ly differ from the CNR group at BL, the BL biomarker profiles of MST patients who achieved SVR did not differ significantly from those of the MST patients 
who had a NR. Within the MST group, a BL to FU comparison for the six patients that 15602004 achieved SVR indicated that no biomarkers significantly decreased with treatment between these two time points. Similarly in the MDT group, no biomarkers changed between BL and FU. In addition, we compared the HCV spontaneous clearance group to all patients who achieved SVR at BL and FU, initially comparing individual C-SVR and MST-SVR groups to the spontaneous clearance group. Only biomarkers that were significantly elevated in the combined-SVR group and in both C-SVR and MST-SVR comparisons were considered. A total of 22 markers were significantly elevated in the combinedSVR group versus the spontaneous group at BL. Of these, 12 remained significantly elevated at FU as well. In contrast, 10 were significantly elevated at BL, but not at FU. Finally, we compared our significant, non-parametric biomarker findings, to both unadjusted and adjusted parametric analyses, taking into account several possible confounding variables. The parametric models yielded qualitatively similar results to the nonparametric analyses; however, estimates became unstable when covariates were added, often resulting in substantially larger odds ratios and wider confidence intervals. We believe that the adjusted models were over parameterized given the small sample sizes, and so these results were not considered any further. Biomarkers in HCV and HIV Infection Discussion We observed distinct differences among biomarker profiles of HCV mono-infected patients, HIV co-infected patients, and those who spontaneously cleared HCV infection. These observations can be summarized as two central conclusions. First, our study confirms that co-infected patients have significantly increased levels of pro-inflammatory cytokines compared to mono-infected patients and enhances the current understanding of this heightened inflammatory state by evaluating 50 different biomarkers. Secondly, though the cytokine profiles of C-SVR and C-NR patients did not significantly differ at BL, they differed considerably at FU after patients received 48 weeks of HCV treatment, and these cross-sectional differences were largely driven by longitudinal changes within the C-SVR group. To our knowledge, this is the first study of HCV mono-infected, HIV/HCV coinfected, and HCV spontaneous clearance patients to both evaluate and report the results of 50 different markers with regard to infection status and treatment outcome. Notably, over 90% of patients were male, sample sizes were small, and the HIV/HCV co-infected group had a larger percentage of African American patients than the HCV mono-infected group, all of which could affect immune 17850214 marker differences between groups. When compared to mono-infected patients at BL, HIV/HCV co-infected patients in our study had significantly higher levels of cytokines involved in inflammation, chemotaxis, hematopoiesis, and fibrosis. This heightened inflammatory state may offer clues as to why CEP32496 conventional antiviral therapy for HCV infection may not be as effective or why prolonged treatment is necessary to achieve an SVR relative to monoinfected patients. This observation is further supported by comparisons of co-infected and mono-infected patients to those who spontaneously cleared HCV and therefore represent the baseline inflam
