Abstract

Human immunodeficiency virus (HIV) enters and infects target cells by a process involving interactions between the envelope glycoprotein gp120 and the host cell CD4 receptor, then one or both of two chemokine co-receptors CCR5 and CXCR4. HIV strains that use the CCR5 receptor to gain entry are called R5-tropic viruses. Those that use the CXCR4 receptor are known as X4-tropic viruses and those that can use both receptors are referred to as dual/mixed tropic. Maraviroc is the first clinically approved CCR5 antagonist. It acts by blocking the interaction of R5-tropic HIV strains with the CCR5 receptor. Currently, knowledge of the tropism of an individual’s infecting HIV strain is required before maraviroc can be prescribed. Treated individuals must be exclusively infected with R5-tropic viruses. Previously the domain of phenotypic assays, recent improvements to genotype-based methods to determine HIV co-receptor utility has enabled genotyping of HIV to determine whether maraviroc is an option for patients failing multiple drug classes.

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