1. ¹Department of Molecular Research and Development, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria, Australia
2. ²Department of Gastroenterology, St Vincent's Hospital, Fitzroy, Victoria, Australia

Correspondence: Dr AJV Thompson, Victorian Infectious Diseases Reference Laboratory, 10 Wreckyn St.North Melbourne, Victoria 3051, Australia. E-mail: alexander.thompson@svhm.org.au

Received 9 June 2007; Accepted 14 June 2007; Published online 31 July 2007.

Abstract

The antiviral innate immune response follows the detection of viral components by host pattern recognition receptors (PRRs). Two families of PRRs have emerged as key sensors of viral infection: Toll-like receptors (TLRs) and retinoic acid inducible gene-I like RNA helicases (RLHs). TLRs patrol the extracellular and endosomal compartments; signalling results in a type-1 interferon response and/or the production of pro-inflammatory cytokines. In contrast, RLHs survey the cytoplasm for the presence of viral double-stranded RNA. In the face of such host defence, viruses have developed strategies to evade TLR/RLH signalling. Such host–virus interactions provide the opportunity for manipulation of PRR signalling as a novel therapeutic approach.