Chemokine mRNA levels in mononucleated cells of HIV-infected patients before and after initiation of PI- versus NNRTI-containing HAART.
To compare CC chemokine mRNA levels from native peripheral blood mononucleated cells (PBMCs) before and 6 months after the initiation of two different regimens of highly active antiretroviral therapy (HAART), we treated group 1 (n = 11) with two nucleoside analogues and the protease inhibitor (PI) indinavir boosted by ritonavir (800/100 mg b.i.d.); group 2 (n = 8) was treated with the non-nucleoside reverse transcriptase inhibitor (NNRTI) efavirenz instead of PI. CC chemokine mRNA levels (regulated upon T cell activation expressed secreted [RANTES], macrophage inhibitory protein [MIP]-1alpha, MIP-1beta, monocyte chemotactic protein [MCP]-1, MCP-2) were quantified from PBMCs before and 6 months after the initiation of HAART using a reverse transcription/real-time polymerase chain reaction (PCR) assay. The mRNA levels of MCP-1 and MCP-2 were significantly decreased in both groups (P < 0.05), while MIP-1alpha and MIP-1beta were decreased significantly only in the PI-treated group, but not in the NNRTI group. A moderate decrease of RANTES was observed in both treatment groups. The data suggest that HAART regimens containing either NNRTI or PI are not equivalent with regard to modification of CC chemokine mRNA profiles.
Wasmuth
Jan-Christian
JC
Department of Medicine I, University of Bonn, Sigmund Freud Str. 25, 53105 Bonn, Germany. j-c.wasmuth@uni-bonn.de
Nischalke
Hans-Dieter
HD
Jütte
Alexander
A
Fätkenheuer
Gerd
G
Salzberger
Bernd
B
Sauerbruch
Tilman
T
Spengler
Ulrich
U
Rockstroh
Jürgen K
JK
Dumoulin
Franz L
FL
D000328:Adult; D000480:Alkynes; D023241:Antiretroviral Therapy, Highly Active; D048588:Benzoxazines; D018932:Chemokine CCL2 / Q000032:analysis / Q000235:genetics; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000032:analysis / Q000235:genetics; D054412:Chemokine CCL8; D018925:Chemokines / Q000032:analysis* / Q000235:genetics; D003521:Cyclopropanes; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology*; D017320:HIV Protease Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D019469:Indinavir / Q000008:administration & dosage / Q000627:therapeutic use; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D019402:Macrophage Inflammatory Proteins / Q000032:analysis / Q000235:genetics; D008297:Male; D008875:Middle Aged; D018945:Monocyte Chemoattractant Proteins; D010078:Oxazines / Q000008:administration & dosage / Q000627:therapeutic use; D012333:RNA, Messenger / Q000032:analysis; D018894:Reverse Transcriptase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D019438:Ritonavir / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use
D000480:Alkynes; D048588:Benzoxazines; C515453:CCL8 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054412:Chemokine CCL8; D018925:Chemokines; D003521:Cyclopropanes; D017320:HIV Protease Inhibitors; D019402:Macrophage Inflammatory Proteins; D018945:Monocyte Chemoattractant Proteins; D010078:Oxazines; D012333:RNA, Messenger; D018894:Reverse Transcriptase Inhibitors; D019469:Indinavir; C098320:efavirenz; D019438:Ritonavir