that the HPV virion infects epithelial tissues through micro-abrasions, whereby the virion associates with putative receptors such as alpha integrins and laminins, leading to entry of the virions into basal epithelial cells through clathrin-mediated endocytosis and/or caveolin-mediated endocytosis depending on the type of HPV. At this point, the viral genome is transported to the nucleus by unknown mechanisms and establishes itself at a copy number between 10-200 viral genomes per cell. A sophisticated transcriptional cascade then occurs as the host keratinocyte begins to divide and become increasingly differentiated in the upper layers of the epithelium. The viral oncogenes, E6 and E7, are thought to modify the cell cycle so as to retain the differentiating host keratinocyte in a state that is amiable to the amplification of viral genome replication and consequent late gene expression. E6 in association with host E6 AP (associated protein), which has ubiquitin ligase activity act to ubiquitinate p53 leading to its proteosomal degradation. E7 (inoncogenic HPV s) acts as the primary transforming protein. E7 competes for pRb binding, freeing the transcription factor E2F to transactivate its targets, thus pushing the cell cycle forwards. All HPV can induce transient proliferation, but only 16 and 18 can immortalise cell intes (in vitro). It has also been shown that HPV 16 and 18 cannot immortalise primary rat cells alone, there needs to be activation of the ras oncogene. In the upper layers of the host epithelium, the late genes L1 and L2 are transcribed/translated and serve as structural proteins which encapsidate (Encapsidation is the process of incorporating a nucleic acid sequence (e.g., a vector, or a viral genome) into a viral particle) the amplified viral genomes. Virions can then be sloughed off in the dead squames of the host epithelium and the viral lifecycle continues. Latency period Once an HPV viron invades a cell, an active infection occurs, and the virus can be transmitted. Several months to years may elapse before squamous intraepithelial lesions (SIL) develop and can be clinically detected. The time from active infection to clinically detectable disease makes it difficult for someone who has become infected to establish which partner was the source of infection.

untrue

weird question