Effect of opportunistic infections on the frequency of leukocyte subpopulations from type-1 human immunodeficiency virus infected individuals
Keywords:
AIDS-related opportunistic infections/ immunology, leukocytes, HIV-1, lymphocyte activation, dendritic cells, natural killer cells, natural
Abstract
Introduction. The presence of opportunistic infections in patients with acquired immunodeficiency syndrome favors the progression of HIV-1 infection. Despite the key role that several leukocyte subpopulations exhibit during the anti-infectious response, few studies have focused on the role of these cells in HIV-1-infected patients with active opportunistic infections.Objective. The quantity of several innate and adaptive cell subpopulations was evaluated in whole peripheral blood of HIV-1-infected patients, with and without a history of opportunistic infections.
Materials and methods. The absolute number of each leukocyte subpopulation was evaluated by flow cytometry, and for each cell subpopulation, this number was correlated with viral load, CD4+ T cell count and the expression of activation markers on CD4+ and CD8+ T lymphocytes.
Results. Chronically HIV-1 infected patients exhibited a quantitative deficiency in several leukocyte subpopulations; this effect was more pronounced in individuals suffering an active opportunistic infection. This indicated that the coinfection by HIV-1 and opportunistic microorganisms potentiated the immunodeficiency by reducing significantly the frequency of different subpopulations of leukocytes.
Conclusions. This finding underlines the importance of an early diagnose of HIV-1 infection, and the need for the rational use of antiretroviral medications to avoid the development of opportunistic infections. In addition, it points to the necessity of developing immunotherapy strategies for HIV-1-infected patients in order to re-establish the immune competence.
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References
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27. Pacanowski J, Kahi S, Baillet M, Lebon P, Deveau C, Goujard C et al. Reduced blood CD123+ (lymphoid) and CD11c+ (myeloid) dendritic cell numbers in primary HIV-1 infection. Blood. 2001; 98: 3016-21.
28. Fleuridor R, Wilson B, Hou R, Landay A, Kessler H, Al-Harthi L. CD1d-restricted natural killer T cells are potent targets for human immunodeficiency virus infection. Immunology. 2003; 108: 3-9.
29. Rubbert A, Combadiere C, Ostrowski M, Arthos J, Dybul M, Machado E, et al. Dendritic cells express multiple chemokine receptors used as coreceptors for HIV entry. J Immunol. 1998; 160: 3933-41.
30. Turville SG, Cameron PU, Handley A, Lin G, Pohlmann S, Doms RW, et al. Diversity of receptors binding HIV on dendritic cell subsets. Nat Immunol. 2002; 3: 975-83.
31. Valentin A, Rosati M, Patenaude DJ, Hatzakis A, Kostrikis LG, Lazanas M, et al. Persistent HIV-1 infection of natural killer cells in patients receiving highly active antiretroviral therapy. Proc Natl Acad Sci USA. 2002; 99: 7015-20.
32. Shearer GM. HIV-induced immunopathogenesis. Immunity. 1998; 9: 587-93.
33. Finkel TH, Tudor-Williams G, Banda NK, Cotton MF, Curiel T, Monks C, et al. Apoptosis occurs predominantly in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes. Nat Med. 1995; 1: 129-34.
34. Herbeuval JP, Grivel JC, Boasso A, Hardy AW, Chougnet C, Dolan MJ, et al. CD4+ T cell death induced by infectious and noninfectious HIV-1: role of type I interferon-dependent, TRAIL/DR5-mediated apoptosis. Blood. 2005; 106: 3524-31.
35. Sousa AE, Carneiro J, Meier-Schellersheim M, Grossman Z, Victorino RM. CD4 T cell depletion is linked directly to immune activation in the pathogenesis of HIV-1 and HIV-2 but only indirectly to the viral load. J Immunol. 2002; 169: 3400-6.
36. Bofill M, Mocroft A, Lipman M. Increased numbers of primed activated CD8+CD38+CD45RO+ T-cells predict the decline of CD4+ T cells in HIV-1-infected patients. AIDS. 1996; 10: 827-34.
