title: [Innate immunity restoration in patients with HIV/AIDS infection associated with antiretroviral therapy].
abstract: BACKGROUND
  Highly active antiretroviral therapy (HAART) in HIV/AIDS infection induces an important reduction of the viral load (VL) and an immune system reconstitution. CD4+ T lymphocyte count is the immunological measurement commonly used for the follow up of HIV/AIDS patients.
  
  
  OBJECTIVE
  To study prospectively the restoration of the innate immune system in patients with HIV/AIDS infection during their first year on HAART.
  
  
  METHODS
  25 naive HIV/AIDS patients, from San José Hospital and University of Chile Clinical Hospital, Santiago, Chile, were studied between years 2002-2003. Every 4 months after HAART initiation, CD3+, CD4+, CD8+ T lymphocytes and CD16/56+ natural killer (NK) cells were quantified by flow cytometry. NK cell cytotoxicity was measured using radioactive chrome liberation (Cr51). Tumor necrosis factor alpha (TNF-alpha) and interleukin-10 (IL-10) were measured in peripheral blood mononuclear cells and viral load was determined using Amplicor HIV-1 from Roche Diagnostics Systems.
  
  
  RESULTS
  Thirteen of the 25 patients continued in the study. They were all males, average age 35 years old (23-50). At baseline average CD4+ count was 146 cells/microL (31-362) and average viral load was 82.000 copies/mL (4.000-290.000). A raise in CD3+, CD4+, CD8+, and CD16/56 cells was noted at months 9-12 of therapy. Viral load became undetectable in the same period. NK cell function was decreased at the beginning of the therapy (1-4 months), reaching its highest values at months 9-12. There was no significant change in IL-10. TNF-alpha increased in six patients during the study.
  
  
  CONCLUSIONS
  In this group of patients, innate immunity was restored during HAART. These results should be confirmed in studies with a longer follow up period and also measuring cytokines such as MIP-1a, MIP-1ss and RANTES.
authors.affiliation: Hospital Clínico, Universidad de Chile, Santiago, Chile.
authors.forename: Alejandro
authors.initials: A
authors.lastname: Afani
authors.forename: Lorena
authors.initials: L
authors.lastname: Jiusán
authors.forename: Pablo
authors.initials: P
authors.lastname: Raby
authors.forename: Giovanni
authors.initials: G
authors.lastname: Sitia
authors.forename: Javier
authors.initials: J
authors.lastname: Puente
authors.forename: Cecilia
authors.initials: C
authors.lastname: Sepúlveda
authors.forename: Dante
authors.initials: D
authors.lastname: Miranda
authors.forename: Roy
authors.initials: R
authors.lastname: Cabrera
authors.forename: Luca
authors.initials: L
authors.lastname: Guidotti
authors.forename: Paola
authors.initials: P
authors.lastname: Lanza
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy / Q000276:immunology; D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D005500:Follow-Up Studies; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology*; D017320:HIV Protease Inhibitors / Q000627:therapeutic use; D015497:HIV-1 / Q000187:drug effects / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D016753:Interleukin-10 / Q000097:blood; D007694:Killer Cells, Natural / Q000528:radiation effects; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019562:Viral Load
chemical_list: D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10