Conclusion: In a French expert center,14% of HCC complicating HBV infection are diagnosed in a non-cirrhotic liver, are mainly developed in non-fibrotic liver F0–1 (80%), with larger and/or more aggressive tumors (high AFP level) compared with HCC developed in HBV cirrhosis. In addition, non-cirrhotic patients have fewer risk factors for HCC (HCV, HDV and NASH) than patients with cirrhosis suggesting a direct viral mechanism in the process of carcinogenesis. FRI-157 HIV infection adversely influences the natural history of untreated hepatocellular carcinoma (HCC) D.J. Pinato 1 , T.-Y. Chen 2 , E. Allara 3 , F. Trevisani 4 , B. Minguez 5 , M. Zoli 6 , M. Harris 7 , A.D. Pria 8 , N. Merchante 9 , H. Platt 10 , M. Jain 11 , E. Caturelli 12 , L. Kikuchi 13 , J. Pineda 9 , M. Nelson 8 , F. Farinati 14 , G. Ludovico Rapaccini 15 , A. Aytaman 16 , M. Yin 17 , M. Bower 8 , E. Giovanni Giannini 18 , N. Brau 19 . 1 Imperial College London, Surgery and Cancer; 2 VA Central Texas HCS; 3 University of Cambridge; 4 University of Bologna; 5 Hospital Universitario Vall d’Hebron; 6 Università di Bologna, Bologna, Italy; 7 St. Paul’s Hospital, Vancouver, BC; 8 National Centre for HIV Malignancy, Chelsea & Westminster Hospital & Imperial College; 9 Universidad de Sevilla, Spain; 10 MSD, USA; 11 University of Texas Southwestern Medical Center; 12 ASL Viterbo; 13 Universidade de São Paulo, Brazil; 14 Universityof Padova; 15 Universita” Cattolica del Sacro Cuore, Rome; 16 VA New York Harbor HCS; 17 Columbia University, NY; 18 University of Genova; 19 Divisions of Infectious Diseases & Liver Diseases, Mount Sinai School of Medicine Email: david.pinato09@imperial.ac.uk Background and Aims: HCC is a leading cause of mortality in people living with HIV. However, studies evaluating whether HIVcan affect the natural history of HCC have been inconsistent due to heterogen- eity in geographical origin, stage, and treatment status. In this large, multicenter study we aimed to assess the prognostic impact of HIV status in two large cohorts of patients who did not receive active anticancer treatment. Method: HIV-infected patients with untreated HCC were retrospect- ively identified from 47 centers in North and South America, Europe, and Australia and compared to 776 HIV-negative subjects with treatment-naïve HCC recruited from the ITALICA consortium. The primary endpoints were overall survival, with HIV status being tested as prognostic factor in uni- and multivariable survival analyses. Secondary endpoints were presentation and staging of HCC at diagnosis. Results: Among the 132 HIV-positive patients, 56% had undetectable plasma HIV RNA, and the median CD4+ cell count was 256/mm 3 . Compared to the 776 HIV-negative patients, they wereyounger (53 vs. 67 years, p < 0.001), more commonly male (95% vs. 80%, p < 0.001), hepatitis C virus positive (74% vs. 54%, p <0.001), but had similar Child-Turcotte-Pugh (CTP) scores at diagnosis (7 vs. 7, p=0.37). They presented more commonly with larger tumours (median diameter, 6.0 vs. 4.0 cm, p < 0.001), with uni-nodular lesions (62% vs 51%, p = 0.012), had higher AFP level (median 714 vs. 77 ng/dl, <0.001) and a higher proportion of portal venous invasion (36% vs 26%, p = 0.034) and distant metastases (28% vs. 8%, p < 0.001). HIV-positive patients had lower median survival (3.0 vs. 8.0 months HIV [-], Log rank p< 0.001) with estimated 1-year survival rates of 13% vs. 24%. Multivariable Cox regression analysis identified HIV infection as an independent predictor of worse survival (H.R., 1.62; 95% C.I., 1.19– 2.19, p = 0.002) together with age, male sex, living in the Americas vs. Europe, CTP score, AFP level, portal vein invasion and BCLC stage. Among HIV-positive patients, independent predictors of mortality were CTP score, AFP level, and presence of metastases, but not HIV viral load, CD4+ cells or BCLC stage. Median Survival 1-yr 2-yr 5-yr Estimated Survival HIV-positive 3.0 months 13% 5% 3% HIV-negative 8.0 months 34% 17% 4% Conclusion: HIV infection is independently associated with adverse survival in patients who did not receive treatment for HCC. Mechanistic studies to investigate the biologic foundations of such survival difference are urgently required. FRI-158 Factors implicated in the risk of developing hepatocellular carcinoma (HCC) in patients with cirrhosis due to HCV. Implications of Sustained Virological Response (SVR) A. Castaño, A. Gomez, M. Torner, M. Fraile, C. Álvarez-Navascués, V. Cadahía-Rodrigo, M.L.G. Dieguez, M. Varela, M. Rodríguez. Hospital Universitario Central de Asturias, Liver Unit. Division of Gastroenterology&Hepatology, Oviedo, Spain Email: castaogarciacongresos@gmail.com Background and Aims: One of the goals of the treatment of HCV is the reduction in the risk of developing HCC. With the new DAAs, high rates of SVR are obtained in patients with cirrhosis. Aim: To analyze the factors involved in the development of HCC in a series of patients with HCV cirrhosis and to determine if SVR reduces the risk. Method: 699 patients with HCV cirrhosis, Child A/B, included in a surveillance program for the early diagnosis of HCC based on semi- annual AFP and US controls. The patients who reached SVR during the follow-up were considered viremic until that moment, censored at that point and included again as patients with SVR, updating the clinical and demographic variables. Results: 72% male sex, mean age 53 ± 9 years, 89% Child A, 22% with previous decompensation, 60% with varices and 34.6% with SVR (53 with IFN and 189 with DAAs). During a mean follow-up of 44 ± 50 months, 98 patients developed HCC, with a mean annual incidence of 3.7% and a cumulative probabilityat 5 and 10 years of 17% and 33% respectively. The probability of developing HCC was significantly lower in patients with SVR than in those without SVR (annual incidence: 1.7% vs. 4.3%, p =0.013). The follow-up of patients with SVR was lower than that of those without SVR (26 ± 32 vs. 54 ± 55 months, p < 0.001). In the univariate analysis the following other variables were associated with the risk of developing HCC: male gender ( p = 0.051), age > 55 years ( p < 0.001), previous POSTERS PRESENTATIONS S431 Journal of Hepatology 2018 vol. 68 | S365–S604