title: Absence of favourable changes in circulating levels of interleukin-16 or beta-chemokine concentration following structured intermittent interruption treatment of chronic human immunodeficiency virus infection.
abstract: Changes in virological and immunological parameters were analysed following structured intermittent interruption of highly active anti-retroviral therapy (HAART) of patients with chronic human immunodeficiency virus (HIV) infection. Parameters analysed were serum levels of the CD8+ T-cell-derived inhibitory molecules interleukin-16 (IL-16), monocyte inhibitory protein-1beta (MIP-1beta) and RANTES ('regulated upon activation, normal T-cell expressed and presumably secreted'), and the enhancer of HIV replication, monocyte chemotactic protein-1 (MCP-1). Twenty-five patients with chronic HIV infection were evaluated during three cycles of intermittent interruptions of therapy (8 weeks on/4 weeks off) in comparison with 20 healthy sex- and age-matched controls. At enrolment, HIV-infected patients showed significantly higher serum concentrations of IL-16 and RANTES, and significantly lower concentrations of MCP-1, than did healthy controls. Levels of MIP-1beta were similar in both groups. Only the serum levels of IL-16 increased significantly in HIV-infected patients after every treatment interruption. However, differences between the CD4+ or CD8+ T-cell counts/microL, HIV loads and serum concentrations of each cytokine at baseline and at the end of the three cycles of intermittent interruptions of therapy were not significant. It was concluded that structured intermittent interruption of HAART for patients with chronic HIV infection did not modify the immunological parameters, including serum levels of CD8+ T-cell-derived inhibitory molecules, or the virus parameters studied. Thus, the findings do not support the use of this treatment modality for the management of HIV-infected patients.
authors.affiliation: Internal Medicine Service, Hospital Universitario Puerta del Mar, Cádiz, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Montes de Oca Arjona
authors.forename: R
authors.initials: R
authors.lastname: Pérez Cano
authors.forename: M J
authors.initials: MJ
authors.lastname: Orozco
authors.forename: A
authors.initials: A
authors.lastname: Martín Aspas
authors.forename: F
authors.initials: F
authors.lastname: Guerrero
authors.forename: C
authors.initials: C
authors.lastname: Fernández Gutiérrez Del Alamo
authors.forename: J A
authors.initials: JA
authors.lastname: Girón-González
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D018932:Chemokine CCL2 / Q000097:blood; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000097:blood; D019742:Chemokines, CC / Q000097:blood*; D002908:Chronic Disease; D004334:Drug Administration Schedule; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D019410:Interleukin-16 / Q000097:blood*; D019402:Macrophage Inflammatory Proteins / Q000097:blood; D008297:Male; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019742:Chemokines, CC; D019410:Interleukin-16; D019402:Macrophage Inflammatory Proteins