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Journal of Virology, March 2001, p. 2741-2752, Vol. 75, No. 6
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.6.2741-2752.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Antibody Binding and Neutralization of Primary and T-Cell Line-Adapted Isolates of Human Immunodeficiency Virus Type 1

Joanne York,1 Kathryn E. Follis,1 Meg Trahey,1 Phillipe N. Nyambi,2 Susan Zolla-Pazner,2,3 and Jack H. Nunberg1,*

Montana Biotechnology Center, The University of Montana, Missoula, Montana 598121; New York University School of Medicine, New York, New York 100162; and Veterans Affairs Medical Center, New York, New York 100103

Received 9 October 2000/Accepted 19 December 2000

The relative resistance of human immunodeficiency virus type 1 (HIV-1) primary isolates (PIs) to neutralization by a wide range of antibodies remains a theoretical and practical barrier to the development of an effective HIV vaccine. One model to account for the differential neutralization sensitivity between Pls and laboratory (or T-cell line-adapted [TCLA]) strains of HIV suggests that the envelope protein (Env) complex is made more accessible to antibody binding as a consequence of adaptation to growth in established cell lines. Here, we revisit this question using genetically related PI and TCLA viruses and molecularly cloned env genes. By using complementary techniques of flow cytometry and virion binding assays, we show that monoclonal antibodies targeting the V3 loop, CD4-binding site, CD4-induced determinant of gp120, or the ectodomain of gp41 bind equally well to PI and TCLA Env complexes, despite large differences in neutralization outcome. The data suggest that the differential neutralization sensitivity of PI and TCLA viruses may derive not from differences in the initial antibody binding event but rather from differences in the subsequent functioning of the PI and TCLA Envs during virus entry. An understanding of these as yet undefined differences may enhance our ability to generate broadly neutralizing HIV vaccine immunogens.

* Corresponding author. Mailing address: Montana Biotechnology Center, The University of Montana, Missoula, MT 59812. Phone: (406) 243-6421. Fax: (406) 243-6425. E-mail: nunberg{at}selway.umt.edu.

Journal of Virology, March 2001, p. 2741-2752, Vol. 75, No. 6
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.6.2741-2752.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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