Viral hitchhiker inhibits Wolbachia bacteria’s ability to proliferate

Scientists studying the widespread symbiotic bacteria Wolbachia have long been interested in its ability to proliferate. One way it does this is by hijacking sperm of its insect hosts and genetically tricking them to bear more infected females, the only sex that transmits the bacteria. Now, a new study from the MBL (Marine Biological Laboratory), published in the May 18 issue of PLoS Pathogens, demonstrates that a virus common to Wolbachia cells may be a key inhibitor of the cellular process that allows Wolbachia to manipulate insect reproduction.

Because Wolbachia are found in about 75 percent of the world’s insects, the discovery could impact the development of virally delivered biocontrol tools for insects that transmit pathogens to humans or harm agriculture. It might also enable the design of alternative therapies for debilitating illnesses such as river blindness and elephantiasis, whose pathologies are caused by Wolbachia bacteria living in the parasitic worms associated with these diseases.

The new research, led by Seth Bordenstein, an Assistant Scientist in the MBL’s Program in Global Infectious Diseases, shows that a virus known as WO-B interferes with Wolbachia’s ability to cause cytoplasmic incompatibility, the reproductive manipulation of its insect host.

Until now, scientists believed the virus was somehow inducing this process. But viruses pirate cells to reproduce, often killing the cells as a result. So Bordenstein and his colleagues hypothesized that by preying on Wolbachia cells, the WO-B virus might reduce the incidence of cytoplasmic incompatibility in a host, not promote it.

Using DNA analysis and electron microscopy, the scientists quantified the number of WO-B viruses and Wolbachia cells in the testes of a common host: the fruit-fly-sized jewel wasp, Nasonia vitripennis. The researchers found that the virus was indeed associated with reduced bacterial growth. Then they bred the wasps and confirmed fewer incidences of cytoplasmic incompatibility in relation to the reduced presence of the bacteria and increased presence of the virus.

“We’re excited about these findings because there is a great deal of interest in deciphering the genetic and cytological mechanisms of cytoplasmic incompatibility,” says Bordenstein. “We know very little about the virus, but understanding and using it may pave the way for future strategies to control insect-borne diseases.”