On page 313, Hou et al. expose a traitor. Cells producing the cytokine interleukin (IL)-17 protect a virus instead of their host. These results may help explain how chronic viruses, like HIV, establish a long-term foothold.

High levels of IL-17–secreting helper T (Th17) cells coincide with a number of chronic infections, but their role in disease pathogenesis is variable. Th17 cells help protect the body against certain bacterial infections, but they exacerbate tissue damage in autoimmune diseases. Hou et al. now catch IL-17 helping virus-infected cells survive.

Antigen presenting cells infected with the CNS-invading virus Theiler's murine encephalitis virus (TMEV) drove naive T cells toward a Th17 cell fate by secreting IL-6, show the authors. In turn, the IL-17 produced by those cells up-regulated anti-apoptosis genes, allowing infected cells to skirt suicide as well as assassination by killer T cells.

Other groups have shown that IL-6 promotes Th17 responses by triggering a positive feedback loop with IL-17. Here the authors show how TMEV manipulates that loop. Mice that produced higher levels of IL-6 and IL-17 after infection developed more severe disease than did resistant mice, in which protective Th1 responses predominated. Overproduction of IL-17 has been reported during early HIV infection in humans and herpes simplex virus in mice. Now that Hou et al. reveal that IL-17 promotes viral infection, chances are it's playing a similarly insidious role in other chronic infections.