Journal article icon

Journal article

Epitopes of the CD4 antigen and HIV infection.

Abstract:
The CD4 (or T4) surface antigen of human T lymphocytes is an important part of the receptor for the human immunodeficiency virus (HIV). After binding to the receptor, the HIV may enter the T cell and induce the formation of syncytia. In an attempt to identify the receptor site more closely, monoclonal antibodies (Mab's) to CD4 were tested for their ability to block HIV infection in a syncytium formation assay, and the CD4 epitopes so identified were mapped by antibody cross-blocking. The antibodies that showed strong inhibition of HIV fell into two main families while a third group of Mab's blocked syncytia formation weakly or not at all. Several different isolates of HIV as well as the laboratory strain CBL1 grown in CEM cells were used to induce the syncytia. The data indicate that only some epitopes of CD4 are important for virus binding and imply that the virus-binding site for CD4 is conserved in different isolates of HIV with substantially divergent env gene sequences. Preliminary studies of patients suggest that polymorphism of these epitopes does not play a role in determining susceptibility to infection.
Publication status:
Published

Actions

Access Document

Publisher copy:
10.1126/science.2430333

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Pathology Dunn School
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
NDM Experimental Medicine
Role:
Author


Journal:
Science (New York, N.Y.) More from this journal
Volume:
234
Issue:
4780
Pages:
1120-1123
Publication date:
1986-11-01
DOI:
EISSN:
1095-9203
ISSN:
0036-8075


Language:
English
Keywords:
Pubs id:
pubs:25843
UUID:
uuid:2ed0d929-5862-4b68-864a-a03cb744cc3d
Local pid:
pubs:25843
Source identifiers:
25843
Deposit date:
2012-12-19
ARK identifier:

Terms of use


Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP