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Abstract
The immune response to virus infection is initiated when pathogen recognition receptors
(PRRs) of the host cell recognize specific nonself-motifs within viral products (known
as a pathogen-associated molecular pattern or PAMP) to trigger intracellular signaling
events that induce innate immunity, the front line of defense against microbial infection.
The replication program of all viruses includes a cytosolic phase of genome amplification
and/or mRNA metabolism and viral protein expression. Cytosolic recognition of viral
infection by specific PRRs takes advantage of the dependence of viruses on the cytosolic
component of their replication programs. Such PRR-PAMP interactions lead to PRR-dependent
nonself-recognition and the downstream induction of type I interferons and proinflammatory
cytokines. These factors serve to induce innate immune programs and drive the maturation
of adaptive immunity and inflammation for the control of infection. Recent studies
have focused on identifying the particular viral ligands recognized as nonself by
cytosolic PRRs, and on defining the nature of the PRRs and their signaling pathways
involved in immunity. The RIG-I-like receptors, RIG-I and MDA5, have been defined
as essential PRRs for host detection of a variety of RNA viruses. Novel PRRs and their
signaling pathways involved in detecting DNA viruses through nonself-recognition of
viral DNA are also being elucidated. Moreover, studies to identify the PRRs and signaling
factors of the host cell that mediate inflammatory signaling through inflammasome
activation following virus infection are currently underway and have already revealed
specific NOD-like receptors (NLRs) as inflammatory triggers. This review summarizes
recent progress and current areas of focus in pathogen recognition and immune triggering
by cytosolic PRRs.
Copyright 2009 Elsevier Ltd. All rights reserved.