The Scene: A human is fending off a group of pathogenic bacteria.
Human: Hey you, bacteria, don’t come near me. I’ve got a badass virus with me.
Bacteria: Oh, yeah?
Human: It is so bad, man! You try me and you’ll get blisters that you may not even see in your nightmares. [unexpectedly exposes certain body parts]
Bacteria: [scream and run]
Human triumphs, ably supported by herpes virus. End of a bacterial invasion.
Herpes co-evolved with us for the past tens of millions of years. In a study reported at ScienceNow, we learn that herpes virus in mice keeps bacterial pathogens away indirectly. A similar twisted symbiosis may be at work in humans too.
Eight human herpesviruses are known, and most people are infected with several of them at an early age. They can cause serious disease: The cytomegalovirus (CMV), for instance, can blind people with compromised immune systems, and the Epstein-Barr virus (EBV) can cause tumors. But in the vast majority of cases, herpesviruses become latent: They just hang out in the body, never leaving but never causing trouble.
A key player in maintaining this equilibrium is a host molecule called interferon-γ (IFN-γ). But that’s not all it does. IFN-γ also helps fight bacterial infection by activating macrophages, a type of white blood cell that gobbles up microbes. So viral immunologist Herbert Virgin of Washington University School of Medicine in St. Louis, Missouri, reasoned that latently infected mice might be more resistant to bacterial infection, because those mice have higher blood levels of IFN-γ.