Abstract
Naïve CD4(4) T cells are resistant to both HIV R5 env and vesicular stomatitis virus G protein (VSV-G)-mediated fusion. However, viral particles carrying both HIV R5 env and VSV-G infect naïve cells by an unexplained mechanism. We show that VSV-G-pseudotyped virus cannot fuse to unstimulated cells because the viral particles cannot be endocytosed. However, virions carrying both HIV R5 env and VSV-G can fuse because CD4 binding allows viral uptake. Our findings reveal a unique mechanism by which R5 HIV env and VSV-G cooperate to allow entry to naïve CD4(+) T cells, providing a tool to target naïve CD4(+) T cells with R5 HIV to study HIV coreceptor signaling and latency.
Publication types
-
Research Support, N.I.H., Extramural
MeSH terms
-
CD4-Positive T-Lymphocytes / virology*
-
HIV-1 / genetics
-
HIV-1 / metabolism
-
Humans
-
Membrane Fusion*
-
Membrane Glycoproteins / genetics
-
Membrane Glycoproteins / metabolism*
-
Receptors, CCR5 / metabolism
-
Vesicular stomatitis Indiana virus / genetics
-
Vesicular stomatitis Indiana virus / metabolism
-
Vesicular stomatitis Indiana virus / pathogenicity
-
Viral Envelope Proteins / genetics
-
Viral Envelope Proteins / metabolism*
-
Virion / genetics
-
Virion / metabolism*
-
Virus Internalization*
-
env Gene Products, Human Immunodeficiency Virus / genetics
-
env Gene Products, Human Immunodeficiency Virus / metabolism*
Substances
-
G protein, vesicular stomatitis virus
-
Membrane Glycoproteins
-
Receptors, CCR5
-
Viral Envelope Proteins
-
env Gene Products, Human Immunodeficiency Virus