![]() Then, RIG-I undergos a conformational change resulting in the exposure of the CARDs to the cytoplasm, which ultimately leads to CARD ubiquitination. During virus infection, prepackaged single-stranded RNA (ssRNA) and double-stranded RNA (dsRNA) generated by viral RNA polymerases, can be recognized by the CTD through the RNA-binding domain. RIG-I, a 925 amino acid protein, is composed of two N-terminal tandem caspase activation and recruitment domains (CARDs), a central DExD/H-box RNA helicase domain, and a Zn 2+-containing regulatory C-terminal domain (CTD), which is also known as an autorepression domain. The RLRs, which consist of RIG-I, MDA5 (melanoma differentiation associated gene 5), and LGP2 (laboratory of genetics and physiology 2), are the major cytoplasmic PRRs of RNA viruses. The recognition of virus-specific pathogen-associated molecular patterns (PAMPs) by host cells is mediated by pathogen recognition receptors (PRRs), including Toll-like receptors (TLRs), Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) and Nod-like receptors (NLRs). This difference in virus resistance among waterfowl, pigeon, and chicken has been ascribed to their individual immune systems, especially their respective innate immune systems. As natural reservoirs, ducks and pigeons have been called the “Trojan horse” and “dead end” for susceptibility to infection however, they are ineffective propagators and disseminators of the virus. Both HPAIV and IBDV cause high morbidity and mortality in chicken poultry but typically do not cause these effects in wild waterfowl and pigeon. Another major problem in the domestic poultry industry is infectious bursal disease (IBD) caused by the infectious bursal disease virus (IBDV) characterized by acute, highly contagious, immunosuppressive disease in the young chicken. Despite its weak virulence, H9N2 influenza genotype evolution has facilitated the genesis of the novel H7N9 virus, which has caused the deaths of at least 115 people. H9N2 avian influenza virus (AIV) has been the major threat against domestic poultry in China during the last few decades. In conclusion, these results demonstrated that pigeon RIG-I and CARDs have a strong antiviral ability against AIV H9N2 and IBDV in chicken DF-1 cells but not in human 293T cells. Furthermore, chicken melanoma differentiation associated gene 5(MDA5)/ mitochondrial antiviral signaling (MAVS) silencing combined with RIG-I transfection suggested that pigeon RIG-I can restore the antiviral response in MDA5-silenced DF-1 cells but not in MAVS-silenced DF-1 cells. Our data indicated that waterfowl RIG-I are more effective in the induction of antiviral genes and the repression of ZB07 and IBDV TS/CJ-801 strain replication than pigeon RIG-I. We also compared the antiviral abilities of RIG-I proteins from waterfowl (duck and goose) and pigeon. The exogenous expression of enhanced green fluorescence protein (EGFP)-tagged pigeon RIG-I and caspase activation and recruitment domains (CARDs), strongly induced antiviral gene ( IFN-β, Mx, and PKR) mRNA synthesis, decreased viral gene ( M gene and VP2) mRNA expression, and reduced the viral titers of ZB07 and IBDV TS/CJ-801 virus strains in chicken DF-1 cells, but not in 293T cells. ![]() ![]() Pigeon mRNA encoding the putative pigeon RIG-I analogs was identified. Consequently, we sought to identify pigeon RIG-I and investigate its roles in the detection of A/Chicken/Shandong/ZB/2007 (H9N2) (ZB07), Gansu/Tianshui (IBDV TS) and Beijing/CJ/1980 (IBDV CJ-801) strains in chicken DF-1 fibroblasts or human 293T cells. Like ducks, pigeons are also susceptible to infection but are ineffective propagators and disseminators of AIVs, i.e., “dead end” hosts for AIVs and even highly pathogenic avian influenza (HPAI). ![]() Previous studies have shown that mammalian RIG-I (human and mice) and waterfowl RIG-I (ducks and geese) are essential for type I interferon (IFN) synthesis during AIV infection. Retinoic acid-inducible gene I (RIG-I), a cytosolic pattern recognition receptor (PRR), can sense various RNA viruses, including the avian influenza virus (AIV) and infectious bursal disease virus (IBDV), and trigger the innate immune response.
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