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Synergistic pathogenesis of chicken infectious anemia virus and J subgroup of avian leukosis virus.

ABSTRACT: As important immunosuppressive viruses, chicken infectious anemia virus (CIAV) and subgroup J avian leukosis virus (ALV-J) have caused huge economic losses to the poultry industry globally. Recently, the co-infection of CIAV and ALV-J frequently occurred in the domestic chicken flocks in China. However, the synergistic pathogenesis of CIAV and ALV-J has not been fully investigated. Here, a co-infection study was performed to further understand the potential synergistic pathogenesis of CIAV and ALV-J. In vitro study showed that CIAV could promote the replication of ALV-J in HD11 cells, but ALV-J could not increase the replication of CIAV. Chicken infection study showed both CIAV and ALV-J with synergistic effects caused significant body weight loss to the infected chickens. Although ALV-J had no effect on CIAV viral shedding and tissue load, CIAV did significantly increase ALV-J viremia, viral shedding and tissue load in the co-infection group. Moreover, both CIAV and ALV-J could significantly inhibit the humoral immunity to H9N2 influenza virus and serotype 4 fowl adenovirus (FAdV-4). All these data demonstrate the synergistic pathogenesis for the co-infection of CIAV and ALV-J, and highlight the positive effect of CIAV on the pathogenesis of ALV-J.

SUBMITTER: Zhang J

PROVIDER: S-EPMC8503663 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature

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Synergistic pathogenesis of chicken infectious anemia virus and J subgroup of avian leukosis virus.

Zhang Jun J Ma Li L Li Tuofan T Li Luyuan L Kan Qiuqi Q Yao Xiaohui X Xie Quan Q Wan Zhimin Z Shao Hongxia H Qin Aijian A Ye Jianqiang J

Poultry science 20210904 11

As important immunosuppressive viruses, chicken infectious anemia virus (CIAV) and subgroup J avian leukosis virus (ALV-J) have caused huge economic losses to the poultry industry globally. Recently, the co-infection of CIAV and ALV-J frequently occurred in the domestic chicken flocks in China. However, the synergistic pathogenesis of CIAV and ALV-J has not been fully investigated. Here, a co-infection study was performed to further understand the potential synergistic pathogenesis of CIAV and A ...[more]

PMID: 34624772

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Project description:Different from other subgroups of avian leukosis viruses (ALVs), ALV-J is highly pathogenic. It is the main culprit causing myeloid leukemia and hemangioma in chickens. The distinctiveness of the env gene of ALV-J, with low homology to those of other ALVs, is linked to its unique pathogenesis, but the underlying mechanism remains unclear. Previous studies show that env of ALV-J can be grouped into three species based on the tyrosine motifs in the cytoplasmic domain (CTD) of Gp37, i.e., the inhibitory, bifunctional, and active groups. To explore whether the C terminus or the tyrosine motifs in the CTD of Gp37 affect the pathogenicity of ALV-J, a set of ALV-J infectious clones containing different C termini of Gp37 or the mutants at the tyrosine sites were tested in vitro and in vivo Viral growth kinetics indicated not only that ALV-J with active env is the fastest in replication and ALV-J with inhibitory env is the lowest but also that the tyrosine sites essentially affected the replication of ALV-J. Moreover, in vivo studies demonstrated that chickens infected by ALV-J with active or bifunctional env showed higher viremia, cloacal viral shedding, and viral tissue load than those infected by ALV-J with inhibitory env Notably, the chickens infected by ALV-J with active or bifunctional env showed significant loss of body weight compared with the control chickens. Taken together, these findings reveal that the C terminus of Gp37 plays a vital role in ALV-J pathogenesis, and change from inhibitory env to bifunctional or active env increases the pathogenesis of ALV-J.IMPORTANCE ALV-J can cause severe immunosuppression and myeloid leukemia in infected chickens. However, no vaccine or antiviral drug is available against ALV-J, and the mechanism for ALV-J pathogenesis needs to be elucidated. It is generally believed that gp85 and LTR of ALV contribute to its pathogenesis. Here, we found that the C terminus and the tyrosine motifs (YxxM, ITIM, and ITAM-like) in the CTD of Gp37 of ALV-J could affect the pathogenicity of ALV-J in vitro and in vivo The pathogenicity of ALV-J with Gp37 containing ITIM only was significantly less than ALV-J with Gp37 containing both YxxM and ITIM and ALV-J with Gp37 containing both YxxM and ITAM-like. This study highlights the vital role of the C terminus of Gp37 in the pathogenesis of ALV-J and thus provides a new perspective to elucidate the interaction between ALV-J and its host and a molecular basis to develop efficient strategies against ALV-J.

Dataset Information

Synergistic pathogenesis of chicken infectious anemia virus and J subgroup of avian leukosis virus.

Publications

Synergistic pathogenesis of chicken infectious anemia virus and J subgroup of avian leukosis virus.

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