There are 170 established HPV types. Cancerous human papillomavirus (HPV) viruses are the main cause of cervical cancer, and are found in close to 100% of cervical tumors.
Cervical cancer and genital warts are caused by HPV. However, testing for the virus using standard techniques can sometimes give a negative result - in these cases, the condylomas are called ‘virus-negative’ warts.
In a new study published in Virology, researchers assessed the DNA found in samples taken from 40 patients with ‘virus-negative’ genital warts. Through a general DNA sequencing approach, the researchers showed that several of the negative samples did in fact contain HPV DNA.
This means that virus-negative warts can harbor small amounts of more distantly related viruses that escaped previous detection. According to the research, there is a diverse pool of previously unknown HPV types that infect humans and are detectable on genital warts.
The findings have implications for the knowledge of diversity of HPV types, as these viruses are currently undetectable using traditional testing methods.
Ten pools of four samples taken from virus-negative warts were tested using genetic material straight from the patient - including viral, bacterial and human DNA. Five of the pools contained HPV, and three of these contained new strains of the virus.
There are more than 100 types of HPV. About 30 or so types can cause genital infections. Some can cause genital warts; other types can cause cervical or other genital cancers. The other 70 or so HPV types can cause infections and warts elsewhere on the body, such as on the hands.
Many sexually active women and men will contract HPV at some point in their lifetime. Most will never even know it. Usually, this virus does not cause any symptoms and doesn’t cause disease. Often, the body can clear HPV infection on its own within two years or less.
Some types of HPV, typically HPV 6 and HPV 11, cause genital warts. The warts are rarely associated with cervical cancers. They are considered “low-risk” HPV.
HPV and Cervical Cancer
Certain HPV types are classified as “high-risk” because they lead to abnormal cell changes and can cause genital cancers: cervical cancer as well as cancer of the vulva, anus, and penis. In fact, researchers say that virtually all cervical cancers - more than 99% - are caused by these high-risk HPV viruses. The most common of the high-risk strains of HPV are types 16 and 18, which cause about 70% of all cervical cancers.
If the body clears the infection, the cervical cells return to normal. But if the body doesn’t clear the infection, the cells in the cervix can continue to change abnormally. This can lead to precancerous changes or cervical cancer.
Rates of Cervical Cancer
Actual cervical cancer is rare in the U.S. because most women get Pap tests and have abnormal cells treated before they turn into cancer. The American Cancer Society predicts that about 12,170 women will find out they have cervical cancer in the U.S. this year. They also say that roughly 4,220 women will die of the disease the same year.
Altogether, 1337 pieces of HPV-related DNA were detected, representing 23 new types of HPV, 10 established types of HPV and two known HPV DNA sequences.
This new style of testing has highlighted previously unknown forms of the virus. As such, we learn more about the evolution of different HPV types. It is possible that the previously unknown forms of the virus do not cause condyloma but may be secondary invaders of condyloma.
HPV can infect anyone who has ever had a sexual encounter, even without going “all the way.”
HPV is spread through skin-to-skin contact, not through an exchange of bodily fluid.
In most cases, the virus is harmless and most people have no symptoms. The body clears most HPV infections naturally.
HPV can be contracted from one partner, remain dormant, and then later be unknowingly transmitted to another sexual partner, including a spouse.
Though usually harmless, some high-risk types cause cervical cell changes that, if not detected in time, can turn into cancer. The majority of women with an HPV infection will not develop cervical cancer, but regular Pap tests are important.
Cervical cancer most commonly takes 10 years to 20 years or more to develop; women who are no longer sexually active should still have Pap tests.
Cervical cancer is the first cancer in women to be identified as being caused almost exclusively by a virus.
The best way to screen for cervical cancer is a Pap test, which may be done alone or, for women age 30 and older, in combination with an HPV DNA test.
HPV infections in women over 30 are less likely to be cleared naturally, so an HPV test can be helpful in letting health care providers know which women are at greatest risk of cervical cancer.
Regular Pap tests, supplemented by appropriate HPV testing, will detect virtually all pre-cancerous changes and cervical cancers.
Cervical cancer is completely preventable if precancerous cell changes are detected and treated early.
Genital warts usually appear as a small bump or group of bumps in the genital area. They can be small or large, raised or flat, or shaped like a cauliflower. Health care providers typically 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.
Latex condoms can reduce - but not totally eliminate - the risk of HPV transmission.
HPV type 16 is linked to some head and neck cancers.
Approximately thirty percent of oral carcinoma is related to HPV.
Oropharayngeal cancers (cancer of the tonsils, back of throat or base of the tongue) are rare, but the risk increases with the number of oral sex partners.
Notes for editors
This article is “Metagenomic sequencing of “HPV-negative” condylomas detects novel putative HPV types” by Hanna Johansson, Davit Bzhalava, Johanna Ekström, Emilie Hultin, Joakim Dillner, and Ola Forslund (DOI: 10.1016/j.virol.2013.01.023) and appears in Virology published by Elsevier.
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