Negredo Eugenia, Puigdomènech Isabel, Marfil Silvia, Puig Jordi, Pérez-Alvarez Núria, Ruiz Lidia, Rey-Joly Celestino, Clotet Bonaventura, Blanco Julià
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.
J Antimicrob Chemother. 2008 Feb;61(2):400-4. doi: 10.1093/jac/dkm470. Epub 2007 Dec 14.
Cellular cholesterol is essential for HIV replication and may control HIV spread. HIV, in turn, appears to control cholesterol metabolism.
To describe the relationships between serum lipids, cellular cholesterol and viral replication during highly active antiretroviral therapy (HAART) interruption.
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.
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.
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.
细胞胆固醇对HIV复制至关重要，可能控制HIV传播。反过来，HIV似乎也控制胆固醇代谢。
描述在高效抗逆转录病毒治疗（HAART）中断期间血清脂质、细胞胆固醇与病毒复制之间的关系。
我们将病毒学参数与血清中循环脂质水平以及外周血单核细胞（PBMC）中细胞胆固醇含量进行了关联分析。该研究纳入了33例中断HAART治疗的患者，其中23例接受阿托伐他汀治疗，10例未接受阿托伐他汀治疗。
HAART中断后第4周，阿托伐他汀治疗未改变PBMC胆固醇水平，尽管它显著降低了血清胆固醇（总胆固醇和低密度脂蛋白胆固醇，其中LDL代表低密度脂蛋白）（P<0.05）。血清胆固醇或低密度脂蛋白胆固醇对PBMC胆固醇的影响微乎其微，因为在HAART中断后0周或4周，这些参数之间均未发现显著相关性。对所有患者的病毒学数据进行分析发现，基线PBMC胆固醇与基线绝对CD4 T细胞计数之间呈负趋势（P = 0.07），但与第4周的病毒载量（VL）相关性较差（P = 0.18）。对对照组患者进行单独分析显示，基线PBMC胆固醇与第4周的VL之间存在相关性（P = 0.01）。然而，阿托伐他汀治疗通过增加细胞胆固醇水平较低个体的病毒复制，消除了这种相关性。
我们的数据强调了PBMC胆固醇在体内HIV复制中的潜在相关性，以及阿托伐他汀的复杂作用，这些作用似乎与PBMC胆固醇无关。
