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. Author manuscript; available in PMC: 2011 Jun 20.
Published in final edited form as: Virology. 2010 Apr 9;402(1):135–148. doi: 10.1016/j.virol.2010.03.009

Figure 3. CCR5 use on CD4+ lymphocytes correlates with resistance to inhibition by ECL2-directed CCR5 mAbs and small molecule antagonists.

Figure 3

U87/CD4/CCR5 cells were treated for 1 hour with or without 10 μg/ml of CCR5-specific mAbs (A) or increasing concentrations of CCR5 antagonists M657 or Maraviroc (B), then infected with HIV-1 luciferase pseudotype viruses in the continued presence of mAb or blocker. Three days later, infection was determined by luciferase activity in cell lysates and normalized to luciferase activity in untreated cells. Each symbol represents an individual R5X4 virus, and results are presented as the proportion of total lymphocyte entry mediated by CCR5 (from Figure 2b) on the X-axis versus the percentage of U87/CD4/CCR5 infection resistant to inhibition by CCR5 mAbs (A) or the EC50 values for the small molecule CCR5 antagonists (B) on the Y axis. Data are means for three experiments each carried out in duplicate.