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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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Published in: | Nature (London) 1986-07, Vol.322 (6078), p.470-474 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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. |
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ISSN: | 0028-0836 1476-4687 |
DOI: | 10.1038/322470a0 |