RT Journal Article
SR Electronic
T1 Rapid complementation assays measuring replicative potential of human immunodeficiency virus type 1 envelope glycoprotein mutants.
JF Journal of Virology
JO J. Virol.
FD American Society for Microbiology
SP 2416
OP 2420
VO 64
IS 5
A1 Helseth, E
A1 Kowalski, M
A1 Gabuzda, D
A1 Olshevsky, U
A1 Haseltine, W
A1 Sodroski, J
YR 1990
UL http://jvi.asm.org/content/64/5/2416.abstract
AB Rapid assays which measure the ability of mutant human immunodeficiency virus type 1 envelope glycoproteins to mediate cell-free and/or cell-to-cell transmission of virus are described. By using these assays, envelope glycoprotein mutants with varying degrees of syncytium-forming ability were tested for ability to complement viral replication in trans. As expected, mutants that dramatically affect association of the gp120-gp41 envelope subunits, CD4 binding, or membrane fusion were unable to form syncytia or to support cell-free or cell-to-cell transmission. Surprisingly, some membrane fusion-defective mutants significantly attenuated in syncytium-forming ability were able to complement viral replication. Conversely, mutations in the carboxyl terminus of gp41 transmembrane glycoprotein, although not affecting syncytium-forming ability, significantly attenuated both forms of virus transmission. These results indicate that syncytium formation is not sufficient for cell-to-cell transmission of human immunodeficiency virus type 1. Furthermore, virus transmission appears to be less sensitive to inhibition of membrane fusion than is syncytium formation.