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JAC Advance Access originally published online on December 14, 2007
Journal of Antimicrobial Chemotherapy 2008 61(2):400-404; doi:10.1093/jac/dkm470
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Association between HIV replication and cholesterol in peripheral blood mononuclear cells in HIV-infected patients interrupting HAART

Eugenia Negredo1, Isabel Puigdomènech2, Silvia Marfil2, Jordi Puig1, Núria Pérez-Álvarez1,3, Lidia Ruiz2, Celestino Rey-Joly4, Bonaventura Clotet1,2 and Julià Blanco2,*

1 Lluita contra la SIDA Foundation, Institut de Recerca en Ciències de la Salut Germans Trias i Pujol, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, 08916 Badalona, Barcelona, Spain 2 Fundació irsiCaixa, Institut de Recerca en Ciències de la Salut Germans Trias i Pujol, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, 08916 Badalona, Barcelona, Spain 3 Departamento de Estadística e Investigación Operativa, Universitat Politècnica de Catalunya, C \ Jordi Girona, 1-3, 08034 Barcelona, Spain 4 Internal Medicine Department, Institut de Recerca en Ciències de la Salut Germans Trias i Pujol, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, 08916 Badalona, Barcelona, Spain

Received 14 August 2007; returned 13 September 2007; revised 5 November 2007; accepted 14 November 2007

* Corresponding author. Tel: +34-93-497-88-87; Fax: +34-93-465-76-02; E-mail: jblanco{at}irsicaixa.es

Background: Cellular cholesterol is essential for HIV replication and may control HIV spread. HIV, in turn, appears to control cholesterol metabolism.

Objectives: To describe the relationships between serum lipids, cellular cholesterol and viral replication during highly active antiretroviral therapy (HAART) interruption.

Methods: We have correlated virological parameters with the level of circulating lipids in serum and the content of cellular cholesterol in peripheral blood mononuclear cells (PBMCs). The study included 33 patients interrupting HAART with (n = 23) or without (n = 10) atorvastatin treatment.

Results: Atorvastatin treatment did not modify PBMC cholesterol levels at week 4 after HAART interruption, although it significantly reduced serum cholesterol (total and LDL, where LDL stands for low density lipoprotein) (P < 0.05). Serum cholesterol or LDL marginally influenced PBMC cholesterol since no significant correlations were found between these parameters either at 0 or 4 weeks after HAART interruption. Analysis of virological data in all patients revealed a negative trend (P = 0.07) between baseline PBMC cholesterol and absolute CD4 T cell counts at baseline but a poor correlation (P = 0.18) with the viral load (VL) at week 4. Separate analysis of control patients showed a correlation between baseline PBMC cholesterol and VL at week 4 (P = 0.01). However, atorvastatin treatment abrogated this correlation by increasing viral replication in individuals with low cellular cholesterol.

Conclusions: Our data underscore the potential relevance of PBMC cholesterol in in vivo HIV replication and the complex effects of atorvastatin that seem to be unrelated to PBMC cholesterol.

Keywords: lipid , metabolism , membrane , replication , atorvastatin , PBMC


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