CROI 2015 Program and Abstracts

Abstract Listing

Poster Abstracts

Results: The best-fit parameter values indicated that the HCV epidemic was mainly driven by the increase in sexual risk behaviour in recent years. The epidemic threshold (R 0 = 1) was crossed in 2010. A pessimistic scenario assuming that the frequency of unsafe sex continues to rise predicts a steep increase in HCV incidence, with little differences between treatment strategies (Figure). A scenario where the frequency of unsafe sex remains stable results in declining HCV incidence with or without DAA therapy, provided that treatment rate increases considerably. The optimistic assumption that the frequency of unsafe sex reduces considerably leads to an immediate and steep decrease in the future HCV incidence, even in the absence of improvements in treatment rate and/or efficacy (Figure).

Figure. Projected HCV incidence in HIV-infected MSM assuming different treatment and behavioural scenarios. Conclusions: Treatment interventions are only effective in reducing HCV transmission among HIV-infected MSM if the frequency of high risk sexual behaviour does not increase as in recent years. However, if unsafe sex behaviour stabilizes, increased treatment uptake and efficacy are predicted to curb the epidemic within 10 years.

WEDNESDAY, FEBRUARY 25, 2015 Session P-N7 Poster Session

Poster Abstracts

Poster Hall

2:30 pm– 4:00 pm Immunopathogenesis of HCV Infection 676 Macrophage Activation and Hepatitis C (HCV) Disease Progression in HIV-InfectedWomen Participating in theWomen’s Interagency HIV Study (WIHS) Audrey L. French 1 ; Charlesnika Evans 3 ; Marion G. Peters 2 ; Mary A.Young 4 ; Mark Kuniholm 6 ; Michael Augenbraun 7 ; Seema N. Desai 5

1 CORE Center/ Stroger Hospital of Cook County, Chicago, IL, US; 2 University of California San Francisco, San Francisco, CA, US; 3 Northwestern University, Chicago, IL, US; 4 Georgetown University, Washington, IL, US; 5 Rush University Medical Center, Chicago, IL, US; 6 Montefiore Medical Center, University Hospital for Albert Einstein College of Medicine, Bronx, NY, US; 7 State University of New York Downstate, Brooklyn, NY, US Background: Hepatic macrophage activation by endotoxin is thought to contribute to hepatic fibrosis in HCV infection. We measured changes in markers of macrophage activation, microbial translocation and inflammation in HIV/HCV co-infected women comparing women who had rapid liver disease progression to liver disease non-progressors. Methods: Soluble CD163 and CD14, lipopolysaccharide (LPS), tumor necrosis factor receptor II (TNFRII), chemokine ligand-2 (CCL2) and interleukin-6 (IL-6) were measured by ELISA at 3 timepoints (T) on stored serum from HIV/HCV infected women. Women were retrospectively defined as liver disease progressors (LDP) or non-progressors (NP).). T1 for all women was a visit at which serummarkers (APRI and FIB-4) or liver biopsy were consistent with no/minimal fibrosis. T3 was approximately 5 years after T1. For NP, biopsies or fibrosis markers continued to reflect minimal or no fibrosis at T3. Progressors had severe fibrosis by histology, imminent liver-related death or both serummarkers consistent with cirrhosis/significant fibrosis at T3. T2 was ~equidistant between T1 and T3. Women with any hazardous alcohol consumption (>7 drinks/week) between T1 and T3 were excluded. Results: Soluble markers were measured in 31 liver disease progressors and 84 non-progressors. The median time between the T1 and 3 was 4.9 years. Median age, CD4 and HIVRNA at T1 for LDP and NP were 42 and 40 years, 462 and 487 cells/cmm and 1100 and 763 copies respectively and the groups were well-matched for race, HAART use and drug abuse (p>0.5 for all). LPS, CCL-2, IL-6 and sCD14 levels were not different in slope or quantity over time between LDP and NP. TNFRII levels were higher overall in progressors at T3 in unadjusted analysis (p=0.0005) and adjusted for HIVRNA (p=0.04) with a trend at T2 (p=0.01 unadjusted and 0.13 adjusted). SCD163 (figure) was significantly higher at T2 (p=0.007) and T3 (p<0.0001), (p=0.02 and <0.0001 respectively in the adjusted model) and for sCD163 the slope differed significantly between LDP and NP (p=0.02)

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CROI 2015