MOPE011 - Poster Exhibition
Differences in CD4+ T cell immune activation in HIV, hepatitis C (HCV) and HIV/HCV co-infection are influenced by HIV and HCV infection status
A. Hodowanec1,2, K.E. Brady3, W. Gao4, S. Kincaid1, J. Plants3, M. Bahk1, A. Landay3, G. Huhn1,2
1Ruth M Rothstein CORE Center, Infectious Diseases, Chicago, United States, 2Rush University Medical Center, Infectious Diseases, Chicago, United States, 3Rush University Medical Center, Immunology and Microbiology, Chicago, United States, 4University of Illinois at Chicago, Center for Clinical and Translational Sciences, Chicago, United States
Background: HIV/HCV-coinfected patients have accelerated liver disease compared to HCV-monoinfection. In poorly-controlled HIV with chronic hepatitis C (CHC), immune activation has been primarily attributed to CD8 T-cell subsets. In well-controlled HIV, data comparing inflammatory cytokines and immune activation between HIV/HCV-coinfection with CHC to HIV/HCV-seropositive patients with cleared-HCV are underreported.
Methods: Fifty-nine age (median, 53 years) and sex (male=43/female=16)-matched patients were stratified: A) HIV-monoinfection (N=15), B) HCV-monoinfection with CHC (N=15), C) HIV/HCV-coinfection with CHC (N=14), and D) HIV/HCV-seropositive with cleared-HCV (N=15). All HIV+ patients had undetectable HIV viremia, and current CD4 counts in strata A and C were matched to CD4 at estimated timepoint of HCV clearance in strata D (median, CD4=420 cells/ml). Risk factors were recorded and serum collected for CD4 and CD8 immune activation (CD38/HLADR) and immune senescence (CD28) markers via flow cytometry, and luminex-multiplex cytokine assay. Immune and inflammatory markers were analyzed across strata using pair-wise t-tests; additional correlations of immune markers and cytokines were examined by multivariate analysis.
Results: CD38+HLADR+ and total HLADR+ expression on CD4+ T-cells was significantly increased in HIV/HCV-coinfection with CHC versus HIV-monoinfection, HCV-monoinfection, and HIV/HCV-seropositive with cleared-HCV. Total CD4+CD38+ expression was significantly lower in HIV/HCV-coinfection with CHC than HIV-monoinfection, but higher in HIV/HCV-coinfection with CHC than HCV-monoinfection(Figure 1). Other potential predictors of CD4+ activation included elevated transaminases and habits (Table 1). IL10 production was significantly higher in HIV-monoinfection versus HIV/HCV-coinfection with CHC (p=0.0002). No other differences in cytokines or CD28 across strata were detected.
Conclusions: In contrast to previously reported increased CD8 activation in poorly-controlled HIV, there were no differences in CD8 activation in our populations with undetectable HIV viremia. CD4 immune activation with HLADR+ expression in HIV/HCV-coinfection with well-controlled HIV may arise from chronic HCV viremia. Conversely, CD38+ expression in CD4 cells may be driven by underlying HIV infection in both HIV-monoinfection and HIV/HCV-coinfection.
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