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.