OK, if you insist. This comes with the usual caveat directed at scientists that I know this is oversimplified, but I wish to reach the largest audience possible. Feel free to correct my mistakes, but please don’t bother me about oversimplification.
So here’s the deal. Several decades ago, it became scientifically fashionable to believe that most cancer had a viral cause. This belief coincided with the discovery that some viruses do cause cancer. And while it turns out that most cancers are not caused by viruses (probably), many of them are. Viruses can cause cancers in a number of ways, but since you said you were interested in HPV (human papilloma virus) we can use this as an example.
First, there is no scientific question about the causal relationship between HPV and cervical cancer (and certain oral cancers, anal cancers, and penile cancers, but we’ll use cervical cancer as shorthand for all of them). There is excellent epidemiologic evidence to support this, and virologic evidence that proves it.
Now that we’ve got that out of the way, how does this cancer virus thing work?
First of all, we need a very basic understanding of what “cancer” is. Cancer refers to hundreds of different diseases that have one thing in common—uncontrolled growth of cells that are no longer restricted to their usual place of residence.
For cells to be “cancerous” they must lose their ability to die off in the usual way. This allows a mass of cells (which are clonal, meaning they are all daughter cells of an cancerous mother cell) to continue to divide and to fail to die. Cell division increases the population of cells, and forgetting to die prevents a reduction in the population. In addition to this, a cancerous cell has gained the ability to escape its usual home, that is it can grow out of the space this type of cell was designed for.
So, for example, in colon cancer, a particular type of colon cell my sustain a genetic injury that causes it not to die at the proper time, and another that allows it continue to divide and produce daughter cells. As this goes on, more mutations can accumulate, until a fortuitous one allows the cells to grow beyond the inner wall of the colon and invade the deeper layers. Eventually, these cells may even gain the ability to break free and thrive in distant tissues (“metastasis”—in the case of colon cancer, to the nearby lymph nodes, and then the liver).
This is the “Knudson Two-Hit Hypothesis” (or the more modern “multi-hit hypothesis”). A cell needs a defect causing immortality, and another causing uncontrolled division. Many genes involved in this process have been identified. Two broad classes of the genes involved in cancers are tumor-suppressor genes and oncogenes. TSGs are genes that normally prevent uncontrolled cell division—they regulate the cell cycle and tell a cell when it is or is not appropriate to reproduce. Oncogenes, on the other hand, stimulate cell growth in a variety of ways. These two classes of genes create a balance as the brakes and accelerator of cell growth. When one is damaged, the other can still control cell growth, but when both are gone, cell growth goes unabated.
What? HPV?
Oh yeah, sorry. Let’s get back to HPV.
The strains of HPV that cause cancer are rather interesting. They produce a protein that inhibits the products of the powerful tumor suppressor genes Rb and p53. That’s one hit, which helps to explain why only a minority of people with HPV actually get cancer—they still need that second hit. We aren’t sure yet what constitutes the second hit in cervical cancer, but there are lots of candidates.
So HPV causes cervical cancer by screwing with two of our most powerful tumor suppressor genes. The rest in commentary. Go and learn it.
Related Links (which I was too lazy to embed)
http://whitecoatunderground.com/2008/01/29/hpv-and-cervical-cancer/
http://www.brown.edu/Courses/Bio_160/Projects1999/hpv/path.html
http://virology-online.com/viruses/Papillomaviruses3.htm
http://www.cinj-genetics.org/health_pro/health_pro.htm
http://jncimono.oxfordjournals.org/cgi/content/full/2003/31/35
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