Avian leukosis virus (ALV) is an enveloped and oncogenic retrovirus. Avian leukosis caused by the members of ALV subgroups A, B and J has become one of the major problems challenging the poultry industry in China. However, the cellular factors such as signal transduction pathways involved in ALV infection are not well defined. In this study, our data demonstrated that ALV-J strain NX0101 infection in primary chicken embryo fibroblasts or DF-1 cells was correlated with the activity and phosphorylation of Akt. Akt activation was initiated at a very early stage of infection independently of NX0101 replication. The specific phosphatidylinositol 3-kinase (PI3K) inhibitors LY294002 or wortmannin could suppress Akt phosphorylation, indicating that NX0101-induced Akt phosphorylation is PI3K-dependent. ALV-A strain GD08 or ALV-B strain CD08 infection also demonstrated a similar profile of PI3K/Akt activation. Treatment of DF-1 cells with the drug 5-(N, N-hexamethylene) amiloride that inhibits the activity of chicken Na + /H + exchanger type 1 significantly reduced Akt activation induced by NX0101, but not by GD08 and CD08. Akt activation triggered by GD08 or CD08 was abolished by clathrin-mediated endocytosis inhibitor chlorpromazine. Receptor-mediated endocytosis inhibitor dansylcadaverine had a negligible effect on all ALV-induced Akt phosphorylation. Moreover, viral replication of ALV was suppressed by LY294002 in a dose-dependent manner, which was due to the inhibition of virus infection by LY294002. These data suggest that the activation of the PI3K/Akt signalling pathway by exogenous ALV infection plays an important role in viral entry, yet the precise mechanism remains under further investigation.
INTRODUCTIONAvian leukosis virus (ALV) is an oncogenic retrovirus that primarily infects chickens. Based on the identity of the surface region (SU) of its envelope glycoprotein, ALV is divided into different subgroups, designated A through to F and J (Coffin et al., 1997). ALV-E is endogenous virus, while all other subgroups are exogenous. Recently, the disease caused by ALV-J, ALV-A or ALV-B has become one of the major problems facing the poultry industry in China, which has been identified in the commercial meat and eggtype chickens, and also in the Chinese local breeds (Du et al., 2000;Cui et al., 2003;Cheng et al., 2010;Zhang et al., 2010). ALV can induce a rather wide variety of tumours and mortality that cause significant economic losses. The various pathotypes of tumours are mainly lymphomas, myelocytomas and haemangiomas, as well as fibrosarcomas, histiocytic sarcomas, intestinal adenocarcinoma, leiomyosarcoma and so on (Xu et al., 2004;Sun & Cui, 2007;Cheng et al., 2010). The major mechanism of ALV pathogenesis is that of typical oncogene activation by proviral insertion gene deregulation, resulting in tumour formation after chronic infection. Acute-transforming ALV variants have been discovered that have acquired an activated oncogene in their genome and these cause tumours in a short period of time (Graf & Beu...
