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

Xueping Wang,Shuying Chen,Jingyu Wang,Xuefeng Qi,Bo Yang

doi:10.3389/fmicb.2018.01091

Xueping Wang, Shuying Chen + Show 3 more

Open Access

https://doi.org/10.3389/fmicb.2018.01091

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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.

Highlights

Egg drop syndrome (EDS) is one of the most economically important diseases in the poultry industry, and it has wide host range, such as turkey breeder flocks, healthy laying birds, quail, and geese (Brugh et al, 1984; Bidin et al, 2007; Hafez, 2011)
To investigate whether autophagy is induced in duck embryo fibroblasts (DEFs) by Egg drop syndrome virus (EDSV) infection, the cells were mock infected or infected with the EDSV-127 strain or DEFs were treated with rapamycin for 36 hpi, and they were observed through Transmission Electron Microscopy (TEM)
Double-membrane vesicles were rarely observed in mock-infected cells, whereas a large number of single-membrane vesicles and double-or single-membrane vesicles were observed in the cytoplasm of EDSV-infected DEFs (Figure 1b). These double-membrane structures were similar to the autophagosomes in DEFs induced by rapamycin, a wellknown autophagy inducer, suggesting that the autophagosomes were induced in DEFs by EDSV infection (Figure 1c)

Summary

Introduction

Egg drop syndrome (EDS) is one of the most economically important diseases in the poultry industry, and it has wide host range, such as turkey breeder flocks, healthy laying birds, quail, and geese (Brugh et al, 1984; Bidin et al, 2007; Hafez, 2011). The causative agent, egg drop syndrome virus (EDSV) belong to the genus Atadenovirus within the family Adenoviridae, which are non-enveloped viruses with an approximately 30–35 kb linear double-stranded DNA genome (Fu et al, 2013; Larson et al, 2015). Accumulating evidence has demonstrated that adenoviral proteins E1A and E1B play an essential role in establishing a productive virus infection by regulating cell

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