Abstract
The disease caused by duck Tembusu virus (DTMUV) is characterized by severe egg-drop in laying ducks. Currently, the disease has spread to most duck-raising areas in China, leading to great economic losses in the duck industry. In the recent years, DTMUV has raised some concerns, because of its expanding host range and increasing pathogenicity, as well as the potential threat to public health. Innate immunity is crucial for defending against invading pathogens in the early stages of infection. Recently, studies on the interaction between DTMUV and host innate immune response have made great progress. In the review, we provide an overview of DTMUV and summarize current advances in our understanding of the interaction between DTMUV and innate immunity, including the host innate immune responses to DTMUV infection through pattern recognition receptors (PRRs), signaling transducer molecules, interferon-stimulated genes (ISGs), and the immune evasion strategies employed by DTMUV. The aim of the review is to gain an in-depth understanding of DTMUV pathogenesis to facilitate future studies.
Highlights
2 Overview of duck Tembusu virus (DTMUV) 3 DTMUV infection triggers host innate immune responses 3.1 T LR‐mediated signaling pathway in recognition of DTMUV 3.2 RLR‐mediated signaling pathway in recognition of DTMUV 3.3 Other pattern recognition receptors (PRRs) relevant to DTMUV infection 3.4 IF N‐stimulated genes (ISGs) defense against DTMUV infection
Overexpression of duck mitochondrial antiviral-signaling protein (MAVS) significantly reduced DTMUV replication, its disruption increased virus titer in duck embryo fibroblasts (DEF) cells [94], and the knockdown of MAVS impaired the activation of IRF1, NF-κB, and IFN-β induced by DTMUV [95], which suggested that DTMUV can efficiently trigger RLR- and MAVS-dependent signaling pathways
It is demonstrated that the disruption expression of endogenous IFITM1 or IFITM3 markedly enhanced DTMUV replication in DF-1 cells while IFITM2 not, and the overexpression of chicken or duck IFITM1 and IFITM3 can inhibit the replication of DTMUV in DF-1 cells, which indicated that in Interferon-inducible transmembrane (IFITM) family proteins, IFITM1 and IFTIM3 play crucial roles in anti-DTMUV infection [122]
Summary
1 Introduction In April 2010, an outbreak of an unknown duck egg-drop disease occurred in the coastal provinces of southeast China, characterized by a substantial decrease in egg laying and neurological symptoms in infected egg-laying and breeder ducks [1]. Li et al reported that DTMUV can be transmitted by aerosol [26], similar to H9N2 avian influenza virus (AIV) [27, 28], Newcastle disease virus (NDV) [29, 30], and Marek’s disease virus [31] This transmission mode partly explains why DTMUV was capable of spreading to majority of duck-raising areas in China within a short time after the outbreak. In addition to mediating virus entry, E protein is essential for DTMUV pathogenesis [50]; especially, mutations in several important amino acid sites, which can significantly affect viral pathogenicity. Yan et al reported that a single mutation at amino acid residue 156 (S-P) reduced the ability of viral replication and transmission in ducks, and further analysis confirmed that the potential mechanism was composed by the disruption of N-linked glycosylation at position 154 and changes in the conformation of the “150 loop” of the E protein [51]. More attention should be paid to epidemiological investigation and evolution analysis
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