The envelope glycoprotein of human endogenous retrovirus HERV-W induces cellular resistance to spleen necrosis virus.
Human endogenous retrovirus type W (HERV-W) envelope glycoprotein (Env) has recently been reported to induce fusion in cells expressing the RD-114 and type D retrovirus receptor (RDR) and to serve as a functional retroviral envelope protein. In this report, another biological function for HERV-W was demonstrated by testing its ability to protect cells against retroviral infection. Spleen necrosis virus (SNV), a gammaretrovirus was chosen for testing resistance because it uses RDR to enter cells. An HERV-W Env expression plasmid was transfected into canine osteosarcoma cells (D-17), which are permissive for SNV infection. Cell fusion assays were performed to demonstrate biological function of HERV-W Env in D-17 cells. The presence of HERV-W env sequences was confirmed in stably transfected cell clones by using polymerase chain reaction. Viral infectivity assays were performed with SNV and amphotropic Murine leukemia virus (MLV-A) pseudotyped vector viruses to measure titers in D-17 cells expressing HERV-W Env and in negative control cells. The HERV-W Env caused fusion of D-17 cells in culture and greatly reduced infection by SNV vector virus. A 1000- to 10,000-fold decrease in SNV infectivity was observed for D-17 cells expressing HERV-W Env as compared to D-17 cells that were not expressing HERV-W Env. In contrast, infection by MLV-A pseudotyped vector virus was not significantly reduced. Thus, HERV-W Env confers host cell resistance to infection by SNV. This is the first report of a human endogenous retrovirus gene product blocking infection by any exogenous retrovirus.
Ponferrada
V G
VG
Department of Biochemistry and Molecular Biology, Wright State University School of Medicine, Dayton, Ohio, U.S.A.
Mauck
B S
BS
Wooley
D P
DP
D000818:Animals; D002460:Cell Line; D004285:Dogs; D020077:Endogenous Retroviruses / Q000502:physiology*; D017988:Gammaretrovirus / Q000502:physiology*; D014162:Transfection; D014759:Viral Envelope Proteins / Q000235:genetics / Q000502:physiology*; D014762:Viral Interference; D014779:Virus Replication
D014759:Viral Envelope Proteins