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Human papillomavirus (HPV) belongs to Papillomaviruses, a diverse group of DNA-based viruses that infect the skin and mucous membranes of humans and a variety of animals. Over 100 different human papillomavirus (HPV) types have been identified on the basis of difference in the virus genome nucleotide sequences (e.g. type 1, 2 etc.) Today genital HPV infection is one of the most widespread sexually transmitted diseases. Approximately 20 million people around the world are currently infected with HPV. At least 50 percent of sexually active men and women acquire genital HPV infection at some point in their lives. By age 50, at least 80 percent of women will have acquired genital HPV infection. In accordance with WHO information, genital HPV infection was a reason of over 99% of cervical cancer cases, i.e. about 1.4 million women were affected worldwide and 239 000 of them died each year.
All HPVs are transmitted by skin-to-skin contact. A group of about 30-40 HPVs is typically transmitted through sexual contact and infect the anogenital region. Some sexually transmitted HPVs, types 6 and 11, may cause genital warts. However, other HPV types which may infect the genitals do not cause any noticeable signs of infection.
Persistent infection with a subset of about 13 so-called “high-risk” sexually transmitted HPVs, including types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 and 68 — different from the ones that cause warts — may lead to the development of cervical intraepithelial neoplasia (CIN), vulvar intraepithelial neoplasia (VIN), penile intraepithelial neoplasia (PIN), and/or anal intraepithelial neoplasia (AIN). These are precancerous lesions and can progress to invasive cancer. HPV infection is a necessary factor in the development of nearly all cases of cervical cancer.
The HPV lifecycle begins from infection of epithelial tissues through micro-abrasions. At this point, the viral genome is transported to the nucleus 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 make them amiable to the amplification of viral genome replication and consequent late gene expression. In the upper layers of the host epithelium, the late genes L1 and L2 are transcribed/translated and serve as structural proteins which encapsidate the amplified viral genomes.
Hytest offers a wide spectrum of monoclonal antibodies specific to oncoprotein E7 of “high-risk” HPV types 16 and 18 as well as of less oncogenic HPV type 11. MAbs can be used in routine immunoassays (direct or indirect ELISA, sandwich immunodetection systems, Western blotting). Some MAbs display high specificity to definite type of HPV while others can be used for determination of E7 proteins for all four types of viruses.
Search Human papilloma virus references from PubMed.
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