Simian Polyoma Virus 40 [Image licensed under the Creative Commons Phoebus87 at English Wikipedia, Symian virus, CC BY-SA 3.0]
What is even stranger about viruses is that while some of the more familiar ones, such as colds, flu, measles, invade the host, make him/her sick, and eventually (with luck) are cleared from the body -- some of them leave behind remnants that can make their presence known later. This behavior is what makes the herpes family of viruses so insidious. If you've been infected once, you are infected for life, and the latent viruses hidden in your cells can cause another eruption of symptoms, sometimes decades later.
Even weirder is when those latent viral remnants cause havoc in a completely different way than the original infection did. There's a piece of a virus left in the DNA of many of us called HERV-W (human endogenous retrovirus W) which, if activated, can trigger multiple sclerosis or schizophrenia. Another one, Coxsackie virus, has an apparent connection to type-1 diabetes and Sjögren's syndrome. The usual sense is that all viral infections, whether or not they're latent, are damaging to the host. So it was quite a shock to me to read a piece of recent research that there's a viral remnant that not only is beneficial, but is critical for creating myelin -- the coating of our nerve cells that is essential for speeding up nerve transmission!
The paper -- which appeared last week in the journal Cell -- is by a team led by Tanay Ghosh of the Cambridge Institute of Science, and looked at a gene called RetroMyelin. This gene is one of an estimated forty (!) percent of our genome that is made up of retrotransposons, DNA that was inserted by viruses during evolutionary history. Or, looking at it another way, genes that made their way to us using a virus as a carrier. Once inside our genome, transposons begin to do what they do best -- making copies of themselves and moving around. Most retrovirus-introduced elements are deleterious; HIV and feline leukemia, after all, are caused by retroviruses. But sometimes, the product of a retroviral gene turns out to be pretty critical, and that's what happened with RetroMyelin.
Myelin is a phosopholipid/protein mixture that surrounds a great many of the nerves in vertebrates. It not only acts as an insulator, preventing the ion distribution changes that allow for nerve conduction to "short-circuit" into adjacent neurons, it is also the key to saltatory conduction -- the jumping of neural signals down the axon, which can increase transmission speed by a factor of fifty. So this viral gene acted a bit like a neural accelerator, and gave the animals that had it a serious selective advantage.
"Retroviruses were required for vertebrate evolution to take off," said senior author and neuroscientist Robin Franklin, in an interview in Science Daily. "There's been an evolutionary drive to make impulse conduction of our axons quicker because having quicker impulse conduction means you can catch things or flee from things more rapidly. If we didn't have retroviruses sticking their sequences into the vertebrate genome, then myelination wouldn't have happened, and without myelination, the whole diversity of vertebrates as we know it would never have happened."
The only vertebrates that don't have myelin are the jawless fish, such as lampreys and hagfish -- so it's thought that the retroviral infection that gave us the myelin gene occurred around the same time that jaws evolved on our branch of the vertebrate family tree, on the order of four hundred million years ago.
So even some fundamental (and critical) traits shared by virtually all vertebrates, like the myelin sheaths that surround our neurons, are the result of viral infections. Just proving that not all of 'em are bad. Something to think about the next time you feel a sore throat coming on.
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