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Pure speculation - but interesting if true..
Published on June 26, 2005 By Phil Osborn In Biology
Ok, so we've got this information packet called a virus. It inserts itself into the DNA of a cell and uses the cellular machinery to make lots and lots of copies of itself.

But, suppose there already is another virus in the cell, doing the same. Things can get confused real easily, which is apparently how these new flu strains move from duck to pig to human. It isn't generally a simple mutation by the original virus, but rather a mix-up of genes from another virus already adapted to the new host animal.

So far, we have described a purely predatory, parasitical process. The virus adds nothing to the functionality of the cell. It just converts, steals, pillages, corrupts and destroys.

So, how come the cell lets this happen? Is it SO hard to keep the viruses out? And, what about the viruses that are endemic in one population, and seemingly innocuous, but deadly in another population, even one closely genetically related, such as certain monkey viruses that are deadly to humans? These viruses definitely serve as a defense mechanism for the monkeys, and there are many similar examples. Most of the deaths of indigenous peoples at the hands of invaders from a faraway land were not due to military actions, or executions, or starvation or anything deliberately genocidal on the part of the invaders.

Rather, most fatalities were from diseases that the invaders had acquired at least a partial immunity or tolerance to. When european settlers arrived in what became New England, they faced a tolerable amount of fierce resistance by the natives. But what the history books don't typically mention is that roughly 90% of the normal native population was already gone, due to waves of pandemics brought in by the early settlers and the Grand Banks fishermen before them. Even worse, an entire civilization that built the enormous mounds along the Mississippi River was utterly wiped off the globe by a single peaceful Spanish exploring party.

It if works for humans, then it works in animals as well, and we should perhaps look for examples of such microbal genocide in the processes of speciation and invasion of new ecosystems. I suspect, however, that immune-based speciation, while fairly common, is only one piece of the package.

Viruses are information packages. They require energy and resources to replicate and survive. If they are a pure parasite, then they are truly an exception to the rule that parasites tend to evolve towards symbiosis. In that light, the real question I pose is:

How many viruses have indeed achieved some kind of working relationship - a symbiosis - with the host, and what are the limits and intensity of this mutuality?

We notice the viruses that make us ill - or, we notice the illness, anyway, and someone in some lab traces it to a signature in the immune system and uses that signature to track down the viral agent.

But what about all the times that we acquire a new virus that DOESN'T make us ill? At least not noticeably, or not right away. There are the stealth viruses that hide out in places that the immune system can't reach effectively, such as nervous tissues or immune cells themselves, ultimately causing such diseases as AIDS or shingles.

What kinds of other viruses might possibly exist? We know that the simple model of DNA directly coding RNA to create protein is rapidly evolving into a much more nuanced and complex system involving meta-changes in DNA expression modulated or triggered apparently by small RNA molecules and sourced from the so-called "junk DNA." I think that some or a lot of that "junk" has been identified or assumed to be leftover viral sequences that managed to get into a germ cell - egg or sperm, and thus continues to be passed forward with each new generation.

We also know, however, that it is quite possible for a virus to pick up DNA from the host and accidentally incorporate it into its own information package. This is likely what happens in the case of the recombinant flu viruses, even though the new DNA came from another virus. It didn't HAVE to come from another virus is my point. It could be a working segment of the host DNA.

Wouldn't it be convenient to have a mechanism, such as the transfer of DNA between bacteria to convey resistance to drugs, that worked with higher, more complex multi-cellular creatures, like us? What if both our vulnerability to viruses and the recent discoveries that mature cells and tissues can assume new stable functionalities or system configurations are linked to an evolved sybiosis with viruses that specifically transfer useful meta-genetic information?

I recall reading a few years back that scientists were astonished to discover that a single drop of common seawater held millions of viruses, of which only a tiny number were identifiable. What if there is a whole dimension to health, disease, mutation and evolution that we have hitherto missed, simply because we have been so busy working with the pieces we DO understand? What if there are established communication systems based on viral information transmission? Such a system would be evolutionarily stable, benefitting the survival of both virus and host.

Questions remain:

With respect to enhancing positive mutations and spreading them around: How could a "good" mutation be identified and then transmitted? Perhaps certain cellular indicators connected with the meta-configurations could trigger a release of a virus when the cell was performing exceptionally well? Then, how does the cell know that something IS a new mutation at all? Perhaps the system that checks correspondence to RNA in the DNA - the one that was recently identified as being capable or rewriting damaged DNA from the RNA - would assume that something was new.... Again, pure speculation. But, if true, I'm anticipating that Nobel money.

Now how to test this.... ???

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