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The CCR5 coreceptor may be a therapeutic target to block HIV infection. HIV-1–infected patients who had received previous antiretroviral treatment were enrolled in one of two phase 3, placebo-controlled, double-blind international studies of treatment with maraviroc (a CCR5 antagonist). Maraviroc significantly lowered the HIV-1 viral load and increased the CD4 cell count at 48 weeks. The CCR5 coreceptor may be a therapeutic target to block HIV infection. In two studies, maraviroc (a CCR5 antagonist) significantly lowered the HIV-1 viral load and increased the CD4 cell count at 48 weeks. For the past decade, treatment of human immunodeficiency virus type 1 (HIV-1) has consisted of a multiple-drug regimen targeting one or more of three HIV-1 proteins: reverse transcriptase, protease, and the glycoprotein envelope subunit gp41. 1 Although these antiretroviral combinations are successful in suppressing viral replication and delaying disease progression, drug resistance and toxic effects may occur. 2 – 4 There is therefore a need for better-tolerated, convenient antiretroviral agents with reduced toxicity and activity against multidrug-resistant viruses. Agents with novel mechanisms of action provide options for patients with drug-resistant virus. 4 CC chemokine receptor 5 (CCR5) is an attractive therapeutic target, since people . . .

In key subgroups of the HIV-infected patients in the MOTIVATE 1 and MOTIVATE 2 studies, a consistent treatment benefit of maraviroc over placebo was seen at 48 weeks. These subgroups include patients with a low baseline CD4 cell count and a high HIV viral load at screening and those receiving no active background antiretroviral agents. In patients in whom maraviroc failed, the CXCR4-using virus was often present at failure. In key subgroups of HIV-infected patients, a consistent treatment benefit of maraviroc over placebo was seen at 48 weeks. These subgroups include patients with a low baseline CD4 cell count and a high HIV viral load at screening and those receiving no active background antiretroviral agents. The CC chemokine receptor 5 (CCR5) antagonist maraviroc has shown potent antiviral activity in vitro and in vivo against the R5 human immunodeficiency virus type 1 (HIV-1). 1 , 2 As reported by Gulick et al. 3 elsewhere in this issue, treatment with maraviroc plus optimized background therapy was associated with significantly greater virologic and immunologic efficacy and had a similar safety profile, as compared with placebo plus optimized background therapy, in the Maraviroc versus Optimized Therapy in Viremic Antiretroviral Treatment-Experienced Patients (MOTIVATE) 1 and MOTIVATE 2 studies at 48 weeks. Subgroup analyses of data from recent trials evaluating new drugs in patients . . .