Current drugs in the early stages of development by pharmaceutical companies could have a new, and important benefit: this is the ability to cancel out the HPV virus. This comes from new research carried out at the University of Leeds and University of Birmingham, both in the U.K. The research is focused on Human Papillomavirus (HPV).
Human papillomavirus infection refers to an infection by human papillomavirus. The majority of HPV infections cause no symptoms and they resolve spontaneously. However, in some of the general population an HPV infection persists and will result in the development of warts or precancerous lesions. These precancerous lesions increase the risk of cancer of the cervix, vulva, vagina, penis, anus, mouth, or throat.
There are over 100 types of HPV, and about 30 types of HPV infection can affect the genital area. The main route of transmission is during sexual intercourse and skin-to-skin contact of the genital areas. Nearly all cervical cancers (99.7 percent) are caused by infection with a high-risk type of HPV.
The new research was led by Dr Andrew Macdonald at the University of Leeds. The research team have discovered the role of one of the crucial proteins responsible for allowing HPV to infect cells. This is called STAT3 and it is essential for HPV to replicate. Importantly, by ucovering the identity and role of these enzymes which ‘switch on’ STAT3 completes the chain and means that scientists have a new pathway to work through to target HPV based cancers.
Dr Macdonald has said that drugs are already being developed which targeted the same enzymes for other uses meant the possibility of a new treatment could be much closer to becoming a reality. In communication sent to Digital Journal, the researcher states: “We need to find new ways of treating HPV cancers, so we have been working towards understanding how the virus works and interacts with cells. Now we have identified both the role of STAT3 and how it is activated, we have a potential target for future studies in combating HPV associated disease.”
He also added, with reference to drug development: “We know there are various drugs being developed that have the potential to target the enzymes we are dealing with for other purposes. This is great news because it means that while there is still a long way to go, we are already over the first hurdle.”
The new research has been published in the journal PLoS Pathogens, with the research paper titled “STAT3 activation by E6 is essential for the differentiation-dependent HPV18 life cycle.”
