The cells were then

The cells were then Dabrafenib cost treated with IFN for 6 hours and harvested. To evaluate the interferon responsiveness, ISG mRNA levels were quantified by real time PCR. Results: In the clinical study, more than 1 Log IU/ml reduction of HBsAg titer was achieved in 11 of 37 patients (interferon mono-therapy: 2, Sequential therapy: 9). By univariate analysis, the following factors, gender, serum HBsAg level, the existence of HBeAg, and prior NA therapy, were associated with HBsAg reduction (P=0.007, P=0.027, P=0.031, P=0.037, respectively). From the clinical results, it was predicted that interferon responsiveness might be improved by prior NA therapy. To verify these results, in vitro experiments were performed.

In the absence of HBV, the ISGs MxA and OAS1 were significantly induced by interferon treatment (19.2-fold, 9.7-fold, respectively). However, in T23 cells, inductions of these ISGs was suppressed (P=0.0495, P=0.0495, respectively). After entecavir treatment, interferon responsiveness was restored and ISG induction increased (P=0.0495, P=0.0339, respectively). Conclusions: Prior NA therapy could improve interferon responsiveness

in HBV infected human hepatocytes. To improve the anti-viral effects in chronic hepatitis B patients, it might be necessary to revise the way of using NAs and interferons. Disclosures: Kazuaki Chayama – Consulting: Abbvie; Grant/Research Support: Dainippon Sumitomo, Chugai, Mitsubishi Tanabe, DAIICHI SANKYO, Toray, BMS, MSD; Kinase Inhibitor Library concentration MCE公司 Speaking and Teaching: Chugai, Mitsubishi Tanabe, DAIICHI SANKYO, KYO-RIN, Nihon Medi-Physics, BMS, Dainippon Sumitomo, MSD, ASKA, Astellas, AstraZeneca, Eisai, Olympus, GlaxoSmithKline, ZERIA, Bayer, Minophagen, JANSSEN, JIMRO, TSUMURA, Otsuka, Taiho, Nippon Kayaku, Nippon Shin-yaku, Takeda, AJINOMOTO, Meiji Seika, Toray The following people have nothing to disclose: Masataka Tsuge, Nobuhiko Hiraga, Eisuke Murakami, Michio Imamura, Hiromi Abe, Daiki Miki, Hidenori Ochi, C. Nelson Hayes Background/Aim: Nucleoside analogue (NA) can decrease risk of hepatocellular carcinoma (HCC), but not prevent to develop HCC in some patients. Objects: Of 926 HBV carriers during 1979 and 2014 in our hospital, 277 were taken nucle-oside

analogue therapy. Among 277 patients, 146 patients ((sex: M/F 96/50, age: 47.4±10.7, genotype: A/B/C/E/ undetermined 6/12/120/1/7, ALT 85.5 (13-2273) IU/L, platelet count 16.7±6.3×104/|jL, HBeAg +/− 76/70, HBeAb +/- 86/60, HBV DNA 6.7±1.7 log copies/ml, HBcrAg 5.8±1.8 log U/ml, HBsAg 2490 IU/ml (0.69-287000 IU/ ml), history of interferon therapy(+/-) 28/ 118, diabetes (+/-) 7/139, significant intake of alcohol (+/-) 6/140, NA: LVD/ETV/TDF 42/99/5) showed good efficacy (HBV DNA <2.1 log copies/ml at the last observation point). Methods: During 53 (13-172) months observation period, 15 of 146 patients developed HCC (HCC group) and 131 patients did not (non-HCC group). We conducted an univariate analysis to compare two groups and Kaplan-Meier method search for HCC risk factor.

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