Journal article
GBV-C viremia is associated with reduced CD4 expansion in HIV-infected people receiving HAART and interleukin-2 therapy
AIDS (London), Vol.23(5), pp.605-610
2009
DOI: 10.1097/QAD.0b013e32831f1b00
PMCID: PMC2739595
PMID: 19194270
Abstract
Objective: Interleukin-2 (IL-2) is a cytokine with multiple effects on lymphocytes including induction of CD4 T-cell proliferation. IL-2 administration has been shown to increase CD4 cell counts in HIV-infected people receiving antiretroviral therapy. GB virus C (GBV-C) is an apparently nonpathogenic flavivirus that replicates in CD4 T cells and inhibits HIV replication in vitro by mechanisms including downregulation of HIV entry coreceptors (CCR5 and CXCR4) and induction of chemokines (RANTES, MIP-1alpha, MIP-1 beta, and SDF-1). GBV-C replication is significantly inhibited in vitro by activation of primary CD4 cell cultures with IL-2 and phytohemagglutinin. We sought to determine if there is an interaction between GBV-C and IL-2 in vivo.
Methods: GBV-C viremia status was characterized in 92 HIV-infected individuals participating in a randomized trial of IL-2 and antiretroviral therapy [AIDS Clinical Trials Group Study (ACTG) 328]. Changes in CD4 cell counts and HIV RNA levels in individuals assigned IL-2 were compared with those in individuals assigned antiretroviral therapy alone.
Results: Individuals lacking GBV-C viremia had a significantly greater rise in CD4 cell count with IL-2, compared with GBV-C viremic individuals (by 511 cells/microl at week 84; interaction P = 0.02): GBV-C viremic individuals assigned IL-2 did not demonstrate a significant increase in CD4 cell count compared with individuals not assigned to receive IL-2 (95% CI for difference -255 to 397 cells/microl).
Conclusion: GBV-C viremia was associated with a block in CD4 cell expansion following IL-2 therapy in the ACTG 328 study, and GBV-C status may be an important factor in IL-2 treatment response.
Details
- Title: Subtitle
- GBV-C viremia is associated with reduced CD4 expansion in HIV-infected people receiving HAART and interleukin-2 therapy
- Creators
- Jack T STAPLETON - Department of Internal Medicine, The University of Iowa, Iowa City, Iowa, United StatesKathryn CHALONER - Department of Biostatistics, The University of Iowa, Iowa City, Iowa, United StatesJINGYANG ZHANG - Department of Biostatistics, The University of Iowa, Iowa City, Iowa, United StatesDonna KLINZMAN - Iowa City VA Medical Center, The University of Iowa, Iowa City, Iowa, United StatesInara E SOUZA - Department of Internal Medicine, The University of Iowa, Iowa City, Iowa, United StatesJINHUA XIANG - Department of Internal Medicine, The University of Iowa, Iowa City, Iowa, United StatesAlan LANDAY - Rush Medical College, United StatesJohn FAHEY - University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, United StatesRichard POLLARD - University of California, Davis, School of Medicine, Sacramento, California, United StatesRonald MITSUYASU - University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, United States
- Resource Type
- Journal article
- Publication Details
- AIDS (London), Vol.23(5), pp.605-610
- DOI
- 10.1097/QAD.0b013e32831f1b00
- PMID
- 19194270
- PMCID
- PMC2739595
- NLM abbreviation
- AIDS
- ISSN
- 0269-9370
- eISSN
- 1473-5571
- Publisher
- Lippincott Williams & Wilkins
- Language
- English
- Date published
- 2009
- Academic Unit
- Microbiology and Immunology; Infectious Diseases; Internal Medicine
- Record Identifier
- 9984094522902771
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