37. Hunt PW, Martin JN, Sinclair E, Bredt B, Hagos E, Lampiris H, et al. T cell activation is associated with lower CD4+ T cell gains in human immunodeficiency virus-infected patients with sustained viral supression during antiretroviral therapy. J Infect Dis. 2003; 187: 1534-43.
38. Carcelain G, Debre P, Autran B. Reconstitution of CD4+ T lymphocytes in HIV-infected individuals following antiretroviral therapy. Curr Opin Immunol. 2001; 13: 483-8.
39. Li TS, Tubiana R, Katlama C, Calvez V, Ait- Mohand H, Autran B. Long-lasting recovery in CD4 T-cell function and viral-load reduction after highly active antiretroviral therapy in advanced HIV-1 disease. Lancet. 1998; 351: 1682-6.
40. Gorochov G, Neumann AU, Kereveur A, Parizot C, Li T, Katlama C, et al. Perturbation of CD4+ and CD8+ T-cell repertoires during progression to AIDS and regulation of the CD4+ repertoire during antiviral therapy. Nat Med. 1998; 4: 215-21.
41. Connors M, Kovacs JA, Krevat S, Gea-Banacloche JC, Sneller MC, Flanigan M, et al. HIV infection induces changes in CD4+ T-cell phenotype and depletions within the CD4+ T-cell repertoire that are not immediately restored by antiviral or immune-based therapies. Nat Med. 1997; 3: 533-40.
42. Montoya CJ, Moreno ME, Rugeles MT. Reacciones y alteraciones del sistema inmune durante la infección por el VIH-1. Infectio. 2006; 10: 250-65.
43. Montoya CJ, Rugeles MT, Landay AL. Innate immune defences in HIV-1 infection: prospective for a novel immune therapy. Expert Rev Anti Infec Ther. 2006; 4: 767-80.
2. Cohen DE, Walker BD. Human immunodeficiency virus pathogenesis and prospects for immune control in patients with established infection. Clin Infect Dis. 2001; 32: 1756-68.
3. Clerici M, Clivio A, Shearer GM. Resistance to HIV infection: the genes are only part of the solution. Trends Microbiol. 1997; 5: 2-4.
4. OBrien SJ, Nelson GW. Human genes that limit AIDS. Nat Genet. 2004; 36: 565-74.
5. Touloumi G, Hatzakis A. Natural history of HIV-1 infection. Clin Dermatol. 2000; 18: 389-99.
6. Chaisson RE, Bishai W. No news is good news: opportunistic infections. Hopkins HIV Rep. 1998; 10: 2-11.
7. Equils O, Schito ML, Karahashi H, Madak Z, Yarali A, Michelsen KS, et al. Toll-like receptor 2 (TLR2) and TLR9 signaling results in HIV-long terminal repeat trans-activation and HIV replication in HIV-1 transgenic mouse spleen cells: implications of simultaneous activation of TLRs on HIV replication. J Immunol. 2003; 170: 5159-64.
8. Rotchford K, Strum AW, Wilkinson D. Effect of coinfection with STDs and of STD treatment on HIV shedding in genital-tract secretions: systematic review and data synthesis. Sex Transm Dis. 2000; 27: 243-8.
9. Sulkowski MS, Chaisson RE, Karp CL, Moore RD, Margolick JB, Quinn TC. The effect of acute infectious illnesses on plasma human immunodeficiency virus (HIV) type 1 load and the expression of serologic markers of immune activation among HIV-infected adults. J Infect Dis . 1998; 178: 1642-8.
10. Rodriguez B, Sethi AK, Cheruvu VK, Mackay W, Bosch RJ, Kitahata M, et al. Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection. JAMA. 2006; 296: 1498-506.
11. Hazenberg MD, Otto SA, van Benthem BH, Roos MT, Coutinho RA, Lange JM, et al. Persistent immune activation in HIV-1 infection is associated with progression to AIDS. AIDS. 2003; 17: 1881-8.
