Adaptation of a CCR5-using, primary human immunodeficiency virus type 1 isolate for CD4-independent replication

被引:159
作者
Kolchinsky, P
Mirzabekov, T
Farzan, M
Kiprilov, E
Cayabyab, M
Mooney, LJ
Choe, H
Sodroski, J
机构
[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Dept Pathol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Childrens Hosp, Perlmutter Lab, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA
[5] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
关键词
D O I
10.1128/JVI.73.10.8120-8126.1999
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The gp120 envelope glycoprotein of the human immunodeficiency virus type 1 (HIV-I) promotes virus entry by sequentially binding CD4 and chemokine receptors on the target cell. Primary, clinical HIV-1 isolates require interaction with CD4 to allow gp120 to bind the CCR5 chemokine receptor efficiently. We adapted a primary HIV-1 isolate, ADA, to replicate in CD4-negative canine cells expressing human CCR5. The gp120 changes responsible for the adaptation were limited to alteration of glycosylation addition sites in the V2 loop-V1-V2 stem. The gp120 glycoproteins of the adapted viruses bound CCR5 directly, without prior interaction with CD4. Thus, a major function of CD4 binding in the entry of primary HN-I isolates can be bypassed by changes in I-he gp120 V1-V2 elements, which allow the envelope glycoproteins to assume a conformation competent for CCR5 binding.
引用
收藏
页码:8120 / 8126
页数:7
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