Innate sensing of viruses by pattern recognition receptors in birds

Abstract

Similar to mammals, several viral-sensing pattern recognition receptors (PRR) have been identified in birds including Toll-like receptors (TLR) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLR). Avian TLR are slightly different from their mammalian counterparts, including the pseudogene TLR8, the absence of TLR9, and the presence of TLR1La, TLR1Lb, TLR15, and TLR21. Avian TLR3 and TLR7 are involved in RNA virus recognition, especially highly pathogenic avian influenza virus (HPAIV), while TLR15 and TLR21 are potential sensors that recognize both RNA viruses and bacteria. However, the agonist of TLR15 is still unknown. Interestingly, chickens, unlike ducks, geese and finches, lack RIG-I, however they do express melanoma differentiation-associated gene 5 (MDA5) which functionally compensates for the absence of RIG-I. Duck RIG-I is the cytosolic recognition element for HPAIV recognition, while chicken cells sense HPAIV through MDA5. However, the contributions of MDA5 and RIG-I to IFN-β induction upon HPAIV infection is different, and this may contribute to the chicken’s susceptibility to highly pathogenic influenza. It is noteworthy that the interactions between avian DNA viruses and PRR have not yet been reported. Furthermore, the role for avian Nod-like receptors (NLR) in viral immunity is largely unknown. In this review, recent advances in the field of viral recognition by different types of PRR in birds are summarized. In particular, the tissue and cellular distribution of avian PRR, the recognition and activation of PRR by viruses, and the subsequent expression of innate antiviral genes such as type I IFN and proinflammatory cytokines are discussed.

Apoptosis induction and release of inflammatory cytokines in the oviduct of egg-laying hens experimentally infected with H9N2 avian influenza virus

“…The activation of PRRs by viral nucleic acids triggers the expression of innate antiviral genes such as interferon (Chen et al, 2013). In the present study, TLR3 was slightly decreased in the early stage of infection and was slightly increased in late stage that may trigger the down-regulation of IFN-a mRNA expression, as TLR3 plays two-faced role in the induction of antivirus IFN-a or IFN-b in different situation (Okahira et al, 2005;Kogut et al, 2005).…”

Identification of an infectious bronchitis coronavirus strain exhibiting a classical genotype but altered antigenicity, pathogenicity, and innate immunity profile

“…As RIG-I is absent in chickens, IFIH1 is a functional compensate16. Avian TLRs are different from their mammalian counterparts, lacking TLR9 but possessing TLR1LA, poultry-specific TLR15, and a TLR9 homologue TLR2117. TLR3 and TLR7 are known to be involved in RNA virus recognition, and its stimulation leads to activation of IRF3 and IRF7 (IFN-regulatory factor 3 and 7).…”

“…TLR3 and TLR7 are known to be involved in RNA virus recognition, and its stimulation leads to activation of IRF3 and IRF7 (IFN-regulatory factor 3 and 7). These factors then signal IFN transcription to trigger IFN-stimulated genes (ISGs) through JAK-STAT pathway to express various antiviral proteins151718. A global gene expression profiling of chicken kidney has revealed that 103 immune and inflammatory-related genes are involved in the host defense response during the first week of IBV infection19.…”

Genetic variants in IFIH1 and DDX58 influence hepatitis C virus clearance in Chinese Han population

“…IFIH1 and DDX58 can distinguish different RNA viruses and play a crucial role in host antiviral responses . Previous studies also suggested that IFIH1 and DDX58 can identify RNA viruses in the cells via binding to the pathogen‐associated molecular pattern . The current study recruited 3065 participants to investigate the effect of the IFIH1 rs3747517 and DDX58 rs9695310 on the susceptibility and clinical outcome of HCV infection, with a statistical power of 0.964.…”