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Abstract
BackgroundSubgroup J avian leukosis virus (ALV-J) infection can induce tumor-related diseases in chickens. Previous studies by our laboratory demonstrated that ALV-J infection of DF-1 cells resulted in altered activity and phosphorylation of AKT. However, little is known about the subsequent activation of host DF-1 cells.ResultsIn the current study, autophagy inhibition was observed for ALV-J infected DF-1 cells. Our data showed that the autophagosome protein, microtubule-associated protein 1 light chain 3-II (LC3-II), was reduced considerably in DF-1 cells infected with active ALV-J, while no change was observed for cells infected with inactivated ALV-J. Autophagy inhibition was also confirmed by fluorescence microscopy and transmission electron microscopy. Interestingly, when autophagy was promoted by rapamycin, the titers of ALV-J replication were decreased, and the replication level of ALV-J was significantly enhanced when atg5 (autophagy-related gene 5) was knocked out.ConclusionsThese results suggested that ALV-J infection could down-regulate autophagy in DF-1 cells during viral replication. This study is the first to report on the relationship between ALV-J infection and autophagy in DF-1 cells.
Highlights
Subgroup J avian leukosis virus (ALV-J) infection can induce tumor-related diseases in chickens
Autophagy is down-regulated in Avian leukosis viruses (ALV)-J infected DF-1 cells ALV-J inhibition of autophagy was determined by examining autophagosome formation in DF-1 cells
Further confirmation of autophagy inhibition by ALV-J infection was established from autophagy levels, Figure 1 ALV-J infection inhibits autophagy in DF-1 cells. (A) Fluorescence microscopy revealed limited numbers of GFP-LC3 puncta in ALV-J-infected cells
Summary
Subgroup J avian leukosis virus (ALV-J) infection can induce tumor-related diseases in chickens. Previous studies by our laboratory demonstrated that ALV-J infection of DF-1 cells resulted in altered activity and phosphorylation of AKT. Avian leukosis viruses (ALV) are avian retroviruses responsible for inducing tumor-related diseases in poultry. Chicken ALVs are classified into six subgroups according to antigenic differences in the surface envelope glycoprotein; endogenous viruses belong to subgroup ALV-E while all exogenous viruses belong to subgroups A–D and J [1]. Since its first isolation from meat-type chickens in the early 1990s, ALV-J has induced a high incidence of myeloid tumors in some chicken lines and their hybridizing passages [2]. ALV-J tumor-related diseases are not restricted to commercial meat-type poultry, with reports of egg-type poultry and some local Chinese
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