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. Author manuscript; available in PMC: 2015 Apr 30.
Published in final edited form as: Virology. 2005 Jun 5;336(2):184–197. doi: 10.1016/j.virol.2005.03.032

Fig. 3.

Fig. 3

The R3A Env shows enhanced binding efficiency for CXCR4, but similar sensitivity to Tak-779 and T20. (A) R3A and R3B Envs show equal sensitivity to a CCR5 antagonist. Infection of U373-MAGI-CCR5E cells was performed in the presence of the CCR5 antagonist TAK-779. Infection was quantitated by counting blue colonies and was normalized to the number of colonies observed with no TAK-779. Shown is a representative of two independent experiments with error bars derived from quadruplicate samples. (B) R3A shows enhanced affinity for CXCR4 relative to R3B. Infection of Sup-T1 cells was performed with NL4-luc-pseudotyped virus in the presence of AMD-3100. Infection was quantitated by luciferase assay after 48 h and was normalized to levels obtained with no AMD-3100. Shown is a representative of seven independent experiments with error bars derived from triplicate samples (*P <0.05 for R3A vs. either NL4-3 or R3B). (C) Sup-T1 cells transduced with vector or X4h shRNA, which reduces CXCR4 surface levels by ~97%, were infected with NL4-luc pseudotyped with the indicated Env. Infection was quantitated by luciferase assay after 48 h and was normalized to levels obtained on vector-transduced cells. Shown is a representative of three independent experiments with error bars derived from triplicate samples (*P <0.05 in comparison to R3A Env or to infection of parental cells). (D) R3A and R3B Envs show equal sensitivity to the fusion inhibitor T20. TZM-bl cells were infected with virus in the presence of the indicated dose of T20. Infection was quantitated and normalized as in A. Shown is a representative of 2 experiments with error bars derived from duplicate samples (*P <0.05 for NL4-R3A vs. either NL4-3 or NL4-R3B).