Other scientists previously had shown that interferon gamma helps the immune system fight off some strains of bacteria. This led Virgin and his colleagues to test herpes-infected mice with exposure to the bacteria Yersinia pestis, which causes plague, and Listeria monocytogenes, which is a minor cause of food poisoning and can infect the central nervous system. Many aspects of Listeria infection in mice are also similar to those that occur in humans infected with tuberculsis. They found that when mice had a latent herpes infection, the bacteria replicated more slowly and were less likely to kill the mice.
When herpes was still in the acute phase of infection, no protective effect was present. When scientists exposed the mice to a mutant herpes virus that can infect but cannot establish latency, the herpes infection did not confer resistance. The protective effect could be produced by two different mouse herpes viruses.
"We have a good feel for who the main players are in this protective effect, but we need further research to better understand the exact mechanisms that underlie the process," Virgin says.
He suspects that the virus may be prompting the immune system to produce more interferon gamma to keep itself from emerging from latency. If the virus stays latent, it prevents itself from seriously endangering the host and can continue to spread to new hosts from its current perch.
"We need to explore whether there are additional costs and benefits to the host from this," Virgin says. "Are there additional pathogens that find it harder to come in as a secondary infection after herpes becomes latent" Do other latent infections convey similar protective effects" These are not the kinds of questions we're accustomed to asking about such infections, but our findings suggest that we need to start."
Source:Washington University School of Medicine