title: Human cytomegalovirus (HCMV)-specific CD4+ T lymphocyte response in AIDS patients with no past or current HCMV disease following HAART.
abstract: BACKGROUND
  The incidence of Human Cytomegalovirus (HCMV) end-organ disease has dramatically decreased since the implementation of highly active antiretroviral therapies (HAARTs), but the precise immune mechanism whereby HCMV is controlled remains to be elucidated.
  
  
  OBJECTIVE
  To investigate the effect of (HAART) on CD4+ T-cell immunity to HCMV in AIDS patients with no past or current HCMV disease.
  
  
  METHODS
  Seventeen patients were prospectively examined for CD4+ (CD45RO+ and CD45 RA+) T-cell counts (flow cytometry), HIV RNA load (Amplicor HIV test), HCMV leukoDNAemia and HCMV DNA in urine (nested PCR), lymphoproliferative response (LPR) to HCMV, phytohemagglutinin (PHA) and purified protein derived from Mycobacterium tuberculosis (PPD) by measurement of 5-bromo-2'-deoxyuridine incorporation to DNA (ELISA) and cytokine secretion (IFN-gamma, IL-4 and IL-10) by HCMV-stimulated peripheral blood mononuclear cell (PBMC) cultures (ELISA).
  
  
  RESULTS
  Fifteen patients responded favorably to HAART (virologically, immunologically, or both). Of these, six patients presented LPR to HCMV at least once during follow-up, whereas most displayed detectable LPRs to PHA. IFN-gamma was detected at least once in supernatants of HCMV-stimulated PBMC cultures from 14 of the 17 patients. All but one patient tested negative for HCMV leukoDNAemia and HCMV DNA in urine, and none developed HCMV disease during the observation period.
  
  
  CONCLUSIONS
  Control of HCMV replication and the absence of HCMV disease are not consistently associated with recovery and/or maintenance of LPR to HCMV in AIDS patients under HAART and with no prior HCMV disease. Whether detection of IFN-gamma by PBMCs upon HCMV antigenic stimulation may serve as a surrogate marker for protection against HCMV disease requires further investigation.
authors.affiliation: Department of Microbiology, School of Medicine, University of Valencia, Spain.
authors.forename: Amparo
authors.initials: A
authors.lastname: Tamarit
authors.forename: Juan
authors.initials: J
authors.lastname: Alberola
authors.forename: Amparo
authors.initials: A
authors.lastname: Mir
authors.forename: Isabel
authors.initials: I
authors.lastname: Benet
authors.forename: Josep Vicent
authors.initials: JV
authors.lastname: Mira
authors.forename: Carlos
authors.initials: C
authors.lastname: Muñoz
authors.forename: María José
authors.initials: MJ
authors.lastname: Galindo
authors.forename: David
authors.initials: D
authors.lastname: Navarro
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000276:immunology* / Q000821:virology; D000163:Acquired Immunodeficiency Syndrome / Q000150:complications / Q000188:drug therapy*; D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D003587:Cytomegalovirus / Q000276:immunology* / Q000302:isolation & purification; D003586:Cytomegalovirus Infections / Q000276:immunology* / Q000821:virology; D004279:DNA, Viral / Q000097:blood / Q000652:urine; D005260:Female; D006678:HIV / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D019562:Viral Load; D014766:Viremia
chemical_list: D016207:Cytokines; D004279:DNA, Viral; D012367:RNA, Viral; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma