N. Imami, Department of Immunology, Imperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK.
E-mail: [email protected]

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Abstract

Summary Interleukin-16 (IL-16) and the β-chemokines (RANTES, monocyte chemotactic protein-1 (MCP-1), macrophage inhibitory protein (MIP)-1α and (MIP)-1β) are soluble in vitro suppressors of macrophage tropic HIV-1 strains. The reduction of HIV-1 RNA plasma levels in late-stage patients receiving protease inhibitors has been associated with increased concentrations of MIP-1α, MIP-1β, RANTES and IL-16 and a decrease in levels of MCP-1. We determined plasma levels of MCP-1, MIP-1α, MIP-1β, RANTES and IL-16 during the first 16 weeks of highly active antiretroviral therapy (HAART) in chronic HIV-1-infected patients. Patients were administered one of two therapeutic regimens based on either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI). No differences were seen in the levels of RANTES and IL-16 over the first 16 weeks of HAART in either treatment group. MCP-1 decreased significantly in the PI-treated group over the first 16 weeks of HAART (P = 0·0003). A significant increase was observed in the levels of MIP-1α and MIP-1β in the NNRTI cohort (P = 0·0010 and P = 0·0012, respectively). A significant decrease in levels of MIP-1α and MIP-1β (P = 0·0015 and P = 0·0299, respectively) was observed over the 16 weeks in the PI cohort. A significant difference was seen when the levels of MIP-1α and MIP-1β were compared between the NNRTI and the PI cohorts at week 16 (P = 0·04 and P = 0·05, respectively). Evaluation of CCR5 expression ex vivo revealed no difference between the two treatment groups. Patients were genotyped for CCR5 Δ32 and the incidence of heterozygosity was lower than in the HIV-1 seronegative controls (3% compared to 19%).

References

1 Doranz BJ, Rucker J, Yi Y et al. A dual-tropic primary HIV-1 isolate that uses fusin and the beta-chemokine receptors CKR-5, CKR-3, and CKR-2b as fusion cofactors. Cell 1996; 85: 1149–58.
10.1016/S0092-8674(00)81314-8
CAS PubMed Web of Science® Google Scholar
2 Berson JF, Long D, Doranz BJ, Rucker J, Jirik FR, Doms RW. A seven-transmembrane domain receptor involved in fusion and entry of T-cell-tropic human immunodeficiency virus type 1 strains. J Virol 1996; 70: 6288–95.
10.1128/JVI.70.9.6288-6295.1996
CAS PubMed Web of Science® Google Scholar
3 Liu R, Paxton WA, Choe S et al. Homozygous defect in HIV-1 co-receptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection. Cell 1996; 86: 367–77.
10.1016/S0092-8674(00)80110-5
CAS PubMed Web of Science® Google Scholar
4 Samson M, Libert F, Doranz BJ et al. Resistance to HIV-1 infection in Caucasian individuals bearing mutant alleles of the CCR-5 chemokine receptor gene. Nature 1996; 382: 722–5.
10.1038/382722a0
CAS PubMed Web of Science® Google Scholar
5 Quillent C, Oberlin E, Braun J et al. HIV-1-resistance phenotype conferred by combination of two separate inherited mutations of CCR5 gene. Lancet 1998; 351: 14–8.
10.1016/S0140-6736(97)09185-X
CAS PubMed Web of Science® Google Scholar
6 Paxton WA, Kang S, Liu R et al. HIV-1 infectability of CD4⁺ lymphocytes with relation to beta-chemokines and the CCR5 co-receptor. Immunol Lett 1999; 66: 71–5.
10.1016/S0165-2478(98)00154-0
CAS PubMed Web of Science® Google Scholar
7 Eugen-Olsen J, Iversen AK, Garred P et al. Heterozygosity for a deletion in the CKR-5 gene leads to prolonged AIDS-free survival and slower CD4 T-cell decline in a cohort of HIV-seropositive individuals. AIDS 1997; 11: 305–10.
10.1097/00002030-199703110-00007
CAS PubMed Web of Science® Google Scholar
8 Roda Husman AM, Koot M, Cornelissen M et al. Association between CCR5 genotype and the clinical course of HIV-1 infection. Ann Intern Med 1997; 127: 882–90.
10.7326/0003-4819-127-10-199711150-00004
PubMed Web of Science® Google Scholar
9 Cocchi F, DeVico AL, Garzino-Demo A, Arya SK, Gallo RC, Lusso P. Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8⁺ T cells. Science 1995; 270: 1811–5.
10.1126/science.270.5243.1811
CAS PubMed Web of Science® Google Scholar
10 Baier M, Werner A, Bannert N, Metzner K, Kurth R. HIV suppression by interleukin-16. Nature 1995; 378: 563.
10.1038/378563a0
CAS PubMed Web of Science® Google Scholar
11 Dragic T, Litwin V, Allaway GP et al. HIV-1 entry into CD4⁺ cells is mediated by the chemokine receptor CC-CKR-5. Nature 1996; 381: 667–73.
10.1038/381667a0
CAS PubMed Web of Science® Google Scholar
12 Amara A, Gall SL, Schwartz O et al. HIV co-receptor downregulation as antiviral principle. SDF-1alpha-dependent internalization of the chemokine receptor CXCR4 contributes to inhibition of HIV replication. J Exp Med 1997; 186: 139–46.
10.1084/jem.186.1.139
CAS PubMed Web of Science® Google Scholar
13 Alkhatib G, Locati M, Kennedy PE, Murphy PM, Berger EA. HIV-1 co-receptor activity of CCR5 and its inhibition by chemokines: independence from G protein signaling and importance of co-receptor downmodulation. Virology 1997; 234: 340–8.
10.1006/viro.1997.8673
CAS PubMed Web of Science® Google Scholar
14 Zagury D, Lachgar A, Chams V et al. C-C chemokines, pivotal in protection against HIV type 1 infection. Proc Natl Acad Sci USA 1998; 95: 3857–61.
10.1073/pnas.95.7.3857
CAS PubMed Web of Science® Google Scholar
15 Ullum H, Cozzi LA, Victor J et al. Production of beta-chemokines in human immunodeficiency virus (HIV) infection: evidence that high levels of macrophage inflammatory protein-1beta are associated with a decreased risk of HIV disease progression. J Infect Dis 1998; 177: 331–6.
10.1086/514192
CAS PubMed Web of Science® Google Scholar
16 Bisset LR, Rothen M, Joller-Jemelka HI, Dubs RW, Grob PJ, Opravil M. Change in circulating levels of the chemokines macrophage inflammatory proteins 1 alpha and 11 beta, RANTES, monocyte chemotactic protein-1 and interleukin-16 following treatment of severely immunodeficient HIV-infected individuals with indinavir. AIDS 1997; 11: 485–91.
10.1097/00002030-199704000-00012
CAS PubMed Web of Science® Google Scholar
17 Carter LM, Peters BS, Ellis BA, Wolstencroft RA. Highly active antiretroviral therapy normalizes the potential for MIP-1alpha production in HIV infection. J Infect 2000; 41: 252–5.
10.1053/jinf.2000.0742
PubMed Web of Science® Google Scholar
18 Baier M, Bannert N, Werner A, Lang K, Kurth R. Molecular cloning, sequence, expression, and processing of the interleukin 16 precursor. Proc Natl Acad Sci USA 1997; 94: 5273–7.
10.1073/pnas.94.10.5273
CAS PubMed Web of Science® Google Scholar
19 Amiel C, Darcissac E, Truong MJ et al. Interleukin-16 (IL-16) inhibits human immunodeficiency virus replication in cells from infected subjects, and serum IL-16 levels drop with disease progression. J Infect Dis 1999; 179: 83–91.
10.1086/314550
CAS PubMed Web of Science® Google Scholar
20 Palella FJ Jr, Delaney KM, Moorman AC et al. Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators. N Engl J Med 1998; 338: 853–60.
10.1056/NEJM199803263381301
CAS PubMed Web of Science® Google Scholar
21 Gazzard B, Moyle G. revision to the British HIV Association guidelines f or antiretroviral treatment of HIV seropositive individuals. BHIVA Guidelines Writing Committee. Lancet 1998; 352: 314–6.
10.1016/S0140-6736(98)04084-7
CAS PubMed Web of Science® Google Scholar
22 Carpenter CC, Cooper DA, Fischl MA et al. Antiretroviral therapy in adults. updated recommendations of the International AIDS Society-USA Panel. JAMA 2000; 283: 381–90.
10.1001/jama.283.3.381
CAS PubMed Web of Science® Google Scholar
23 Staszewski S, Morales-Ramirez J, Tashima KT et al. Efavirenz plus zidovudine and lamivudine, efavirenz plus indinavir, and indinavir plus zidovudine and lamivudine in the treatment of HIV-1 infection in adults. Study 006 Team. N Engl J Med 1999; 341: 1865–73.
10.1056/NEJM199912163412501
CAS PubMed Web of Science® Google Scholar
24 Podzamczer D, Ferrer E, Consiglio E et al. Preliminary results of a randomised multicenter study comparing combivir (ZDV/3TC) plus nelfinavir or nevirapine in HIV-infected naive patients (COMDINE) study. 7th Conference on Retroviruses and Opportunistic Infections, 2 February 2000.
Google Scholar
25 Murphy R, Katlama C, Johnson VA. The Atlantic Study: a randomised open-label trial comparing two protease inhibitors-sparing antiretroviral strategies versus a standard PI-containing regimen, 48-week data. 39th Conference on Antimicrobial Agents and Chemotherapy, 1999.
Google Scholar
26 Leonard EJ, Yoshimura T. Human monocyte chemoattractant protein-1 (MCP-1). Immunol Today 1990; 11: 97–101.
10.1016/0167-5699(90)90035-8
CAS PubMed Web of Science® Google Scholar
27 Mengozzi M, De Filippi C, Transidico P et al. Human immunodeficiency virus replication induces monocyte chemotactic protein-1 in human macrophages and U937 promonocytic cells. Blood 1999; 93: 1851–7.
10.1182/blood.V93.6.1851.406k12_1851_1857
CAS PubMed Web of Science® Google Scholar
28 Pakker NG, Notermans DW, De Boer RJ et al. Biphasic kinetics of peripheral blood T cells after triple combination therapy in HIV-1 infection: a composite of redistribution and proliferation. Nat Med 1998; 4: 208–14.
10.1038/nm0298-208
CAS PubMed Web of Science® Google Scholar
29 Giovannetti A, Ensoli F, Mazzetta F et al. CCR5 and CXCR4 chemokine receptor expression and beta-chemokine production during early T cell repopulation induced by highly active anti-retroviral therapy. Clin Exp Immunol 1999; 118: 87–94.
10.1046/j.1365-2249.1999.01033.x
CAS PubMed Web of Science® Google Scholar
30 Polo S, Veglia F, Malnati MS et al. Longitudinal analysis of serum chemokine levels in the course of HIV-1 infection. AIDS 1999; 13: 447–54.
10.1097/00002030-199903110-00002
CAS PubMed Web of Science® Google Scholar
31 Havlir DV, Bassett R, Levitan D et al. Prevalence and predictive value of intermittent viremia with combination HIV therapy. JAMA 2001; 286: 171–9.
10.1001/jama.286.2.171
CAS PubMed Web of Science® Google Scholar

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Volume130, Issue2

November 2002

Pages 286-292

Impact of NNRTI compared to PI-based highly active antiretroviral therapy on CCR5 receptor expression, β -chemokines and IL-16 secretion in HIV-1 infection

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Impact of NNRTI compared to PI-based highly active antiretroviral therapy on CCR5 receptor expression, β -chemokines and IL-16 secretion in HIV-1 infection

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