Boom or bust.
Viruses turn their bacterial hosts into viral replication factories, but they are more likely to die as "offspring" numbers soar.

A Viral Drive to Survive

Having children can be costly, even deadly. And the larger the brood, the greater the risk. So most living things make a tradeoff, producing enough young to effectively pass on their genes without sacrificing too much of their own life span. The strategy is so universal, it even extends to nonliving entities such as viruses, according to a new study.

Viruses are the ultimate parasites. Consisting of little more than strands of DNA or RNA stuffed into a protein capsule, they are entirely dependent on their host for survival and replication. As such, the jury's still out on whether viruses are actually alive.

To see whether viruses adopt one of the near-universal signs of life--namely, the offspring tradeoff strategy--molecular biologists François Taddei and Marianne de Paepe of INSERM and the University of Paris in France watched how 16 kinds of viruses replicated in Escherichia coli bacteria. As expected, the viruses were soon replicating at a violent pace, as measured by the rate at which the bacteria burst. But when the researchers examined the offspring of this viral baby boom under an electron microscope, they noticed that many of the viruses had thin protein capsules--a sign that they themselves would probably burst before too long.

The team thinks that as viruses push to increase their numbers, the bacteria's machinery struggles to keep up and does shoddier work. "It's a case of quality versus quantity," says Taddei. These second-rate viruses are likely less able to infect bacteria, leading to less viral offspring. As a result, viruses may eventually reach a steady state in which offspring quality is not sacrificed for quantity, suggests Taddei, whose team reports its findings online today in PLoS Biology. Although not exactly analogous to the tradeoff model seen in other organisms, this is as close as viruses are likely to come, he says.

These results could have important implications for the modeling of disease virulence and transmission, says evolutionary biologist Martin Ackermann of the Swiss Federal Institute of Technology in Zurich. If other viruses behave as these do, he says, disease transmission would depend on how much a virus multiplies before the tradeoff kicks in.

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