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Host response

Viral persistence: IL-10 is the key

Nature Reviews Immunology volume 6, pages 878–879 (2006)Cite this article

Intensive research has been directed towards understanding the mechanisms that underlie virus persistence. Cell-mediated immunity is essential for virus clearance, but persistent viruses can avoid this antiviral response by inducing immunosuppression. Strategies for inducing immunosuppression include physical deletion of virus-specific T-cell subsets, a useful tactic that is used by HIV-1, hepatitis B and C viruses and lymphocytic choriomeningitis virus (LCMV). Concomitant with the deletion of T-cell subsets is the loss of T-cell cytolytic functions, which results in an inability to kill virus-infected cells. The latest research from groups led by Michael Oldstone and Matthias von Herrath has established a clear link between cytokine production and T-cell function in persistent LCMV infection.

One extremely useful model system for probing the subtle interplay between virus replication and the host response during persistence is the infection of rodents with LCMV. Infection with LCMV can produce either an acute or a persistent infection depending on the virus strain, the route of infection and the infectious dose. Both of the studies investigated the basis of persistence using this model.

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ORIGINAL RESEARCH PAPERS

  1. Ejrnaes, M. et al. Resolution of a chronic viral infection after interleukin-10 receptor blockade. J. Exp. Med. 203, 2461–2472 (2006)

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  2. Brooks, D. G. et al. Interleukin-10 determines viral clearance or persistence in vivo. Nature Med. 12, 1301–1309 (2006)

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  1. Senior Editor, Nature Reviews Microbiology,

    Susan Jones

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  1. Susan Jones
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Jones, S. Viral persistence: IL-10 is the key. Nat Rev Immunol 6, 878–879 (2006). https://doi.org/10.1038/nri1989

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