| Autor: |
Anthony DD, Conry SJ, Medvik K, Sandhya Rani MR, Falck-Ytter Y, Blanton RE, Lederman MM, Rodriguez B, Landay AL, Sandberg JK, Anthony, Donald D, Conry, Sara J, Medvik, Kathy, Sandhya Rani, M R, Falck-Ytter, Yngve, Blanton, Ronald E, Lederman, Michael M, Rodriguez, Benigno, Landay, Alan L, Sandberg, Johan K |
| Zdroj: |
Journal of Infectious Diseases; Sep2012, Vol. 206 Issue 6, p969-973, 5p |
| Abstrakt: |
Disease progression of human immunodeficiency virus type 1 (HIV-1) is associated with immune activation. Activation indices are higher during coinfection of hepatitis C virus (HCV) and HIV. The effect of immune activation on interferon α (IFN-α) therapy response is unknown. We evaluated soluble CD14 (sCD14) and natural killer (NK)-cell subsets at baseline, and during pegIFN-α2a/ribavirin therapy in HCV-HIV coinfection. The sCD14 level increased during therapy. Baseline sCD14 positively correlated with baseline HCV level and CD16(+)56(-) NK-cell frequency, and both sCD14 and CD16(+)56(-) NK cells correlated negatively with magnitude of HCV decline. IL28B genotype was associated with therapy response but not sCD14 or CD16(+)56(-) NK frequency. Markers of innate immune activation predict poor host response to IFN-α-based HCV therapy during HCV-HIV coinfection. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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