Andrew Masterson
Andrew Masterson is a former editor of Cosmos.
In a counter-intuitive result, researchers have found that viruses that infect and kill individual bacterial cells can end up benefitting the same bacterial species on a population level.
The finding – made by scientists from the Institute of Science and Technology Austria (IST Austria) and published in the journal Nature Ecology & Evolution – sheds further light on the complex evolutionary relationship between bacteria and viruses.
Viruses that infect bacteria are known as bacteriophages. Some are lethal to the target microbe, while others end up in a more complex relationship, sometimes actually integrating some of their genetic material with their host. This kind of transfer has long been recognised as an important mechanism by which bacteria adapt and evolve.
Viruses that can blend in rather than kill outright are called temperate, but their friendliness can’t be taken for granted. Whether the outcome for an individual bacterium is useful or lethal appears to be random – an observation that caused a team led by IST Austria’s Maros Pleska to wonder if there was some type of governing mechanism at work on either side of virus-bacteria divide that somehow determined the outcome.
What they discovered surprised them.
The key, they suspected, was a bit of bacterial kit known as a Restriction-Modification system (RMS), a collection of specialist enzymes that attack viral genetic material and cut it up into fragments. Bacteria deploy their RMS, sometimes successfully, to defeat lethal viral types. Pleska and colleagues wanted to know if the RMS behaved differently when confronted with a temperate virus that might be potentially beneficial to the individual bacterium.
The answer, it turned out, was no: the RMS always attacked, but the virus usually won — and usually killed the host.
The team then scaled up their experiment to a population level, essentially introducing a large temperate virus horde to an even larger single-species bacterial colony. Based on the individual results, the researchers predicted that the bacteria would use its RMS to battle the infection but that in the end the size of the colony would be significantly reduced.
The actual result was confounding: in a much higher proportion than was predicted, the viruses integrated with the bacteria, passing on genetic material. On a population level, the bacteria benefitted, even though any given microbe, in isolation, was likely to die.
The explanation, they discovered, lay in a misunderstanding regarding the role of the RMS. Rather than simply being there to kill, or try to kill, an invading virus, Pleska’s team discovered its function was more nuanced. Its job was not to defeat, but to delay infection.
The delay bought time for the bacteria, allowing the colony to grow. Beyond an optimum size, the virus-bacteria battle became a numbers game, with more bacteria able to integrate viral DNA than be killed by it.
The researchers found that small bacterial colonies were much more likely than large ones to suffer high casualty rates from viral infections. Similarly, a growing colony was much more likely to fare badly if it was infected early in the growth process.
The results, says Pleska, illustrate how poorly scientists sometimes predict the large-scale dynamics that grow from multiple small-scale interactions.
“In fact,” he explains, “our observations ran completely opposite to what anyone would expect. Thus, ecological and evolutionary interactions between even the simplest biological elements can be very complex and we need new ways of looking at them, if we ever want to understand their role in nature.”
