Membrane-associated GRP78 helps subgroup J avian leucosis virus enter cells.

Lin Wang,Kun Qian,Hongxia Shao,Jianqiang Ye,Aijian Qin,Mei Mei

doi:10.1186/s13567-016-0373-6

Lin Wang, Kun Qian + Show 4 more

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https://doi.org/10.1186/s13567-016-0373-6

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Abstract

We previously identified chicken Annexin A2 (chANXA2) as a novel receptor for retrovirus avian leucosis virus subgroup J (ALV-J), using a DF1 cell line expressing the viral envelope (env) protein. To further probe whether other proteins participate in virus infection, we investigated several host proteins from co-immunoprecipitation with the DF1 cell line expressing viral env. Mass spectrometry analysis indicates that the chicken glucose-regulation protein 78 (chGRP78) of the DF1 membrane interacted with the ALV-J env protein. The results revealed that antibodies or siRNA to chGRP78 significantly inhibited ALV-J infection and replication, and over-expression of chGRP78 enabled the entry of ALV-J into non-susceptible cells. Taken together, these results are the first to report that chGRP78 functions to help ALV-J enter cells.

Highlights

Virus infection relies on the interaction between surface proteins and host receptors
Previous studies with Japanese encephalitis virus (JEV) have reported the possible involvements of a 57-kDa protein derived from BHK-21 cells, the GAG protein from CHO cells and a 74-kDa molecule from Vero cells as possible receptors [31]
In addition to the identified host receptors chicken Annexin A2 (chANXA2) and chNHE1, we found that chicken glucose-regulation protein 78 (chGRP78) is another important protein for AVL-J infection of DF1 cells. chGRP78 is a member of the HSP70 family that is located in both the membrane and plasma of various types of cells [33]

Summary

Introduction

Virus infection relies on the interaction between surface proteins and host receptors. In addition to virus receptors, other proteins may interact with the virus and mediate infection. HIV, a member of the retrovirus family, uses its glycoprotein gp120 to bind with CD4, CCR5 and CXCR4 as receptors to infect host cells [1–3]. Certain other proteins, such as CCR1, CCR8, CXCR6 (BONZO), GPR15 (BOB), GPR1, APJ, CX3CR1 (V28), CXCR5, and RDC1, interact with gp120 and mediate virus entry into host cells [4–10]. According to the antigenicity of its envelope glycoprotein, ALV can be divided into six subgroups (A, B, C, D, E, and J). The high variability of ALV-J’s envelope (env) protein distinguishes it from other subgroups, and results in alternations of the virus’s pathogenicity, tumourigenicity and host range [11].

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