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Role of the HTLV-III/LAV envelope in syncytium formation and cytopathicity

Acquired immune deficiency syndrome (AIDS) is characterized by marked depletion of the T4 + helper subset of T cells 1–3 . The aetiological agent of the disease, the human T-lymphotropic virus type III (HTLV-III)/lymphadenopathy-associated virus (LAV), specifically kills T4 + cells in vitro 4–10 . P...

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Bibliographic Details
Published in:Nature (London) 1986-07, Vol.322 (6078), p.470-474
Main Authors: Sodroski, Joseph, Goh, Wei Chun, Rosen, Craig, Campbell, Kathryn, Haseltine, William A.
Format: Article
Language:English
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Summary:Acquired immune deficiency syndrome (AIDS) is characterized by marked depletion of the T4 + helper subset of T cells 1–3 . The aetiological agent of the disease, the human T-lymphotropic virus type III (HTLV-III)/lymphadenopathy-associated virus (LAV), specifically kills T4 + cells in vitro 4–10 . Part of this specificity for the T4 + population residues in the relative efficiency with which HTLV-III infects these cells, as a result of a specific interaction between the T4 molecule and the virus envelope glycoprotein 11–13 . In addition, the cytotoxic consequences of HTLV-III replication are dependent on cell type, as certain lymphoid and myeloid cells can be productively infected without notable cytopathic effect 14,15 . Here we investigate the basis for the specific cytotoxicity of the virus, and report that high-level expression of the HTLV-III envelope gene induces syncytia and concomitant cell death in T4 + cell lines but not in a B-lymphocyte line. Syncytium formation depends on the interaction of envelope-expressing cells with neighbouring cells bearing surface T4 molecules. These results explain, at least in part, the specific cytopathic effect of HTLV-III infections.
ISSN:0028-0836
1476-4687
DOI:10.1038/322470a0