A30 Abstracts / Digestive and Liver Disease 41 (2009) A1–A45 LLQ < 12 IU/mL). LSM was evaluated by FibroScan ® (Echo- sens, Paris, France) at entry and during treatment. Results. Fourteen patients were excluded due to LSM success rate <65% or interquartile range >30%. In the 104 patients enrolled (median age 57-year, 69% male, 85% HBeAg nega- tive, 40% cirrhosis) baseline median LSM value was 10 kPa (range: 4–65) and was significantly higher in cirrhotic than in non-cirrhotic patients (14 kPa vs. 8 kPa, p < 0.0001), in closed relationship with serum ALT levels (r = 0.24, p = 0.011). After 6–18 months (median 11 months) of treatment, 89% of patients had undetectable HBV DNA and normal ALT and a follow up LSM was available in 85 patients. LSM declined in all but five (94%) patients by median value of 3 kPa (range: 0.4–37). A significant decrease of LSM from median val- ues of 10 to 6.9 kPa (p < 0.0001) was seen in both the 79 patients who normalized ALT and with persistently >1.5 unL ALT. LSM significantly declined from median values of 14.5 (range: 4–65) to 10 (range: 3–28) kPa in cirrhotics and from 8.1 (range 4.3–25) to 5.6 (range 3–22.3) kPa in non-cirrhotic patients (p < 0.0001). Nineteen (63%) patients with a base- line value of LSM >12.5 kPa switched to a LSM value <12.5 in the follow up. Conclusions. The high rates of HBV suppression and ALT normalization following ETV therapy correlated with sig- nificant reduction of LSM indicative of treatment-related regression of hepatic inflammation and fibrosis. doi:10.1016/j.dld.2008.12.062 TRUNCATED FORMS OF HCV CORE PROTEIN LOCALIZE IN DISTINCT SUBCELLULAR COM- PARTMENTS M. Burlone a,b,∗ , R. Minisini a,b , A. Cerutti a,b , E. Alaimo a,b , P. Maillard a,b , A. Budkowska a,b , M. Pirisi a,b a DiMeCS, University of Eastern Piedmont, Novara, Italy b Unité des Hepacivirus, Institute Pasteur, Paris, France Background. Hepatitis C virus (HCV) core protein localizes in cytoplasmatic and nuclear compartments in vitro and in vivo, but the mechanisms of core transport between cellular compartments remain elusive. Nuclear localization signals (NLSs) and nucleolar localization signal (NoLS), have been detected in N-terminal core sequence, which could direct core to nucleus/nucleolus upon its synthesis in the cytoplasm. We aimed to investigate cellular localization of core proteins of various length and mechanisms of core cytoplasmic-nuclear shuttling. Methods. Truncated HCV core proteins (aa 1–120, p120; 1–140, p140; 1–163, p163; and 1–172, p172) were cloned in a pEGFP vector, while full-length core 1–191 (p191), and core-E1 were cloned into a pCDNA vector. These plasmids were transfected in HuH7, HepG2, Fa2N-4, CHO or HEK293 cell lines. The localization of core in transfected cells was assessed by immunofluorescence microscopy. To determine the role of microtubules in core transport, cells were treated with the microtubule affecting drug taxol at different times after transfection and analysed for the subcellular localization of core. Results. HCV core proteins p120 and p140 showed only nuclear/nucleolar localization. Both nuclear and cytoplas- matic localization was observed for core p163 and p172 in HuH7, HepG2 and Fa2N4 cells, while these proteins showed only nuclear localization in CHO and HEK293 cells, suggesting that cytoplasmic localization was hepatocyte- specific. Exclusive cytoplasmic localization of p191 core was observed in hepatoma cells. All core proteins in nucleoli co- localized with nucleolin and B23. Treatment with taxol of cells expressing p163 and p172 proteins induced accumula- tion of core proteins in the nuclei, suggesting a microtubule mediated shuttling of core proteins between nucleus and cyto- plasm. Conclusions. These observations indicate that distribution of core in nuclear/cytoplasmic compartments is specific for hepatic cells and related to microtubule polymerisation mech- anisms. More studies are carried out to determine whether hepatocyte-specific shuttling of core protein takes place between nuclear and cytoplasmic compartments. doi:10.1016/j.dld.2008.12.063 LONG-TERM TREATMENT WITH -IFN IN HEP- ATITITS C RECURRENCE AFTER OLT F. Buonfiglioli a,∗ , M.R. Tamè a , F. Lodato a , A. Colecchia a , P. Cecinato a , F. Azzaroli a , V. Feletti a , M. Vivarelli b , M. Del Gaudio b , F. Piscaglia a , E. Roda a , A.D. Pinna b , G. Mazzella a a Dept of Clinical Medicine, University of Bologna, Italy b Dept of Surgery and Organ Transplantation, University of Bologna, Italy Background and aim. Long-term treatment effects of nat- ural IFN (n-IFN) and Ribavirin (RBV) on hepatitis C recurrence after liver transplant are lacking. Primary end point of the present study is to evaluate the effect of long-term administration of n-IFN + RBV on: histology, viral response, and survival according to severity at inclusion. MedCalc soft- ware package was used for statistical analysis; χ 2 , Wilcoxon for paired test, t-test, Kaplan–Meier survival curves were used when appropriate. Materials and methods. 31 patients (19M, 12F; mean age 56.2 ± 1.6 years; median time from OLT 10 ± 6.3 months, six genotype 2, 22 genotype 1, and three genotype 4) were prospectively included in the protocol study. All patients received 3 MU/day of n-IFN and 800 mg/day RBV with dose adjustment according to subjective maximal tolerability. Responders have been treated for further 12 months after viral undetectability, while non-responders (NR) have continued treatment at the same dose. Liver biopsies were obtained at baseline, 18 and 30 months. Eleven patients had a severe HCV related disease (SC-RD) (five fibrosing cholestatic relapse