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Maraviroc, a CCR5 Coreceptor Antagonist That Blocks Entry of Human Immunodeficiency Virus Type 1
Author(s) -
Hunt Joshua S.,
Romanelli Frank
Publication year - 2009
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1592/phco.29.3.295
Subject(s) - maraviroc , ccr5 receptor antagonist , virology , tropism , cxcr4 , viral entry , viral load , entry inhibitor , tissue tropism , chemokine receptor , virus , biology , human immunodeficiency virus (hiv) , chemokine , viral replication , immunology , inflammation
Inhibition of the human immunodeficiency virus type 1 (HIV‐1) coreceptor is an encouraging new approach to pharmacotherapy against HIV. The HIV‐1 strain makes use of either the CCR5 or the CXCR4 coreceptor to gain access into host CD4 + cells. Maraviroc, the first HIV‐1 CCR5 coreceptor antagonist, blocks entry of HIV‐1. This recently approved drug has demonstrated clinically significant decreases in plasma concentrations of HIV‐1 RNA and increases in CD4 + cell counts; however, it is indicated only for use as salvage therapy. Drug resistance is a concern, as is selective pressure on viral coreceptor use, because viral coreceptor targets may switch as disease progresses. In addition, before maraviroc therapy can be started, costly assays are required to determine the host's viral coreceptor tropism. Emerging therapies targeting CXCR4, the other HIV coreceptor, have shown promise in decreasing plasma concentrations of HIV‐1 RNA. Long‐term studies with both targets are required to explore the critical issues of efficacy and immunologic safety, as the function of these coreceptors is linked to host chemokine pathways.