Viruses and bacteria often act as parasites, infecting a host, reproducing at its expense and causing disease and death. But not always – sometimes, their infections are positively beneficial and on rare occasions, they can actually defend their hosts from parasitism rather than playing the role themselves.
In the body of one species of aphid, a bacterium and a virus have formed a unlikely partnership to defend their host from a lethal wasp called Aphidius ervi. The wasp turns aphids into living larders for its larvae, laying eggs inside unfortunate animals that are eventually eaten from the inside out. But the pea aphid (Acyrthosiphon pisum) has a defence – some individuals are infected by guardian bacteria (Hamiltonella defensa) that save their host by somehow killing the developing wasp larvae.
H.defensa can be passed down from mother to daughter or even sexually transmitted. Infection rates go up dramatically when aphids are threatened by parasitic wasps. But not all strains are the same; some provide substantially more protection than others and Kerry Oliver from the University of Georgia has found out why.
H.defensa‘s is only defensive when it itself is infected by a virus – a bacteriophage called APSE (or “A.pisum secondary endosymbiont” in full). APSE produces toxins that are suspected to target the tissues of animals, such as those of invading wasp grubs. The phage infects the bacteria, which in turn infect the aphids – it’s this initial step that protects against the wasps.
When the bacteria that cause anthrax (Bacillus anthracis) aren’t ravaging livestock or being used in acts of bioterrorism, they spend their lives as dormant spores. In these inert but hardy forms, the bacteria can weather tough environmental conditions while lying in wait for their next host. This is the standard explanation for what B.anthracis does between infections, and it’s too simple by far. It turns out that the bacterium has a far more interesting secret life involving two unusual partners – viruses and earthworms.
A dying animal can release up to a billion bacterial cells in every single millilitre of blood. This torrent of microbes provides a feast of riches for bacteriophages – viruses that infect bacteria. Raymond Schuch and Vincent Fischetti from the Rockefeller University have found that the anthrax bacterium depends on becoming infected by phages. They began by isolating several strains of phages that specifically infect B.anthracis. The viruses hailed from a range of sources, including the soil, plant roots and worm guts. <
When these phages find bacterial targets, they inject their own DNA, which insinuates itself into the genome of the host. This process is called lysogeny and it is essential for the bacterium’s survival. The added viral DNA encodes proteins called sigma factors that change how bacterial genes are switched on. In doing so, they change the behaviour of the bacteria, giving them new abilities that boost their survival and allow them to colonise an intermediate host – the earthworm.
With their newly incorporated viral DNA, some bacteria formed spores while others were actually prevented from doing so, depending on the phage. Regardless, all the anthrax bacteria grew at almost twice the rate. The phage DNA brought out the social side of the bacteria, inducing them to cluster in groups. It also made them more likely to secreted more complex sugar molecules that form the building blocks of biofilms – the bacterial equivalent of towns and cities. Amid this matrix of sugars, the cells find shelter and protection.
Small wonder then that the infected bacteria are much better are surviving for long durations. Their advantage was so great in comparison to virus-free strains that Schuch and Fischetti suggest that phage infections may actually be necessary if anthrax bacteria are to survive in soil. Indeed, duo identified three bacterial genes that are activated by the phages and that are necessary for eking out a living in soil. When they inactivated these genes, the bacteria survived in these environments for the briefest of times.