Article
Adaptive mutations in a human immunodeficiency virus type 1 envelope protein with a truncated V3 loop restore function by improving interactions with CD4.
Journal of virology - 1 Nov 2009
Agrawal-Gamse Caroline, Lee Fang-Hua, Haggarty Beth, Jordan Andrea P O, Yi Yanjie, Lee Benhur, Collman Ronald G, Hoxie James A, Doms Robert W, Laakso Meg M
Abstract excerpt
We previously reported that a human immunodeficiency virus type 1 (HIV-1) clade B envelope protein with a severely truncated V3 loop regained function after passage in tissue culture. The adapted virus, termed TA1, retained the V3 truncation, was exquisitely sensitive to neutralization by the CD4 binding site monoclonal antibody b12 and by HIV-positive human sera, used CCR5 to enter cells, and was completely...
Topics
- Adaptation, Biological
- Animals
- Anti-HIV Agents
- Antibodies, Monoclonal
- CCR5 Receptor Antagonists
- CD4 Antigens
- Cell Line
- Cyclohexanes
- HIV Envelope Protein gp120
- HIV-1
- Humans
- Maraviroc
- Mutation