HPVs are a large and diverse group of DNA viruses – nearly 200 types characterised.
Together the oncogenic types may cause as many as 5 % of human cancers – cervical, anal, vulvar, vaginal, penile and oropharyngeal.
Approximately 80 % of sexually active women will get a HPV infection during their lifetime – mostly asymptomatic and cleared by the immune system relatively quickly.
- However in a small number of cases, infection persists, and after a period of latency progresses to CIN which can progress to cervical carcinoma.
HPV in penile cancer
The most common culprits associated with penile cancer are HPV 16 and 18, followed by 31 and 33.
HPV DNA is found in 70 – 100 % of PeIN lesions, and 50 % of invasive penile carcinomas.
HPV genome encodes for oncoprotein E6, which complexes with tumour suppressor genes Rb and p53 pathways.
HPV positive tumours may have more favourable prognoses overall cf. non HPV.
Buschke-Lowenstein tumour
Differs from condylomata in that BLT can displace, invade and destroy adjacent structures by compression (cf condylomata which despite increasing size, always remain superficial and never invade adjacent tissue).
However, BLT does not seem to metastasise, but can invade and cause destructive local growth.
DNA from HPV 6 and 8 found in these tumours, similar to condyloma.
Vaccination
The Gardasil-9 vaccine currently covers HPV 6, 11, 16, 18, 31, 33, 45, 52 and 58 (previously quadrivalent 6, 11, 16 and 18).
Boys and girls are included in Australian programs from age 12-13.