Disclosures: Hyung Joon Yim – Grant/Research Support: GSK Korea, Handok Pharm, Gilead Korea; Speaking

and Teaching: BMS Korea The following people have nothing to disclose: Hyoung Su Kim, Myoung Kuk Jang, Sang Jun Suh, Yeon Seok Seo, Sun Young Yim, Soon Ho Um, Ji Hoon Kim, Bo Hyun Kim, Sang Jong Park, Sae Hwan Lee, Sang Gyune Kim, Young Seok Kim, Jung Il Lee, Jin-Woo Lee, In Hee Kim, Tae Yeob Kim, Jin Wook Kim, Sook-Hyang Jeong, Young Kul Jung, Hana Park, Seong Gyu Hwang Complete virololgical suppression of HIV RNA and HBV DNA is the therapeutic goal of nucelos(t)ide analogue containing combination antiretroviral therapy (cART) in co-infected patients. Lamivudine/emtricitabine (3TC/FTC) and tenofovir (TDF) target reverse transcriptase of both viruses. Adding TDF improves viral response with pre-existing HBV 3TC/FTC resistance. Despite full HIV RNA suppression, indicating optimal cART adherence, some patients S1P Receptor inhibitor have a slow HBV viral response. Serological (HBeAg status and HBsAg levels), viro-logical (HBV DNA, mutation profile) and immunological (plasma IP 1 0 levels) markers and their change during therapy may explain differences between HBV viral responders (VR) and slow responders (SR) after add-on/switch to TDF and were investigated in this study. Patients: 46 HIV/HBV co-infected patients

(37 males, median age 42y, 67%HBeAg+, 1 3%cir-rhosis) were treated for HIV infection for median 5 years and TDF containing cART for a median 48 months. They were divided into 2 groups according to HBV viral

response (HBV DNA<20IU/ml) after 1-year post adding/starting TDF: 23 responders Cobimetinib price (VR) and 23 slow responders (SR) Methods: HBsAg plasma levels were measured by Abbott ARCHITECT® assay [log10IU/ml], HBV DNA by real-time PCR [log10IU/ml] and IP-1 0 levels by ELISA [pg/ml] at baseline, year (Y) 1, 2, 3, 4 and 5 of therapy. Drug resistance mutations were assessed at TDF baseline using direct sequencing. Results: 19 patients were exposed to 3TC/FTC therapy (7VR vs 12SR,p=0.13) and 10 had YMDD mutation (4VR vs 6SR,p=0.3); 7 achieved HBeAg seroconversion (5VR vs 2SR,p=0.01). Baseline median HBV DNA and HBsAg were significantly higher in SR than VR (HBV DNA: 5.91 vs 4.63,p=0.02; HBsAg: 4.75 vs 3.74,p<0.01), but IP1 0 levels were similar (IP1 0: 200 vs 232,p=0.6). 上海皓元 The proportion with HBV DNA>106IU/ml was similar in both groups (9VRvs 10SR). HBV DNA was higher in SR than VR at year 1-3 on therapy and similar at 4-5, but HBV DNA reduction from baseline was similar in both groups at all time-points. HBsAg was higher in SR than VR only at year 1 and from then on was similar between VR and SR. HBsAg decline from baseline was more rapid in SR than VR at all treatment years (Y1 :-0.5 vs.-0.1; Y2:-0.8 vs.-0.1; Y3:-0.9 vs.-0.1; Y4:-1.1 vs-0.1 andY5:-1.17 vs.-0.2,all p<0.05). IP10 was similar in VR and SR at all therapy time-points.