Identification of amino-acid residues in the V protein of peste des petits ruminants essential for interference and suppression of STAT-mediated interferon signaling

Ma, Xusheng; Yang, Xing; Nian, Xiaofeng; Zhang, Zhidong; Dou, Yongxi; Zhang, Xuehu; Luo, Xuenong; Su, Junhong; Zhu, Qing; Xue-peng, Cai

doi:10.1016/j.virol.2015.03.039

Cited by 35 publications

(47 citation statements)

References 41 publications

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“…In experiments with the Sungri/96 PPRV vaccine virus, IFN-α/β mRNA were not detected after the infection of PBMC [31] and evasion of IFN-induced antiviral effects by PPRV have been shown to occur through miRNA mediated regulation of IRF3 and IRF7 [32]. In contrast, studies with a virulent PPRV strain demonstrated that genes within the interferon and RIG-1 like receptor signaling pathway, IRF-7 and STAT-1 that regulate the expression of ISGs, were active in lymphocytes [33].…”

Section: Discussionmentioning

confidence: 90%

RNAseq Reveals the Contribution of Interferon Stimulated Genes to the Increased Host Defense and Decreased PPR Viral Replication in Cattle

Tirumurugaan

Pawar

Raj

et al. 2020

Viruses

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Peste des petits ruminants virus (PPRV) is known to replicate in a wide variety of ruminants causing very species-specific clinical symptoms. Small ruminants (goats and sheep) are susceptible to disease while domesticated cattle and buffalo are dead-end hosts and do not display clinical symptoms. Understanding the host factors that influence differential pathogenesis and disease susceptibility could help the development of better diagnostics and control measures. To study this, we generated transcriptome data from goat and cattle peripheral blood mononuclear cells (PBMC) experimentally infected with PPRV in-vitro. After identifying differentially expressed genes, we further analyzed these immune related pathway genes using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and selected candidate genes were validated using in-vitro experiments. Upon PPRV infection, we identified 12 and 22 immune related genes that were differentially expressed in goat and cattle respectively. In both species, this included the interferon stimulated genes (ISGs) IFI44, IFI6, IFIT1, IFIT2, IFIT3, ISG15, Mx1, Mx2, OAS1X, RSAD2, IRF7, DDX58 and DHX58 that were transcribed significantly higher in cattle. PPRV replication in goat PBMCs significantly increased the expression of phosphodiesterase 12 (PDE12), a 2′,5′-oligoadenylate degrading enzyme that contributes to the reduced modulation of interferon-regulated gene targets. Finally, a model is proposed for the differential susceptibility between large and small ruminants based on the expression levels of type-I interferons, ISGs and effector molecules.

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Section: Discussionmentioning

confidence: 90%

RNAseq Reveals the Contribution of Interferon Stimulated Genes to the Increased Host Defense and Decreased PPR Viral Replication in Cattle

Tirumurugaan

Pawar

Raj

et al. 2020

Viruses

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“…Among the cells subject to PPRV infection, Vero cells are usually used to study PPRV infection in vitro [17,44]. It is well known that PPRV can infect a multitude of host cells, such as sheep kidney epithelial cells [45] (PO cell line) and goat peripheral blood mononuclear cells (PBMCs) [46].…”

Section: Discussionmentioning

confidence: 99%

Autophagy enhances the replication of Peste des petits ruminants virus and inhibits caspase-dependent apoptosis in vitro

Yang

Xue

et al. 2018

Virulence

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Peste des petits ruminants (PPR) is an acute and highly contagious disease in small ruminants that causes significant economic losses in developing countries. An increasing number of studies have demonstrated that both autophagy and apoptosis are important cellular mechanisms for maintaining homeostasis, and they participate in the host response to pathogens. However, the crosstalk between apoptosis and autophagy in host cells during PPRV infection has not been clarified. In this study, autophagy was induced upon virus infection in caprine endometrial epithelial cells (EECs), as determined by the appearance of double- and single-membrane autophagy-like vesicles, LC3-I/LC3-II conversion, and p62 degradation. We also found that PPRV infection triggered a complete autophagic response, most likely mediated by the non-structural protein C and nucleoprotein N. Moreover, our results suggest that autophagy not only promotes the replication of PPRV in EECs but also provides a potential mechanism for inhibiting PPRV-induced apoptosis. Inhibiting autophagosome formation by wortmannin and knocking down the essential autophagic proteins Beclin-1 and ATG7 induces caspase-dependent apoptosis in EECs in PPRV infection. However, inhibiting autophagosome and lysosome fusion by NH4Cl and chloroquine did not increase the number of apoptotic cells. Collectively, these data are the first to indicate that PPRV-induced autophagy inhibits caspase-dependent apoptosis and thus contributes to the enhancement of viral replication and maturity in host cells.

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“…For instance, within the Respirovirus genus, the C protein of Sendai virus inhibits the phosphorylation of IRF7 (247), and the V proteins of HPIV-1 and -3 are thought to inhibit STAT-1 and STAT-2 (reviewed in reference 248). Similarly, the V proteins of viral species belonging to the Morbillivirus genus, including measles and canine distemper viruses, prevent the transcription of ISGs by abrogating the nuclear translocation of STAT-1 and STAT-2 (249,250). In addition, V proteins inhibit the phosphorylation of Tyk2 and Jak1, which are key IFNR-associated kinases (251).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Host Immunity by the Human Metapneumovirus

et al. 2016

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SUMMARYGlobally, as a leading agent of acute respiratory tract infections in children <5 years of age and the elderly, the human metapneumovirus (HMPV) has gained considerable attention. As inferred from studies comparing vaccinated and experimentally infected mice, the acquired immune response elicited by this pathogen fails to efficiently clear the virus from the airways, which leads to an exaggerated inflammatory response and lung damage. Furthermore, after disease resolution, there is a poor development of T and B cell immunological memory, which is believed to promote reinfections and viral spread in the community. In this article, we discuss the molecular mechanisms that shape the interactions of HMPV with host tissues that lead to pulmonary pathology and to the development of adaptive immunity that fails to protect against natural infections by this virus.

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Identification of amino-acid residues in the V protein of peste des petits ruminants essential for interference and suppression of STAT-mediated interferon signaling

Cited by 35 publications

References 41 publications

RNAseq Reveals the Contribution of Interferon Stimulated Genes to the Increased Host Defense and Decreased PPR Viral Replication in Cattle

RNAseq Reveals the Contribution of Interferon Stimulated Genes to the Increased Host Defense and Decreased PPR Viral Replication in Cattle

Autophagy enhances the replication of Peste des petits ruminants virus and inhibits caspase-dependent apoptosis in vitro

Modulation of Host Immunity by the Human Metapneumovirus

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