12. Letwin NL, Walker BD. Immunopathogenesis and immunotherapy in AIDS virus infections. Nat Med. 2003; 9: 861-6.
13. Leroy V, Salmi LR, Dupon M, Sentilhes A, Texier-Maugein J, Dequae L, et al. Progression of human immunodeficiency virus infection in patients with tuberculosis disease. A cohort study in Bordeaux, France, 1988-1994. The Groupe dEpidemiologie Clinique du Sida en Aquitaine (GECSA). Am J Epidemiol. 1997; 145: 293-300.
14. Whalen C, Horsburgh CR, Hom D, Lahart C, Simberkoff M, Ellner J. Accelerated course of human immunodeficiency virus infection after tuberculosis. Am J Respir Crit Care Med. 1995; 151: 129-35.
15. Crowe SM, Carlin JB, Stewart KI, Lucas CR, Hoy JF. Predictive value of CD4 lymphocyte numbers for the development of opportunistic infections and malignancies in HIV-infected persons. J Acquir Immune Defic Syndr. 1991; 4: 770-6.
16. Nissapatorn V, Lee CK, Rohela M, Anuar AK. Spectrum of opportunistic infections among HIV-infected patients in Malaysia. Southeast Asian J Trop Med Public Health. 2004; 35 (Suppl 2): 26-32.
17. Levy JA. The importance of the innate immune system in controlling HIV infection and disease. Trends Immunol. 2001; 22: 312-6.
18. Levy JA, Mackewicz CE, Barker E. Controlling HIV pathogenesis: the role of noncytotoxic anti-HIV activity of CD8+ cells. Immunol Today. 1996; 17: 217-24.
19. Levy JA, Scott I, Mackewicz CE. Protection from HIV/AIDS: the importance of innate immunity. Clin Immunol. 2003; 108: 167-74.
20. Centers for Disease Control and Prevention. 1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. MMWR Recomm Rep. 1992; 41: 1-19.
21. Donaghy H, Gazzard B, Gotch F, Patterson S. Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1. Blood. 2003; 101: 4505-11.
22. Cohen O, Weissman D, Fauci AS. The immuno-pathogenesis of HIV infection. En: Paul WE, editor. Fundamental immunology. 4th ed. Philadelphia: Lippincott-Raven Publishers; 1999. p. 1455-98.
23. Donaghy H, Pozniak A, Gazzard B, Qazi N, Gilmour J, Gotch F, et al. Loss of blood CD11c(+) myeloid and CD11c(-) plasmacytoid dendritic cells in patients with HIV-1 infection correlates with HIV-1 RNA virus load. Blood. 2001; 98: 2574-6.
24. Douek DC, Brenchley JM, Betts MR, Ambrozak DR, Hill BJ, Okamoto Y, et al. HIV preferentially infects HIV-specific CD4+ T cells. Nature. 2002; 417: 95-8.
25. Unutmaz D. NKT cells and HIV infection. Microbes Infect. 2003; 5: 1041-7.
26. Giorgi JV, Liu Z, Hultin LE, Cumberland WG, Hennessey K, Detels R. Elevated levels of CD38+ CD8+ T cells in HIV infection add to the prognostic value of low CD4+ T cell levels: results of 6 years of follow-up. The Los Angeles Center, Multicenter AIDS Cohort Study. J Acquir Immune Defic Syndr. 1993; 6: 904-12.
27. Pacanowski J, Kahi S, Baillet M, Lebon P, Deveau C, Goujard C et al. Reduced blood CD123+ (lymphoid) and CD11c+ (myeloid) dendritic cell numbers in primary HIV-1 infection. Blood. 2001; 98: 3016-21.
28. Fleuridor R, Wilson B, Hou R, Landay A, Kessler H, Al-Harthi L. CD1d-restricted natural killer T cells are potent targets for human immunodeficiency virus infection. Immunology. 2003; 108: 3-9.
29. Rubbert A, Combadiere C, Ostrowski M, Arthos J, Dybul M, Machado E, et al. Dendritic cells express multiple chemokine receptors used as coreceptors for HIV entry. J Immunol. 1998; 160: 3933-41.
