Abstract

In 2007, the US Food and Drug Administration (FDA) approved maraviroc for the treatment of human immunodeficiency virus type 1 (HIV-1) infection, making it the first (and to date only) CCR5 antagonist available for clinical use. Approval stipulated that maraviroc be used only in treatment-experienced patients who have viremia with a virus using the CCR5 receptor (R5 virus)—the latter being a critical limitation because maraviroc has no antiviral activity against non– CCR5-using viruses. Because a substantial proportion of treatment-experienced patients harbor these strains—roughly 50% in surveys using the original tropism assay [1]—maraviroc use thus far has been necessarily limited. Unlike in treatment-experienced patients, R5 viruses are the dominant type in transmission and predominate early during HIV disease, with an estimated 80% of untreated patients having R5 strains [2]. It is therefore plausible that maraviroc would have its greatest role earlier during HIV disease, especially among

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