Maraviroc belongs to the family of chemokine (C-C motif) receptor 5 (CCR5) antagonists that prevent the entry of human immunodeficiency virus (HIV) into host CD4+ T cells by blocking the CCR5 co-receptor R5. Maraviroc is currently the only CC5R co-receptor inhibitor that has been approved for clinical use in HIV-1-infected patients carrying the CCR5 tropism who are antiretroviral-naïve or have experienced therapeutic failure following traditional antiretroviral therapies. This article is a review of the main characteristics of maraviroc and the latest data regarding its clinical application. Maraviroc is effective and well tolerated in pre-treated and antiretroviral-naïve patients with HIV-1 infections carrying the CCR5 tropism. Data from the phase III programme of maraviroc, which includes the MOTIVATE 1 and 2 studies and the MERIT study, indicate that maraviroc significantly (p < 0.001) increases CD4+ cell counts compared with placebo in pre-treated patients and to a similar extent as efavirenz in antiretroviral-naïve patients. Even in cases where viral load is not completely suppressed, maraviroc improves immunological response compared with placebo. In addition, promising research suggests that maraviroc has favourable pharmacokinetic and safety profiles in patients with high cardiovascular risk or those co-infected with tuberculosis or hepatitis and could be considered an option for treatment of HIV-infected patients with these co-morbidities. Resistance to maraviroc is low and mainly related to the presence of chemokine (C-X-C motif) receptor 4 (CXCR4) tropism HIV-1-infections or to mutations in the V3 region of glycoprotein (gp) 120; however, the exact mechanisms by which resistance is acquired and their genotypic and phenotypic pattern have not yet been established. It is recommended that a tropism test should be performed when considering maraviroc as an alternate drug in HIV-1-infected patients. Current tropism assays have increased sensitivity to reliably detect CXCR4 HIV with rapid turn-around and at a low cost. Improved detection together with positive data on the drug's efficacy and safety profiles should help physicians to identify more accurately the appropriate candidates for commencement of treatment with maraviroc. In summary, maraviroc improves immunological response and has shown favourable pharmacokinetic and safety profiles in patients with high cardiovascular risk or in those co-infected with tuberculosis or hepatitis. Long-term studies are needed to confirm whether therapeutic expectations resulting from clinical trials with maraviroc translate into a real benefit for HIV-1-infected patients for whom traditional antiretroviral therapies have failed or are not suitable.
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http://dx.doi.org/10.2165/11590700-000000000-00000 | DOI Listing |
Curr HIV Res
September 2024
Department of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Front Cell Infect Microbiol
July 2024
Guangxi Key Laboratory of Major Infectious Disease Prevention Control and Biosafety Emergency Response, Guangxi Key Laboratory of AIDS Prevention Control and Translation, Guangxi Zhuang Autonomous Region Center for Disease Control and Prevention, Nanning, China.
Cell Rep
July 2024
Département de microbiologie, infectiologie et immunologie, Faculté de médecine, Université de Montréal, Montréal, QC, Canada; Centre de recherche du centre hospitalier de l'Université de Montréal (CR-CHUM), Montréal, QC, Canada. Electronic address:
The intestinal environment facilitates HIV-1 infection via mechanisms involving the gut-homing vitamin A-derived retinoic acid (RA), which transcriptionally reprograms CD4 T cells for increased HIV-1 replication/outgrowth. Consistently, colon-infiltrating CD4 T cells carry replication-competent viral reservoirs in people with HIV-1 (PWH) receiving antiretroviral therapy (ART). Intriguingly, integrative infection in colon macrophages, a pool replenished by monocytes, represents a rare event in ART-treated PWH, thus questioning the effect of RA on macrophages.
View Article and Find Full Text PDFHum Reprod
May 2024
Department of Anatomy and Cell Biology, Justus Liebig University of Giessen, Giessen, Germany.
Study Question: Does the chemokine/chemokine receptor axis, involved in immune cell trafficking, contribute to the pathology of testicular inflammation and how does activin A modulate this network?
Summary Answer: Testicular chemokines and their receptors (especially those essential for trafficking of monocytes) are elevated in orchitis, and activin A modulates the expression of the chemokine/chemokine receptor network to promote monocyte/macrophage and T cell infiltration into the testes, causing extensive tissue damage.
What Is Known Already: The levels of CC motif chemokine receptor (CCR)2 and its ligand CC motif chemokine ligand (CCL)2 are increased in experimental autoimmune orchitis (EAO) compared with healthy testes, and mice deficient in CCR2 are protected from EAO-induced tissue damage. Activin A induces CCR2 expression in macrophages, promoting their migration.
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