What Can Cheating Viruses Tell Us About Evolution?

Carol Hsin | carol.hsin@yale.edu April 24, 2010

What Can Cheating Viruses Tell Us About Evolution?

If we replayed the history of evolution on Earth – independent of its past – would we get exactly the same species?

In 1989 Stephen J. Gould coined this thought experiment, “replaying life’s tape,” to ask whether life is determined to evolve by the same exact path­way or whether it is dependent on a multitude of steps and conditions. Despite the progress made in evolutionary biology in the past decades, Gould’s question remains unanswered. Paul Turner, Asso­ciate Professor of Ecology and Evolutionary Biology, now seeks to solve this problem by using a surprising model: “cheating” viruses.

On a molecular level, a virus, which is classified as a parasite, is not particularly impressive. It is genetic material encased in a protein shell, simpler than the most ancient bacteria.

Lacking the vital macromolecular machines for energy production, a virus must hijack its host’s resources in order to replicate. These hijacking instructions, coded within the virus’s genome, often command the cell to make proteins that constitute the structure of the virus’s progeny.

Often, multiple viruses infect the same host – an incidence called co-infection, which increases as the ratio of viral titer to viable cells increases. In co-infection, the genetic material of the viruses can mix, which allows for the production of a new set of “recombinant” viruses in addition to those genetically identical original viruses. Furthermore, co-infection can upgrade viruses to “hyperpara­sites,” or parasites that parasitize other parasites. Mediocre at commanding the cell to make pro­teins, hyperparasites steal the resources their co-infector produces. In other words, they cheat.

“In nature there is a selection to cheat,” Turner said. “Energy is limited; resources are limited; if you can devise a way for other organisms to do the work for you, that is great.”

Cheating is an effective strategy that, as Turner demonstrated, can spread throughout a virus population when co-infection is common. But once cheating also becomes common, overall pro­ductivity drops – a result that opened up further inquiries in the evolution and ecological aspects of cheating, which Turner now investigates using the insect-borne Vesicular stomatitis virus (VSV) as a model.

“If you view the interactions between the cheat­ers and the ordinary viruses as a sort of predator-prey interaction,” Turner said, “with time you can measure the ecological dynamic of the predator and prey genome types. They fluctuate in time, but do they fluctuate the same way?”

When graphing how the cheaters’ population changed with time, Turner observed that their numbers would rise, reach a maximum, fall, reach a minimum, and rise again. The same pattern persisted throughout.

After cheating becomes common, Turner explained, it is no longer a viable survival strategy. As a result, nature selects for the ordinary viruses. However, as the ordinary population prospers, there is a point at which “cheating” viruses will again have the upper hand. “Fitness is not constant,” Turner said. “It depends on whether everyone else is using the same strategy.”

Turner said he had expected the evolutionary dynamic to be more random due to the high rate at which viruses mutate. Revisiting Gould’s original question regarding “life’s tape,” Turner said that two possible scenarios could account for his results. One is that the same genome types are being evolved. The second is that there are different genome types, but the genome types are irrelevant because they are presenting the same dynamic.

“If you take, for instance, ten populations of this virus and you culture them in a laboratory through time in an environment with fewer cells in proportion to the virus,” Turner said, “is there one ideal type of cheater that will be selected, and will you see that evolve through all of them? Or are there many cheating strategies?”

The most popular cheating strategy is for a virus to lose about half of its genome coding for replicase, the enzyme that catalyzes RNA replication. A less common way to cheat is to lose a gene that codes for a structural protein, such as those that make up the virus’ shell. Either way, once inside a cell with a virus that has the completed gene, the shortened mutant can use the resources the other has coded.

Turner is currently tracking genetic and trait changes of cheating viruses to see how paral­lel they are across populations. He wants to determine if a specific cheater will be repeatedly selected across populations. Although it is impos­sible to “reply life’s tape,” Turner may be doing just that with cheating viruses.