Replication-independent activation of human plasmacytoid dendritic cells by the paramyxovirus SV5 Requires TLR7 and autophagy pathways

Manuse, Mary J.; Briggs, Caitlin M.; Parks, Griffith D.

doi:10.1016/j.virol.2010.06.023

Cited by 34 publications

(27 citation statements)

References 46 publications

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“…While intriguing, this would be inconsistent with previous work showing that PIV5 is unable to block signaling through Toll-like receptors [65,67] or RIG-I [68]. These disparate findings may reflect differences in the targeting of TBK-1 pathways in different cell types, including cell lines versus primary cells.…”

Section: Paramyxovirus Interactions With Intracellular Rna-sensing Pacontrasting

confidence: 56%

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Paramyxovirus Activation and Inhibition of Innate Immune Responses

Parks

Alexander-Miller

2013

Journal of Molecular Biology

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Paramyxoviruses represent a remarkably diverse family of enveloped nonsegmented negative-strand RNA viruses, some of which are the most ubiquitous disease-causing viruses of humans and animals. This review focuses on paramyxovirus activation of innate immune pathways, the mechanisms by which these RNA viruses counteract these pathways, and the innate response to paramyxovirus infection of dendritic cells (DC). Paramyxoviruses are potent activators of extracellular complement pathways, a first line of defense that viruses must face during natural infections. We discuss mechanisms by which these viruses activate and combat complement to delay neutralization. Once cells are infected, virus replication drives type I interferon (IFN) synthesis that has the potential to induce a large number of antiviral genes. Here we describe four approaches by which paramyxoviruses limit IFN induction: by limiting synthesis of IFN-inducing aberrant viral RNAs, through targeted inhibition of RNA sensors, by providing viral decoy substrates for cellular kinase complexes, and through direct blocking of the IFN promoter. In addition, paramyxoviruses have evolved diverse mechanisms to disrupt IFN signaling pathways. We describe three general mechanisms, including targeted proteolysis of signaling factors, sequestering cellular factors, and upregulation of cellular inhibitors. DC are exceptional cells with the capacity to generate adaptive immunity through the coupling of innate immune signals and T cell activation. We discuss the importance of innate responses in DC following paramyxovirus infection and their consequences for the ability to mount and maintain antiviral T cells.

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Section: Paramyxovirus Interactions With Intracellular Rna-sensing Pacontrasting

confidence: 56%

“…This finding could account for the profound suppression of IFN-α production from MeV-infected pDC [64]. It is note-worthy that some paramyxoviruses fail to inhibit TLR-7-mediated IFN-α production during infection of pDC [65]. …”

Section: Paramyxovirus Interactions With Intracellular Rna-sensing Pamentioning

confidence: 99%

Paramyxovirus Activation and Inhibition of Innate Immune Responses

Parks

Alexander-Miller

2013

Journal of Molecular Biology

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“…Measles virus, which, like NDV, belongs to the family Paramyxoviridae, induces autophagy through a pathogen receptor CD46-Cyt-1/GOPC pathway (18). Another paramyxovirus, parainfluenza virus type 5 (PIV5), requires autophagy pathways to activate human plasmacytoid dendritic cells (19). In the present study, we demonstrated that autophagy is induced upon NDV infection of chicken cells and tissues.…”

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confidence: 56%

Autophagy Benefits the Replication of Newcastle Disease Virus in Chicken Cells and Tissues

Sun

Ding

et al. 2014

J Virol

102

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bNewcastle disease virus (NDV) is an important avian pathogen. We previously reported that NDV triggers autophagy in U251 glioma cells, resulting in enhanced virus replication. In this study, we investigated whether NDV triggers autophagy in chicken cells and tissues to enhance virus replication. We demonstrated that NDV infection induced steady-state autophagy in chickenderived DF-1 cells and in primary chicken embryo fibroblast (CEF) cells, evident through increased double-or single-membrane vesicles, the accumulation of green fluorescent protein (GFP)-LC3 dots, and the conversion of LC3-I to LC3-II. In addition, we measured autophagic flux by monitoring p62/SQSTM1 degradation, LC3-II turnover, and GFP-LC3 lysosomal delivery and proteolysis, to confirm that NDV infection induced the complete autophagic process. Inhibition of autophagy by pharmacological inhibitors and RNA interference reduced virus replication, indicating an important role for autophagy in NDV infection. Furthermore, we conducted in vivo experiments and observed the conversion of LC3-I to LC3-II in heart, liver, spleen, lung, and kidney of NDV-infected chickens. Regulation of the induction of autophagy with wortmannin, chloroquine, or starvation treatment affects NDV production and pathogenesis in tissues of both lung and intestine; however, treatment with rapamycin, an autophagy inducer of mammalian cells, showed no detectable changes in chicken cells and tissues. Moreover, administration of the autophagy inhibitor wortmannin increased the survival rate of NDV-infected chickens. Our studies provide strong evidence that NDV infection induces autophagy which benefits NDV replication in chicken cells and tissues.

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“…(Manuse et al, 2010) One paramyxovirus, Human Parainflueza Virus 3 (HPIV3), specifically inhibits autophagosome maturation during infection. The virus encodes a protein, P, which is central to viral RNA replication.…”

Section: Induction Of Autophagic Signaling Vs Bona Fide Autophagymentioning

confidence: 99%

Viruses and the autophagy pathway

2015

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Studies of the cellular autophagy pathway have exploded over the past twenty years. Now appreciated as a constitutive degradative mechanism that promotes cellular homeostasis, autophagy is also required for a variety of developmental processes, cellular stress responses, and immune pathways. Autophagy certainly acts as both an anti-viral and pro-viral pathway, and the roles of autophagy depend on the virus, the cell type, and the cellular environment. The goal of this review is to summarize, in brief, what we know so far about the relationship between autophagy and viruses, particularly for those who are not familiar with the field. With a massive amount of relevant published data, it is simply not possible to be comprehensive, or to provide a complete “parade of viruses”, and apologies are offered to researchers whose work is not described herein. Rather, this review is organized around general themes regarding the relationship between autophagy and animal viruses.

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Replication-independent activation of human plasmacytoid dendritic cells by the paramyxovirus SV5 Requires TLR7 and autophagy pathways

Cited by 34 publications

References 46 publications

Paramyxovirus Activation and Inhibition of Innate Immune Responses

Paramyxovirus Activation and Inhibition of Innate Immune Responses

Autophagy Benefits the Replication of Newcastle Disease Virus in Chicken Cells and Tissues

Viruses and the autophagy pathway

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