Aim: To characterize HBV quasispecies in HBX by UDPS, including var with deletions. Patients and Methods: UDPS analysis (GS Junior Roche) of HBX nt1596-1912 in 30 serum samples from 10 chronic HBV patients failing lamivudine (LMV): basal, untreated, www.selleckchem.com/products/Gefitinib.html after LMV. nt substitutions/deletions, aa var in HBx (aa75-154),

and PC were studied. Results: 415,726 sequences obtained. Main HBX var: xK130M, xV131I (19 samples), associated with BCP ntA1762T/G1764Avar. HBX deletions (1->50nt) in all patients (Table), causing early HBX stop in 90.7% of these var, 33% were 8nt deletion in region nt1 758-1776 (9 samples/6 patients). Two main single-nt deletions: 1825 (12%) in 7 samples (4 patients) yields a long HBx, and 1746 (4.9%) causes HBx early stop. Genotype D cases (classified by LiPA) clustered with genotype E in HBX, suggesting D-E recombination (recD-E). Moreover; A/recD-E mixtures were frequent, 14/30 samples (9/10 patients) with changes during follow-up. After LMV, genotype A increased when recD-E was dominant (4 cases). All patients showed PC nonexpression var (Table), deletions being most frequent (17/30 samples, 0.3%-12%). Conclusions: The systematic presence Erlotinib purchase of deletions in X/BCP/PC, mainly causing an early HBX stop, suggests a new multicoding HBV mechanism. Deletions are most frequent cause of PC nonexpression. The recD-E

genotype may be prevalent in our region; the dynamics of genotype mixtures seem to be associated with a different sensitivity to antiviral therapy. Funding by Instituto CarlosIII (PI 12/1983), cofinanced by ERDF Disclosures: Rafael Esteban – Speaking and

Teaching: MSD, BMS, Novartis, Gilead, Glaxo, MSD, BMS, Novartis, Gilead, Glaxo, Janssen Maria Buti – Advisory Committees or Review Panels: Boerhinger Inghelm, Boer-hinger Inghelm; Speaking and Teaching: MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen, MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen The following people have nothing to disclose: Josep Gregori, Andrea Caballero, David Tabernero, Maria Homs, Maria Blasi, Rosario Casillas, Josep Quer, Leonardo Nieto, MCE Xose Costa-Alcaide, Francisco Rodriguez-Frias Background/Aim: Asymptomatic patients with chronic hepatitis B virus (HBV) infection often experience hepatitis flare so-called acute exacerbation depending on the host condition, virologic factors or environmental status. Clinical courses of acute exacerbation in patients with chronic HBV infection vary from asymptomatic to transient self-limited, typical hepatitis symptoms, rarely hepatic decompensation or liver failure. The aim of this study was to explore the causes, clinical features and outcomes of acute exacerbation in asymptomatic patients with chronic HBV infection.