CROI 2019 Abstract eBook

Abstract eBook

Poster Abstracts

untreated were as follows: FIB-4<1.25: 25.6 (23.8,27.5); FIB-4 1.26-3.25: 33.2 (31.2,35.1); FIB-4>3.25: 44 (39.6,48.3). The absolute difference in rate was 6.3 for FIB-4<1.25, 13.3 for FIB-4 1.26-3.25 and 19.5 for FIB-4>3.25. Conclusion: Risk of CVD among HCV infected persons is higher with increasing liver fibrosis stage. Treatment reduces the risk of incident events at all fibrosis stages, but the benefit is highest for those with most advanced fibrosis. HCV infected persons with more advanced liver fibrosis should be targeted for treatment to reduce future risk of CVD events.

patients with liver fibrosis compare to those without liver fibrosis, especially for senescence of CD8 cells (p=0.003) Conclusion: Both the presence of HCV coinfection and liver fibrosis significantly impact on several immune markers of HIV pathogenesis. Eradication of HCV with DAAs ameliorates but does not normalize these alterations, what is hindered by the presence of liver fibrosis. These data prompts HCV treatment in HIV/HCV coinfected patients at the earliest stages of liver damage to enhance restoration of T cell homeostasis 572 IMPACT OF DIRECT-ACTING ANTIVIRALS ON RATES OF HCC IN HCV- AND HIV-INFECTED PATIENTS Taiwo A. Ajose , Michael Flood Morehouse School of Medicine, Atlanta, GA, USA Background: HCV and HIV co-infection is known to be associated with increased risk of HCC. While we have data showing a significant decline in the rate of HCC in HCV patients undergoing treatment with DAA, the rate of HCC in HCV-HIV co-infected patients treated with DAA is not known. The aim of our study was to evaluate the impact of DAA therapy on the incidence of HCC in HCV-HIV co-infected patients. Methods: This retrospective analysis included all patients co-infected with both HCV and HIV, followed at Grady Memorial Hospital between January 2012 and December 2017. Patients were divided into two groups based on whether they received or did not receive DAA therapy and followed for development of HCC. Data included age, sex, race, HCV genotype, type of DAA regimen and SVR (in the treated group), cirrhosis, hepatitis B status, HIV control, CD4 trend and rates of HCC in both groups. Chi-square and Hazard ratio were used to calculate levels of statistical significance. Results: 819 patients co-infected with HIV and HCV were included in the analysis. 387 were treated with DAA while 432 were not. Median age in the treated group was 57 years with 79%males and 86% African americans while in the untreated group the corresponding numbers were 56 years, 78%males and 92% African americans. Median follow up was 42 months. There were 37 cirrhotics in the treated and 42 in the untreated group (p=0. 93). 20 patients were HbsAg positive in the treated group and 11 in the untreated group (p<0. 05). HIV was detectable in 14 patients in the treated and 147 in the untreated group (p<0. 00001). 1 patient developed HCC in the treated group compared to 10 in the untreated group (p<0. 01). Patients who developed HCC had poor HIV control (in 8 out of 11) and had a low CD4 count (median 119 cells/µl). HbsAg was positive in 3 patients with HCC, all in the untreated group. 8 of the 11 patients with HCC had cirrhosis. In the untreated group cirrhosis (p<0. 00001) and HbsAg positivity (p<0. 00001) was significantly associated with the development of HCC. Relative risk of HCC in the HCV HIV co-infected cohort treated with DAA compared with untreated cohort was 0. 11 (95% CI 0. 014 to 0. 868) (p=0. 03). Conclusion: DAA therapy significantly reduced rates of HCC in HCV-HIV co- infected patients. Eradicating HCV appears to overcome the significant role of HBV and cirrhosis in the development of HCC in these patients. Poor HIV control appears to be a big reason for withholding DAA therapy in these patients. 573 BARRIERS TO INITIATING DAA THERAPY IN HCV/HIV COINFECTED PATIENTS Taiwo A. Ajose , Austin Chan Morehouse School of Medicine, Atlanta, GA, USA Background: HCV continues to be a leading cause of liver disease and hepatocellular carcinoma (HCC), both of which are accelerated in HCV- HIV co-infected patients. The advent of DAA has significantly reduced the rate of HCC, but a large proportion of patients continue to be deprived of this beneficial therapy. Our aimwas to determine the barriers to initiation of DAA in co- infected patients. Methods: This retrospective analysis included all patients co-infected with both HCV and HIV, followed at Grady Memorial Hospital between January 2012 and December 2017 but did not receive DAA therapy. We evaluated reasons for not initiating DAA in these patients and looked at patient characteristics including age, sex, race, HCV genotype, cirrhosis, hepatitis B status, HIV control, the presence of other cancers, and social issues including drug abuse and health insurance. Results: Out of 819 patients co-infected with HIV and HCV, 387(47%) received and 432 (53%) did not receive any DAA therapy. The median age in the untreated group was 56 years, 78% of patients were males and 92% African Americans. HIV was detectable in 3. 7% patients in the treated and 34% in the untreated

Poster Abstracts

571 LIVER FIBROSIS HINDERS T-CELL HOMEOSTASIS RESTORATION AFTER HCV ERADICATION WITH DAAs Beatriz Álvarez 1 , Andrea García 2 , Clara Restrepo 2 , Marcial García 2 , María Ángeles Navarrete 2 , Victoria M. de Santisteban 2 , José Ligos 3 , Alfonso Cabello 1 , Laura Prieto 1 , Sara Nistal 4 , María Montoya 3 , Miguel Górgolas 1 , Norma Rallón 2 , José Miguel Benito 2 1 Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain, 2 Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Madrid, Spain, 3 Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain, 4 Hospital Universitario Rey Juan Carlos, Madrid, Spain Background: A significant impact of HCV coinfection on several immune parameters of HIV pathogenesis has been recently shown. However, to what extent these alterations are diminished or even abolished after HCV eradication with direct acting antivirals (DAAs) treatment has not been clarified to date. Herein we have analyzed the effect of HCV on several immune parameters of HIV pathogenesis and its evolution after HCV eradication in HIV patients coinfected with HCV Methods: Twenty-five HIV-monoinfected (HIV group), 25 HIV/HCV coinfected (HIV/HCV group) and 20 healthy controls (HC group) were included. All patients were on antiretroviral therapy and undetectable HIV viremia. Maturation, activation, apoptosis, senescence and exhaustion of CD4 and CD8 T cells were assessed by polychromatic flow cytometry. Cross-sectional and longitudinal (comparing baseline and post-HCV treatment data in HIV/HCV patients) analyses were performed. Non-parametric tests were used to establish inter and intra-group differences Results: Compared to HC group, HIV patients showed increased exhaustion and senescence of CD4 and CD8 cells, and increased activation of CD8 cells (p<0.0001 for all comparisons). Compared to HIV group, HIV/HCV patients presented higher exhaustion of effector CD4 (p=0.001) and CD8 (p=0.006) cells; and higher activation of total (p=0.026) effector memory (p=0.006) and effector (p<0.0001) CD8 cells. HIV/HCV patients with liver fibrosis (stage ≥F2), showed increased senescence and activation in several subsets of CD8 cells (p<0.05 for all comparisons) compared to patients without liver fibrosis (stage F0/F1). After HCV eradication with DAAs, differences between HIV/HCV and HIV groups diminished, except activation (p=0.002) and exhaustion (p=0.053) of effector CD8 cells that remained increased in HIV/HCV group. Interestingly, the effect of HCV eradication on immune parameters restoration (measured as the ratio of post-treatment vs. baseline values) was less pronounced in HIV/HCV

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