title: Cytokine profile of a long-term pediatric HIV survivor with hyper-IgE syndrome and a normal CD4 T-cell count.
abstract: BACKGROUND
  An elevated IgE level and increased production of T(H2) cytokines are factors associated with poor prognosis in HIV infection. We report a pediatric long-term survivor of vertically acquired HIV infection with a normal CD4 count and a low viral burden despite the lack of antiretroviral therapy and a phenotype resembling hyper-IgE syndrome.
  
  
  OBJECTIVE
  We sought to characterize the patient's T(H1) versus T(H2) cytokine profile and anti-HIV-specific immune responses.
  
  
  METHODS
  Supernatants collected from cultures of peripheral blood T cells stimulated with phorbol myristate acetate plus ionomycin were assayed for T(H1) and T(H2) cytokines by means of ELISA. Specific IgE antibodies were determined by immunoblot. HIV-specific cytotoxic T-lymphocyte responses were measured from cell lysis by fresh T cells of autologous B-lymphoblastoid cells expressing recombinant HIV proteins.
  
  
  RESULTS
  Patient CD4(+) T cells secreted significantly more T(H2) cytokines, IL-4 (P <.003) and IL-5 (P <.03), than HIV-infected and seronegative control cells. No difference was noted in T(H1) cytokine production. IgE specific for HIV gp160, p24, p17, and p66 proteins and Aspergillus fumigatus was detected in patient sera. Despite predominance of T(H2) cytokines, HIV-specific cytotoxic T-lymphocyte activity was vigorous.
  
  
  CONCLUSIONS
  The patient demonstrated predominantly T(H2) cytokine production in vitro. Unlike other patients with HIV who have hyper-IgE and increased T(H2) cytokine production, our patient has maintained HIV-specific immune responses, a low viral load, and a normal CD4 count without antiretroviral therapy. These findings support a diagnosis of primary hyper-IgE syndrome. Presence of anti-HIV-specific IgE may represent a protective mechanism against HIV replication in our patient.
authors.affiliation: Department of Pediatrics, Division of Immunology, Allergy, and Rheumatology, University of California, San Francisco, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Seroogy
authors.forename: D W
authors.initials: DW
authors.lastname: Wara
authors.forename: M H
authors.initials: MH
authors.lastname: Bluth
authors.forename: A
authors.initials: A
authors.lastname: Dorenbaum
authors.forename: C
authors.initials: C
authors.lastname: White
authors.forename: H G
authors.initials: HG
authors.lastname: Durkin
authors.forename: M E
authors.initials: ME
authors.lastname: Elder
mesh_terms: D018791:CD4 Lymphocyte Count; D002648:Child; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D015483:HIV Antibodies / Q000097:blood / Q000276:immunology; D015658:HIV Infections / Q000097:blood / Q000150:complications / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007589:Job Syndrome / Q000097:blood / Q000150:complications / Q000276:immunology*; D017741:Survivors; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
chemical_list: D016207:Cytokines; D015483:HIV Antibodies; D007073:Immunoglobulin E