Figure 6: Resistant HIV-1 viruses can enter host cells in the presence of the CCR5 antagonist. The successful viral fusion requires the interaction of the V3 loop in gp120 with the ECL2 and NT of CCR5. CCR5 antagonists bind to the pocket formed by TM helices and induce allosteric conformational changes in the ECL2, thereby disrupting the interaction of gp120 with CCR5. The CCR5 antagonists-resistant viruses containing multiple amino acid substitutions in the V3 loop can recognize antagonist-bound forms of CCR5 by enhanced interaction with the NT..
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