Dataset Information

Autophagy Benefits the Replication of Egg Drop Syndrome Virus in Duck Embryo Fibroblasts.

ABSTRACT: Egg drop syndrome virus (EDSV) is an economically important pathogen with a broad host range, and it causes disease that leads to markedly decreased egg production. Although EDSV is known to induce apoptosis in duck embryo fibroblasts (DEFs), the interaction between EDSV and its host needs to be further researched. Here, we provide the first evidence that EDSV infection triggers autophagy in DEFs through increases in autophagosome-like double-membrane vesicles, the conversion of LC3-I to LC3-II, and LC3 colocalization with viral hexon proteins. Conversely, P62/SQSTM1 degradation, LC3-II turnover, and colocalization of LAMP and LC3 confirmed that EDSV infection triggers complete autophagy. Furthermore, we demonstrated that inhibition of autophagy by chloroquine (CQ) and 3-methyladenine (3MA) or RNA interference targeting ATG-7 decreased the yield of EDSV progeny. In contrast, induction of autophagy by rapamycin increased the EDSV progeny yield. In addition, we preliminarily demonstrated that the class I phosphoinositide 3-kinase (PI3K)/Akt/mTOR pathway contributes to autophagic induction following EDSV infection. Altogether, these finding lead us to conclude that EDSV infection induces autophagy, which benefits its own replication in host cells. These findings provide novel insights into EDSV-host interactions.

SUBMITTER: Wang X

PROVIDER: S-EPMC5986908 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Publications

Autophagy Benefits the Replication of Egg Drop Syndrome Virus in Duck Embryo Fibroblasts.

Wang Xueping X Qi Xuefeng X Yang Bo B Chen Shuying S Wang Jingyu J

Frontiers in microbiology 20180529

Egg drop syndrome virus (EDSV) is an economically important pathogen with a broad host range, and it causes disease that leads to markedly decreased egg production. Although EDSV is known to induce apoptosis in duck embryo fibroblasts (DEFs), the interaction between EDSV and its host needs to be further researched. Here, we provide the first evidence that EDSV infection triggers autophagy in DEFs through increases in autophagosome-like double-membrane vesicles, the conversion of LC3-I to LC3-II, ...[more]

PMID: 29896171

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Project description:In China, the duck industry has been severely impacted by the newly emerging duck Tembusu virus (DTMUV). For DTMUV to successfully infect host cells, it employs several strategies that subvert the host's innate immune response. It has been found that several viral proteins encoded by DTMUV have strategically targeted the crucial molecules of the RIG-I-like Receptor (RLR) signaling pathway to antagonize host antiviral responses. However, it is not well known how the host proteins manipulated by DTMUV contribute to innate immune evasion. The present study reports that duck TRIM35 (duTRIM35) antagonizes DTMUV-induced innate immune responses by targeting duck RIG-I (duRIG-I) in duck embryo fibroblasts. A significant increase in duTRIM35 expression occurred during DTMUV infection. DuTRIM35 overexpression suppressed DTMUV-triggered expression of interferon beta (IFN-β) and interferon-stimulated genes (ISGs), promoting viral replication, whereas knockdown of duTRIM35 augments the innate immune response, reducing viral replication. Furthermore, duTRIM35 significantly impaired the IFN-β expression mediated by duRIG-I but not by other RLR signaling molecules. Mechanistically, duTRIM35 interfered with duRIG-I-duTRIM25 interaction and impeded duTRIM25-mediated duRIG-I ubiquitination by interacting with both duRIG-I and duTRIM25. Our findings indicate that duTRIM35 expression induced by DTMUV infection interfered with the duRIG-I-mediated antiviral response, illustrating a novel strategy in which DTMUV can evade the host's innate immunity. IMPORTANCE Duck Tembusu virus (DTMUV), an emerging flavivirus pathogen causing a substantial drop in egg production and severe neurological disorders in duck populations, has led to massive economic losses in the global duck industry. DTMUV has employed various strategies to subvert the host's innate immune response to establish a productive infection in host cells. In this study, we report that duck TRIM35 (duTRIM35) expression was upregulated upon DTMUV infection in vitro and in vivo, and its expression antagonized DTMUV-induced innate immune responses by targeting duck RIG-I (duRIG-I) in duck embryo fibroblasts. Further studies suggest that duTRIM35 interfered with duRIG-I-duTRIM25 interaction and impeded duTRIM25-mediated duRIG-I ubiquitination by interacting with both duRIG-I and duTRIM25. Together, these results revealed that duTRIM35 expression induced by DTMUV infection downregulated duRIG-I-mediated host antiviral response, which elucidated a novel strategy of DTMUV for innate immune evasion.

Dataset Information

Autophagy Benefits the Replication of Egg Drop Syndrome Virus in Duck Embryo Fibroblasts.

Publications

Autophagy Benefits the Replication of Egg Drop Syndrome Virus in Duck Embryo Fibroblasts.

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