Herpesviruses can establish latent infections, but whether coinfection with other pathogens can reactivate the viruses remains unknown. In Science, Virgin and colleagues show that helminth coinfection stimulates the replication and production of herpesvirus. This effect requires signaling via cytokines that induce the transcription factor STAT6, such as interleukin 4 (IL-4) and IL-13, as well as suppression of interferon-γ signaling. Many herpesviruses, including mouse γ-herpesvirus and human Kaposi's sacoma virus, seem to have evolved the ability to sense these competing signals that regulate the expression of a latent-to-lytic 'switch' gene. Thus, herpesviruses are acutely tuned to the immunological status of their host and undergo latency or productive replication dependent on signaling by IL-4 or interferon-γ.

Science (26 June 2014) doi:10.1126/science.1254517