Gp37 Regulates the Pathogenesis of Avian Leukosis Virus Subgroup J via Its C Terminus
Tuofan Li, Xiaohui Yao, Chunping Li, Jun Zhang, Quan Xie, Weikang Wang, Hao Lü, Hui Fu, Luyuan Li, Jing Xie, Hongxia Shao, Wei Gao, Aijian Qin, Jianqiang Ye
Abstract
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.