| Literature DB >> 28460153 |
Jason T Blackard1, Gang Ma1, Jeffrey A Welge2, Lynn E Taylor3, Kenneth H Mayer4, Robert S Klein5, David D Celentano6, Jack D Sobel7, Denise J Jamieson8, Caroline C King8.
Abstract
A beneficial impact of the Human Pegivirus (HPgV)-formerly called GB virus C (GBV-C)-on HIV disease progression has been reported previously. One possible mechanism by which HPgV inhibits HIV replication is an alteration of the cytokine/chemokine milieu. Their expression has not been specifically evaluated in women despite their influence on disease progression and the possibility of gender-based differences in expression. Moreover, the impact of HPgV genotype on cytokine/chemokine expression is unknown. Sera levels of IL-2, IL-4, IL-7, IL-8, IL-10, IL-12p70, IL-13, IFNγ, TNFα, IP-10, MIP-1α, MIP-1β, and TGF-β1 were quantified in 150 HIV-positive women based on HPgV RNA status. Cytokines/chemokines with detection rates of at least 50% included IL-2, IL-4, IL-8, IL-10, IL-12p70, IFNγ, TNFα, IP-10, MIP-1α, MIP-1β, and TGF-β1 . Absolute values were significantly higher for HPgV positive compared to HPgV negative women for IL-7, IL-13, IL-12p70, and IFNγ. Absolute values were significantly lower for HPgV positive women for IL-4, IL-8, TGF-β1 , and IP-10. IFNγ values were higher for HPgV genotype 2 than for genotype 1 (P = 0.036). Further study of cytokine/chemokine regulation by HPgV may ultimately lead to the development of novel therapeutic agents to treat HIV infection and/or the design of vaccine strategies that mimic the "protective" effects of HPgV replication.Entities:
Keywords: GB virus C (GBV-C); HIV; chemokine; cytokine; human pegivirus (HPgV); women
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Year: 2017 PMID: 28460153 PMCID: PMC5603382 DOI: 10.1002/jmv.24836
Source DB: PubMed Journal: J Med Virol ISSN: 0146-6615 Impact factor: 2.327