Abstract
Subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection. The innate immune system is the first line of defense in preventing bacterial and viral infections, and dendritic cells (DCs) play important roles in innate immunity. Because bone marrow is an organ that is susceptible to ALV-J, the virus may influence the generation of bone marrow-derived DCs. In this study, DCs cultured in vitro were used to investigate the effects of ALV infection. The results revealed that ALV-J could infect these cells during the early stages of differentiation, and infection of DCs with ALV-J resulted in apoptosis. miRNA sequencing data of uninfected and infected DCs revealed 122 differentially expressed miRNAs, with 115 demonstrating upregulation after ALV-J infection and the other 7 showing significant downregulation. The miRNAs that exhibited the highest levels of upregulation may suppress nutrient processing and metabolic function. These results indicated that ALV-J infection of chicken DCs could induce apoptosis via aberrant microRNA expression. These results provide a solid foundation for the further study of epigenetic influences on ALV-J-induced immunosuppression.
Highlights
Avian leukosis viruses (ALVs) are a group of avian retroviruses that induce tumors in chickens[1]
We found that ALV-J was able to infect chicken Dendritic cells (DCs)
After the cells were stimulated with lipopolysaccharide (LPS) for 24 h on the tenth day of culture, most cells exhibited a dendritic structure, which indicates that the DCs are in the final stages of maturation (Fig. 1c)
Summary
Avian leukosis viruses (ALVs) are a group of avian retroviruses that induce tumors in chickens[1]. DCs can regulate the immune response, and these cells express many different pathogen recognition receptors, such as Toll-like receptors, which are helpful for antigen presentation[15]. These functions are dependent on DC maturation, which is regulated largely by microRNAs (miRNAs)[16,17,18,19]. We found that ALV-J was able to infect chicken DCs. Infection altered normal DC functions, including their rate of maturation, while inducing apoptosis and causing aberrant miRNA expression. Infection altered normal DC functions, including their rate of maturation, while inducing apoptosis and causing aberrant miRNA expression These changes in DC function may further result in immunosuppression
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