30. Turville SG, Cameron PU, Handley A, Lin G, Pohlmann S, Doms RW, et al. Diversity of receptors binding HIV on dendritic cell subsets. Nat Immunol. 2002; 3: 975-83.
31. Valentin A, Rosati M, Patenaude DJ, Hatzakis A, Kostrikis LG, Lazanas M, et al. Persistent HIV-1 infection of natural killer cells in patients receiving highly active antiretroviral therapy. Proc Natl Acad Sci USA. 2002; 99: 7015-20.
32. Shearer GM. HIV-induced immunopathogenesis. Immunity. 1998; 9: 587-93.
33. Finkel TH, Tudor-Williams G, Banda NK, Cotton MF, Curiel T, Monks C, et al. Apoptosis occurs predominantly in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes. Nat Med. 1995; 1: 129-34.
34. Herbeuval JP, Grivel JC, Boasso A, Hardy AW, Chougnet C, Dolan MJ, et al. CD4+ T cell death induced by infectious and noninfectious HIV-1: role of type I interferon-dependent, TRAIL/DR5-mediated apoptosis. Blood. 2005; 106: 3524-31.
35. Sousa AE, Carneiro J, Meier-Schellersheim M, Grossman Z, Victorino RM. CD4 T cell depletion is linked directly to immune activation in the pathogenesis of HIV-1 and HIV-2 but only indirectly to the viral load. J Immunol. 2002; 169: 3400-6.
36. Bofill M, Mocroft A, Lipman M. Increased numbers of primed activated CD8+CD38+CD45RO+ T-cells predict the decline of CD4+ T cells in HIV-1-infected patients. AIDS. 1996; 10: 827-34.
37. Hunt PW, Martin JN, Sinclair E, Bredt B, Hagos E, Lampiris H, et al. T cell activation is associated with lower CD4+ T cell gains in human immunodeficiency virus-infected patients with sustained viral supression during antiretroviral therapy. J Infect Dis. 2003; 187: 1534-43.
38. Carcelain G, Debre P, Autran B. Reconstitution of CD4+ T lymphocytes in HIV-infected individuals following antiretroviral therapy. Curr Opin Immunol. 2001; 13: 483-8.
39. Li TS, Tubiana R, Katlama C, Calvez V, Ait- Mohand H, Autran B. Long-lasting recovery in CD4 T-cell function and viral-load reduction after highly active antiretroviral therapy in advanced HIV-1 disease. Lancet. 1998; 351: 1682-6.
40. Gorochov G, Neumann AU, Kereveur A, Parizot C, Li T, Katlama C, et al. Perturbation of CD4+ and CD8+ T-cell repertoires during progression to AIDS and regulation of the CD4+ repertoire during antiviral therapy. Nat Med. 1998; 4: 215-21.
41. Connors M, Kovacs JA, Krevat S, Gea-Banacloche JC, Sneller MC, Flanigan M, et al. HIV infection induces changes in CD4+ T-cell phenotype and depletions within the CD4+ T-cell repertoire that are not immediately restored by antiviral or immune-based therapies. Nat Med. 1997; 3: 533-40.
42. Montoya CJ, Moreno ME, Rugeles MT. Reacciones y alteraciones del sistema inmune durante la infección por el VIH-1. Infectio. 2006; 10: 250-65.
43. Montoya CJ, Rugeles MT, Landay AL. Innate immune defences in HIV-1 infection: prospective for a novel immune therapy. Expert Rev Anti Infec Ther. 2006; 4: 767-80.
How to Cite
1.
Montoya CJ, Ramirez Z, Cataño JC, Román A, Rugeles MT. Effect of opportunistic infections on the frequency of leukocyte subpopulations from type-1 human immunodeficiency virus infected individuals. biomedica [Internet]. 2008 Mar. 1 [cited 2024 May 17];28(1):64-77. Available from: https://revistabiomedica.org/index.php/biomedica/article/view/109
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2008-03-01
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