By Ching Nam Wong
Human papillomavirus (HPV) is a DNA virus, from the Papillomaviridae family, and one of the most common sexually transmitted infections. Studies have shown that if you are a sexually active person, there is a 75% chance of you catching HPV at some stage of your life, given that you live to the standard life expectancy. Whilst it sounds like a horrible disease according to various public health propaganda, ~90% of HPV infected patients can recover within 2 years without symptoms. However, if you are “unlucky”, or immunocompromised, HPV can cause painful warts and lesions in various parts of the body, most commonly male/female genitals, anus, mouth, and throat.
HPV infections can be spread by direct skin to skin contact. There are more than 160 types of HPVs, 40 of them transmitted through sexual contact, targeting keratinocytes (cells of the outermost skin layer) of mainly the genitals, mouth, throat, and anus. HPV is a DNA virus, having DNA as it’s viral genetic material, and replicates using a DNA-dependent DNA polymerase within the cell. This could lead to a series of molecular cascades that disrupt the cell cycle, which is why HPV infection is believed to increase the risk of cancer.
HPV infection occurs when the HPV virus binds to the oral keratinocyte cell surface through heparan sulfate proteoglycan binding proteins. The gradual production of microbial glycoproteins and proteoglycans by HPV causes the host immune system to react by producing an inflammatory response. If this does not occur, the attachment of HPV to oral keratinocytes will disrupt normal intercellular attachment, leading to the loss of mucosa integrity. Weakened oral keratinocytes linings, such as mucosa, eventually provide easier access for other microorganisms to the mucosa basement membrane, stromal tissues, and selective stem cell populations. These microbes can lead to the phosphorylation of the retinoblastoma protein (a tumour suppressor), leading to the loss of cell cycle regulation and assisting the development of malignant tumours.
It is important to note, however, that the production of malignant cancer does not occur quickly. It often happens that a person infected with various different HPV subtypes, develops cancer over several years, alongside other microbial infections and contact with carcinogenic substances. Whilst some HPV subtypes, such as HPV16 and HPV18, do possess higher risks of cervical cancers than others, these factors generally combine to form an increased risk of cancer.
So how can we lower the risk of catching HPV? The simplest way is to take an HPV vaccine, which provides at least 5 years of protection from the high-risk HPV subtypes, HPV16 and HPV18. It is unclear whether further booster doses of vaccine can provide more protection long term. However, if your country does not offer HPV vaccines or vaccine subsidies, the best way is to limit the number of sexual partners you have, since no approved HPV test currently exist.
HPV is a disease that could be deadly and that we may all encounter in some stage of our lives without even noticing. Therefore, understanding of and protection against HPV is important for all of us.
Author’s note: Thanks for reading, hope you learned more about HPV through this article. If you want to know more about HPV and it’s molecular cascades, interaction with microbe communities, etc. feel free to look up the book <HPV and Cancer> by James A Radosevich! This is where I researched the details of the information on infection.
Imperial Bioscience Review 