Pathogenicity of duck plague and innate immune responses of the Cherry Valley ducks to duck plague virus.

Ning Li,Yao Wang,Liangmeng Wei,Yumei Cai,Rong Li,Jinzhou Zhang,Sidang Liu,Tianqi Hong,Mengjiao Guo,Tongjie Chai,Jiyuan Liu

doi:10.1038/srep32183

Ning Li, Yao Wang + Show 9 more

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https://doi.org/10.1038/srep32183

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Abstract

Duck plague caused by duck plague virus (DPV) is an acute and contagious disease. To better understand the pathogenic mechanism of duck plague virus in ducklings, an infection experiment was performed. Our results showed that typical symptoms were observed in the infected ducklings. DPV could replicate quickly in many tissues, leading to pathological lesions, especially on the spleen. Real-time quantitative PCR demonstrated that expression of many innate immune-related genes was mostly up-regulated in the brain, and the antiviral innate immune response was established, but not sufficient to restrict viral replication. In contrast, although the expression of many major pattern recognition receptors (PRRs) increased in the spleen, the expression of most cytokines was declined. Our study indicates that DPV is a pantropic virus that can replicate rapidly in tissues, causing serious pathological lesions but the immune responses are different in the spleen and brain. To our knowledge, this is the first report to systematically explore the expression profiles of the immune genes in the DPV-infected ducks. Our data provide a foundation for further study of the pathogenicity of duck plague.

Highlights

Duck plague (DP), known as duck vial enteritis, is an acute and highly contagious disease in waterfowl such as duck and geese
In addition to TLR2, TLR9 has been reported to play an important role in the pathogenesis of herpes simplex virus (HSV), as it can recognize the CpG motifs of HSV DNA and initiates the type I IFNs and cytokine secretion[12,13]
Given that the replication of the viral genome leads to the production of intermediate double-stranded RNA (dsRNA), which are sensed by retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5), RIG-I like receptors (RLRs) interact with the IFN-βpromoter stimulator 1 (IPS-1) adaptor protein upon recognition to induce the synthesis of the antiviral effectors and establish an antiviral state[20,21,22]

Summary

Introduction

Duck plague (DP), known as duck vial enteritis, is an acute and highly contagious disease in waterfowl such as duck and geese. Among a variety of PRRs, one class of receptors called Toll-like receptors (TLRs), which are a group of conserved type I transmembrane proteins located on the plasma membrane or endosomal membrane, recognize PAMPs such as single- and double-stranded RNA (dsRNA), DNA, and lipopolysaccharide of Gram-negative bacteria[9] Both DPV and herpes simplex virus (HSV) belong to the herpes virus, which have the CpG motif in their genomes. The results from Zhang et al suggest that TLR3-mediated production of type I and II IFN may be crucial in the HSV infection[18] Another class of PRRs, namely RIG-I like receptors (RLRs), including the retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5), are expressed in the cytoplasm and primarily sense dsRNA or 5′-triphosphate single-stranded RNA19. In the present study, clinical symptoms, pathological changes, and the viral distribution in the tissues of the ducks infected with DPV were analyzed, with a special focus on the innate immune response to this virus to systemically explore the pathogenicity of DPV in 21-day-old Cherry Valley ducks

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