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This article is part of the supplement: 16th International Symposium on HIV and Emerging Infectious Diseases

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Impact of maraviroc on immune restoration in an advanced stage HIV-infected patient

Sylvie Bregigeon1, Amélie Menard1, Olivia Faucher1, Catherine Tamalet2, Caroline Solas3, Véronique Obry-Roguet1 and Isabelle Poizot-Martin1*

Author Affiliations

1 Department of Immuno-hematology, HIV-Clinical center, Hospital SainteMarguerite, Marseilles, France

2 Fédération de Microbiologie Clinique, Hôpital de la Timone, Marseilles, France

3 Laboratoire de Pharmacocinétique et de Toxicologie, Hôpital de La Timone, Marseilles, France

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Retrovirology 2010, 7(Suppl 1):P59  doi:10.1186/1742-4690-7-S1-P59

The electronic version of this article is the complete one and can be found online at:

Published:11 May 2010

© 2010 Bregigeon et al; licensee BioMed Central Ltd.


Maraviroc is a CCR5 antagonist with clearly demonstrated virological efficacy in patients refractory to prior treatment and infected with an R5-tropic virus.

This antiretroviral drug would appear to have a special immunomodulatory property, given the significantly higher increase in CD4 count in patients treated with maraviroc in clinical trials.

We report the case of a severely immunocompromised patient in which the introduction of maraviroc reduced viral load to below the threshold of 40 copies/ml, with an increase in CD4 of over 100 in the space of 17 months.


The patient was a 53 year old man diagnosed with HIV in 1987, and classed stage C according to CDC classification for cerebral toxoplasmosis in June 1995. His history includes cerebral histoplasmosis in April 1997 (relapse in April 2006) and stage IV Hodgkin's lymphoma with visceral involvement in October 2006 (CD4 = 1/mm3). The first antiretroviral treatment was given in October 1995 (CD4 <50/mm3), and the first maraviroc-based combination therapy was his 28th line treatment (16 stoppages for treatment failure). In January 2008, the tropism test (trofile test) gave an R5 profile and the genotypic resistance test (ANRS algorithm July 2009) showed, for the RT gene, resistance to AZT, 3TC, D4T, ddI, ABC, EFV, NVR and possibly to TDF and ETV; for the protease gene, resistance to IDVr, SQVr, NFV, FPVr, ATV, DRVr, LPVr and possibly to TPVr.


Table 1 shows viro-immunological changes with treatment:


This case report shows the possibility of being confronted with an R5-tropic virus after 21 years' progression, and 15 years of antiretroviral treatment, with severe immunosuppression. The three successive maraviroc-based combination therapies lead to an increase in CD4 count independent of the virological response, with a delta of +120 CD4 after 17 months. A parallel increase in the CD8 count was also observed, as has been reported in clinical trials.