Helminth infection reactivates latent γ-herpesvirus via cytokine competition at a viral promoter

• DOI: 10.1126/science.1254517
• Publication Date: 2014-06-27T04:47:41Z
• Authors: T. A. Reese; B. S. Wakeman; H. S. Choi; M. M. Hufford; S. C. Huang; X. Zhang; M. D. Buck; A. Jezewski; A. Kambal; C. Y. Liu; G. Goel; P. J. Murray; R. J. Xavier; M. H. Kaplan; R. Renne; S. H. Speck; M. N. Artyomov; E. J. Pearce; H. W. Virgin
• Keywords: Gene Expression Regulation, Viral; 0301 basic medicine; Nematospiroides dubius; Macrophages; Schistosoma mansoni; Virus Replication; Schistosomiasis mansoni; Virus Latency; 3. Good health; Mice, Inbred C57BL; Interferon-gamma; Mice; 03 medical and health sciences; Gammaherpesvirinae; Herpesvirus 8, Human; Herpesvirus 8 -- Human; Animals; Humans; Virus Activation; Interleukin-4; Promoter Regions, Genetic; STAT6 Transcription Factor; Ovum; Strongylida Infections

Parasites make it hard to fight viruses

Microbial co-infections challenge the immune system—different pathogens often require different flavors of immune responses for their elimination or containment (see the Perspective by Maizels and Gause). Two teams studied what happens when parasitic worms and viruses infect mice at the same time. Reese et al. found that parasite co-infection woke up a dormant virus. Osborne et al. found that mice already infected with parasitic worms were worse at fighting off viruses. In both cases, worms skewed the immune response so that the immune cells and the molecules they secreted created an environment favorable for the worm at the expense of antiviral immunity.

Science , this issue p. 573 and p. 578 ; see also p. 517