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. 1990 May;64(5):2416–2420. doi: 10.1128/jvi.64.5.2416-2420.1990

Rapid complementation assays measuring replicative potential of human immunodeficiency virus type 1 envelope glycoprotein mutants.

E Helseth 1, M Kowalski 1, D Gabuzda 1, U Olshevsky 1, W Haseltine 1, J Sodroski 1
PMCID: PMC249407  PMID: 2325207

Abstract

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.

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Selected References

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