Between the commercials & decades of preventative measures available to people as young as teenagers, why isn’t general causation info more transparent?
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HPV does this in a few ways, but a really big one is that its genes are able to mess with the normal regulation of the cell cycle. The cell cycle involves many signals and checkpoints that dictate how fast cells proliferate (grow into more cells). Specifically, the viral genes E6 and E7 cause this dysregulation. HPV infects epithelial cells, the cells that make up the mucosa of the cervix and tonsil, thus two places HPV commonly causes cancer. When active expression of the HPV viral genes occur, the epithelial cells multiply more rapidly, leading to dysplasia or disorganization of the mucosa. Oftentimes the virus will integrate into the DNA of the cells, as it is a DNA virus, and highly express viral genes. This integration is a big risk factor for progression of dysplasia into cancer.
Any time there is more rapid growth of cells, there is a higher chance of mutations occurring because the cells are being pushed through the cell cycle and past the checkpoints where mistakes in DNA duplication can be fixed. Once an important enough mutation is acquired, for example one that promotes even more rapid growth/proliferation, the dysplasia will progress to invasion. At this point, this growing invasive group of cells is no longer restricted to the mucosal tissue, it invades downwards into other tissue as it grows, which we call cancer.
You can think of this whole process in terms of the two hit hypothesis of cancer – the HPV infection is the first hit, and the mutation is the second hit that seals the deal. This explains why HPV does not necessarily lead to cancer every time.
And side note – head and neck cancers caused by HPV are actually more common in men, not women, so men are at risk as well
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