The matrix protein of Newcastle disease virus inhibits inflammatory response through IRAK4/TRAF6/TAK1/NF-κB signaling pathway

Duan, Zhiqiang; Xing, Jingru; Shi, Haiying; Wang, Yanbi; Zhao, Caiqin

doi:10.1016/j.ijbiomac.2022.07.132

Cited by 9 publications

(6 citation statements)

References 67 publications

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“…The nuclear-localized W protein inhibited the production of IFN-β, thereby improving the replication, virulence, and pathogenicity of NDV [16]. Apart from V and W proteins, the N-terminal 180 amino acids (aa) of skeleton protein M also proved to antagonize NF-kB activation via the IRK4/TRAF6/TAK1/NF-kB signaling pathway [99]. However, in this study, the M protein did not directly interact with these proteins.…”

Section: Ifnmentioning

confidence: 54%

Pathologic Mechanisms of the Newcastle Disease Virus

Zhang

Ding

2023

Viruses

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Newcastle disease (ND) has been a consistent risk factor to the poultry industry worldwide. Its pathogen, Newcastle disease virus (NDV), is also a promising antitumor treatment candidate. The pathogenic mechanism has intrigued the great curiosity of researchers, and advances in the last two decades have been summarized in this paper. The NDV’s pathogenic ability is highly related to the basic protein structure of the virus, which is described in the Introduction of this review. The overall clinical signs and recent findings pertaining to NDV-related lymph tissue damage are then described. Given the involvement of cytokines in the overall virulence of NDV, cytokines, particularly IL6 and IFN expressed during infection, are reviewed. On the other hand, the host also has its way of antagonizing the virus, which starts with the detection of the pathogen. Thus, advances in NDV’s physiological cell mechanism and the subsequent IFN response, autophagy, and apoptosis are summarized to provide a whole picture of the NDV infection process.

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Section: Ifnmentioning

confidence: 54%

Pathologic Mechanisms of the Newcastle Disease Virus

Zhang

Ding

2023

Viruses

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“…Additionally, the TRAF gene was overexpressed, indicating enhanced type I interferon production [ 37 ]. Previous research identified TRAF down-regulation caused by NDV M protein plasmids as a strategy to mock the host inflammatory response in vitro [ 38 ]. Differences between the current and cited research could be due to using different experimental models.…”

Section: Discussionmentioning

confidence: 99%

Changes in the Transcriptome Profile in Young Chickens after Infection with LaSota Newcastle Disease Virus

Lopes,

Nankemann,

Breedlove

et al. 2024

Vaccines

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Understanding gene expression changes in chicks after vaccination against Newcastle Disease (ND) can reveal vaccine biomarkers. There are limited data on chicks’ early immune response after ND vaccination. Two trials focused on this knowledge gap. In experiment one, 42 13-day-old specific-pathogen-free (SPF) chicks were used. Harderian glands (Hgs) and tracheas (Tcs) from five birds per group were sampled at 12, 24, and 48 h post-vaccination (hpv) to evaluate the gene transcription levels by RNA sequencing (RNA-seq) and RT-qPCR. The results of RNA-seq were compared by glmFTest, while results of RT-qPCR were compared by t-test. With RNA-seq, a significant up-regulation of interferon-related genes along with JAK-STAT signaling pathway regulation was observed in the Hgs at 24 hpv. None of the differentially expressed genes (DEGs) identified by RNA-seq were positive for RT-qPCR. Experiment 2 used 112 SPF and commercial chickens that were 1 day old and 14 days old. Only the commercial birds had maternal antibodies for Newcastle Disease virus (NDV). By RNA-seq, 20 core DEGs associated with innate immunity and viral genome replication inhibition were identified. Genes previously unlinked to NDV response, such as USP41, were identified. This research present genes with potential as immunity biomarkers for vaccines, yet further investigation is needed to correlate the core gene expression with viral shedding post-vaccination.

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“…In recent years, increasing lines of evidence have indicated that BRD2 plays crucial roles in regulating NF-κB activity [ 37 , 38 , 39 , 40 ] and interferon production [ 41 , 42 ]. The NDV M protein is demonstrated to have an innate immune antagonism feature, which inhibits inflammatory responses through TIFA/TRAF6/NF-κB or IRAK4/TRAF6/TAK1/NF-κB signaling pathways [ 7 , 43 ]. Meanwhile, the reduced production of inflammatory cytokines caused by the M protein promotes the replication and cytopathogenicity of NDV.…”

Section: Discussionmentioning

confidence: 99%

Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity

Duan

Shi

Xing

et al. 2023

IJMS

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The matrix (M) protein of Newcastle disease virus (NDV) contains large numbers of unevenly distributed basic residues, but the precise function of most basic residues in the M protein remains enigmatic. We previously demonstrated that the C-terminus (aa 264–313) of M protein interacted with the extra-terminal (ET) domain of chicken bromodomain-containing protein 2 (chBRD2), which promoted NDV replication by downregulating chBRD2 expression and facilitating viral RNA synthesis and transcription. However, the key amino acid sites determining M’s interaction with chBRD2/ET and their roles in the replication and pathogenicity of NDV are not known. In this study, three basic residues—R283, R286, and K288—in the NDV M protein were verified to be responsible for its interaction with chBRD2/ET. In addition, mutation of these basic residues (R283A/R286A/K288A) in the M protein changed its electrostatic pattern and abrogated the decreased expression of endogenic chBRD2. Moreover, a recombinant virus harboring these mutations resulted in a pathotype change of NDV and attenuated viral replication and pathogenicity in chickens due to the decreased viral RNA synthesis and transcription. Our findings therefore provide a better understanding of the crucial biological functions of M’s basic residues and also aid in understanding the poorly understood pathogenesis of NDV.

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The matrix protein of Newcastle disease virus inhibits inflammatory response through IRAK4/TRAF6/TAK1/NF-κB signaling pathway

Cited by 9 publications

References 67 publications

Pathologic Mechanisms of the Newcastle Disease Virus

Pathologic Mechanisms of the Newcastle Disease Virus

Changes in the Transcriptome Profile in Young Chickens after Infection with LaSota Newcastle Disease Virus

Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity

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