Skip to main content

Advertisement

Figure 5 | Retrovirology

Figure 5

From: A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations

Figure 5

17-Res and 24-Res Envs exhibit a similar increased dependence on the CCR5 N-terminus. Luciferase reporter viruses pseudotyped with Envs from subject 17 (A) or 24 (B) were used to infect NP2-CD4 cells expressing equivalent levels of WT CCR5 or CCR5 with mutations in the N-terminus region. Infections were performed in the absence or presence of 10 µM MVC. Viral entry in cells expressing CCR5 mutants was normalized to entry obtained in cells expressing an equivalent amount of WT CCR5. Compared to background levels of entry by virus pseudotyped with a non-functional Env [66] (~1,300 RLU), the entry levels of 17-Res and 24-Res in cells expressing WT CCR5 the presence of MVC were approximately 60- and 380-fold higher, respectively (~80,000 and 500,000 RLU, respectively). The data shown are the means and SEM from a compilation of 3 independent experiments. * p<0.05 for increases in the dependence on a particular residue for the resistant Envs compared to the respective parental sensitive Env. **p<0.05 for increases in the dependence on a particular residue compared to respective resistant Envs in the absence of drug (unpaired t-test).

Back to article page