The idea that cervical cancer might be caused by a human papillomaviruses (HPVs) was first proposed by Professor Harald zur Hausen, a German physician and virologist, in 1976. Subsequent research over the next two decades confirmed this hypothesis and led to a Nobel Prize in Physiology or Medicine for Dr. zur Hausen in 2008. We now know that cervical cancer is almost entirely associated with infection by a subset of HPVs. More recent research extended the cancer causing role of these viruses to other genital cancers, some oral cancers, and certain types of skin cancer. All HPVs are spread via direct human-to-human skin contact, including sexual activity, so the unfortunate news is that you can literally catch these cancers.
HPVs are a large group of related viruses with over 300 individual strains now identified. These strains are named simply by numbering them starting with HPV 1, HPV 2, HPV 3, and so on, adding an additional number to the list for each new strain discovered. All of these viruses can cause warts, though different strains do have different specificity about what kind of skin they will infect. Some strains only infect general skin, while others only infect mucosal skin such as the oral and genital regions. Fortunately, the vast majority of the strains are relatively harmless and are called low-risk. While the warts caused by low-risk HPVs can be unsightly, painful, or just annoying, they do not typically progress to anything more serious. Unfortunately, 12 HPV strains are called high-risk or oncogenic types because they predispose humans to developing cancer (and there are several other potentially high-risk strains that haven’t yet been verified). In the United States, HPV 16 and HPV 18 are the most prevalent high-risk types, while HPV 6 and HPV 11 are the most common cause of benign genital warts.
Once the causative role of HPVs in cervical cancer was established, development of a vaccine was initiated. The hope for the vaccine was that prevention of HPV infections would ultimately result in lower rates of cervical cancer and possibly other HPV-related cancers. In 2006 the first HPV vaccine, called Gardasil, became publicly available. This vaccine provided protection against the two major high-risk types (HPV 16 and HPV 18) as well as the two most common low-risk types (HPV 6 and HPV 11). Note, the vaccine contains no virus and simply uses a single viral protein from each type to elicit antibodies that protect against infection. A recent publication in the Journal of Adolescent Health has now looked at the rates of HPV infection in the 10 year period following introduction of the Gardasil vaccine. As hoped, the prevalence of the four HPV types targeted by Gardasil dropped 86% among 14-19 year old women and 71% among 20-24 year old women, with similar declines seen across racial/ethnic groups. These dramatic drops in infection rates confirm that the vaccine works effectively in widely diverse populations under real world conditions. More importantly, low rates of high-risk HPV infection should translate to significantly lower rates of cervical cancer in these women as they age. While not examined in this publication, males can also develop HPV-induced cancers, so vaccination of males is now recommended to help prevent these diseases in men.
In 2015, Gardasil9 was introduced that protects against the same four HPVs as the original vaccine plus five additional high-risk types. As of 2017 Gardasil9 replaced the original Gardasil in the United States, but it’s too early for data on the effectiveness of Gardasil9 in reducing incidence of all seven of these high-risk types. However, it’s not unreasonable to hope that as vaccination coverage with Gardasil9 grows that we could see a near end to cervical cancer within a generation or two, as well as a reduction of other HPV cancers in both men and women. Score another conquest for vaccines!
TrueScience 