• The Gaudie

Reviewing the success of HPV vaccination for cervical cancer: How does it work?


Photo by Hyttalo Shuza (Unsplash)

by Holly Leslie

Human Papillomavirus (HPV) is known to increase the risk of developing cervical cancer (in women); additionally, vaccination against HPV has recently been introduced to the male population to prevent genital warts. The uptake of HPV vaccine, since becoming readily available to young women (13-14 years old) in 2013, has remained between 80-87% (England, NHS) to date, however, vaccine safety remains a topic of hot discussion amongst carers/parents.


It is known that 80% of cervical cancers are HPV-positive; although primary infection does not directly cause the cancer, the need for the virus to replicate in host cells (as part of its own life cycle) means that host cells continue dividing and hence, are more likely to obtain a secondary, cancer-causing mutation. Luckily, early changes in cervical cells continue to be detectable following a routine smear test for girls of > 20 years, however, evidence released earlier this year found that it was due to uptake of the HPV vaccine that the need for secondary, invasive screening was significantly reduced (41% cases). Why does the safety and ideal of the HPV vaccine continue to cause concern? Here’s how it works:


Unlike other vaccinations, the HPV vaccine does not contain any form of infectious agent. Whilst other vaccines are synthesised using attenuated (dead) virus, the HPV vaccine allows priming of an individual’s immune response by allowing expression of only “late viral genes” (L1), which encode for the viral coating and are completely distinct from the genes that cause disease. Intramuscular vaccination causes empty shells (or viral like particles) to form, which the immune system recognises, allowing specific antibodies to be made. Like all vaccinations, these HPV-specific antibodies are subsequently produced at a faster rate should a “live” HPV infection occur resulting in a faster eradication of the virus from the host.


Despite overall success of the HPV vaccine, the best type and regime for vaccination continues to be a topic of debate; the two most debated contenders are the quadrivalent vaccine, protecting against HPV types 16, 18, 6 and 11 (licensed 2006) and the bivalent vaccine protects against HPV types 16 and 18 (licensed 2007). The latest vaccine, protecting against 9 types of HPV, was only approved by the FDA in 2014.


Regarding vaccination administration, it is unsurprising the three-dose regime showed less adherence compared to a two-dose regime; whilst efficacy appears to be retained in fewer doses, the significance of patient age on efficacy remains elusive. Evidence suggests that patients < 15 years of age show the highest titre of antibodies compared to other patient groups receiving a two-dose regime; the HPV vaccine is a prophylactic vaccine, meaning its efficacy is only observed if the vaccination has been administered prior to the initial infection. As HPV is most commonly a sexually transmitted infection, vaccination regimes are aimed at girls between the ages of 12-13 years. It has been suggested that adopting a national two-dose regime would vaccinate 50% more women and therefore would be more effective in reducing cervical cancer further. Issues regarding introduction of a one-dose regime include lack of cross-protection (from HPV types) and persistence of antibody being suboptimal, compared to the current two-dose model; further studies are required prior to a single dose HPV vaccine being made available.


Very few people don’t mind having a jab, but evidence repeatedly shows that prevention is better than treatment and the risk of the HPV vaccine could not be any lower.

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