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Cytokine/chemokine expression associated with Human Pegivirus (HPgV) infection in women with HIV

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 ev...

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Bibliographic Details
Published in:Journal of medical virology 2017-11, Vol.89 (11), p.1904-1911
Main Authors: Blackard, Jason T., Ma, Gang, Welge, Jeffrey A., Taylor, Lynn E., Mayer, Kenneth H., Klein, Robert S., Celentano, David D., Sobel, Jack D., Jamieson, Denise J., King, Caroline C.
Format: Article
Language:English
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Summary: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.
ISSN:0146-6615
1096-9071
DOI:10.1002/jmv.24836