Some time ago I learnt that a significant proportion of cancers are started as a result of virus activity (I believe that the figure was something around 20% of them). That left me thinking how neat (intellectually, that is) would be if viruses and tumour cells became mutualistic cooperators. A virus that alters the behaviour of a cell making it proliferate when in other circumstances wouldn’t (as tumour cells do) does provide a fitness benefit to tumour cells. The payback that would make this interaction mutualistic would be something that increases the reproductive rate of the virus.
Virus (even those associated with tumourigenesis) are not normally too concerned about boosting the replicative capabilities of the cells they infect. If they do initiate a tumour that is more likely than not a side effect of the virus taking over the replicative machinery of the host cell. As soon as enough copies of the virus have been produced, the host cell will burst making the virus free to infect new cells.
I am currently reading One renegade cell, a pop science book by the well known cancer biologist Robert Weinberg. The book is not exactly new (first published more than 10 years ago) and, despite mentioning somatic evolution, it is (unsurprisingly) heavily biased towards a genetic interpretation of cancer. Still, Weinberg does a superb job of explaining a complex disease to a non specialist readership without dumbing the topic down and while keeping the book readable and entertaining.
In chapter 3 (The elusive quarry), Weinberg shows that I was not the first one to think that viruses and tumour cells could interact cooperatively (although I doubt that a lot of people framed this idea in terms of cooperation). Apparently a now forgotten school of thought about tumour initiation a few decades ago thought that virus were the prime cause of tumourigenesis. Those viruses would trigger uncontrolled cellular growth as that would allow the viruses to grow a large population without having to expose themselves (as they are particularly vulnerable out of a host cell). This way the virus drives tumour growth and the tumour growth translates into more viruses. A perfect example of mutualism. Still no evidence for this though, but a neat idea.
As most viral infections lead to cancer only in a minority of those infected (e.g. after infections with HIV, HBV or EBV), it is helpful to consider the additional host factors that are required. Also, does the virus more readily replicate in those people that develop cancer compared to those that have a chronic infection? Or, is there actually an evolutionary disadvantage for the virus if the host dies of cancer instead of continueing to live with a chronic infection?
I think the virus out of the host should disappear.
Martin: Those are interesting questions. Specifically, I should think that most viruses are more likely to benefit by being able to spread to other hosts (eg. other humans, not other cells in the same individual) than by keeping their host alive for longer. Although these goals are not incompatible. An individual carrying viruses that lives longer is also more capable of spreading the disease than one that dies almost inmediately.
Alejandro: Viruses do have to survive for brief periods of time outside of a host cell as a result of the cell rupture they themselves produce (lysis).
David, survives for short periods, when the host die with disease.
Hi Alejandro. So let’s clarify as I think I made it a bit confusing by talking about host cells. A virus inside a cell is using the cell as a host, when the cell dies it can survive for a period of time. A virus inside a multicellular organism that is using the cells inside this organism as hosts is unlikely to survice long after it has produced the death of the organism.
It is clear the machinery of the RNA virus displayed necessary to clone. That is why the virus live in the host cell for a short time after her death in the cell host. But the virus does not support changing the environment which means a dead body.
I think there are some drawbacks on being too aggressive and lytic as a virus – either you may kill your host too soon or you may alert the host immune system, which can then clear the virus. In some cases a prolonged latent infection is probably better for the virus. I think that chronic infection and cancer are often not mutually exclusive but rather a chronic infection may lead to cancer – many viruses inactivate tumour supressors etc., which means that fewer additional mutations are required for transformation. Why a chronic infection turns into cancer in some hosts but not others are certainly very interesting.
I don’t like to be aggressive, I am only giving my opinion that can be bad or good, my dear Anna
Hi Anna, I agree with what you said, or at least (from a theoretician’s point of view) it makes a lot of sense to me. It is in the interest of a virus to inactivate cellular mechanisms like the ones that lead to apoptosis which, as you pointed out, leave the cells closer to full tumourigenic potential.
My hypothesis is consistent with apoptosis and then killing the virus.
I think that for every theory we come up with there is probably some virus that fits with it – they are very resourceful…
Is true, have a lot of versatility.