Overall, our data suggests that Ficolin-2 not only play an important role in the pathogenesis of HBV infection but also a functional role in other liver diseases caused by HBV. This current study provides the first insights on contribution of theFCN2gene polymorphisms and the Ficolin-2 serum levels to HBV outcome in a Vietnamese cohort. 0.0002 and P<0.0001) conferring a protective effect. Ficolin-2 levels differed significantly between patients and controls (p<0.0001). Patients with acute hepatitis B had higher serum Ficolin-2 levels compared to other patient groups and controls.The viral load was observed to be significantly distributed among the haplotypes (P = MK 886 0.04) and the AAAG haplotype contributed to higher Ficolin-2 levels and to viral load. Four novel single nucleotide polymorphisms in introns (-941G>T, -310G>A, +2363G>A, +4882G>A) and one synonymous mutation in exon 8 (+6485G>T) was observed. Strong linkage was found between the variant -986G>A MK 886 and -4A>G. The very first study on Vietnamese cohort associates both Ficolin-2 serum levels andFCN2haplotypes to hepatitis B virus infection and subsequent disease progression. == MK 886 Introduction == Hepatitis caused by hepatitis B virus (HBV) is one of the most serious global health problems. HBV infects more than 350 million people worldwide and remains the major cause for acute and chronic hepatitis, liver cirrhosis and for hepatocellular carcinoma (HCC). HBV related deaths constitute approx a million people worldwide[1]. In Vietnam KIAA0700 where HBV is epidemic, individuals with chronic HBV infection were estimated around 8.4 million cases with 23,300 registered deaths in 2005[2]. Studies have well documented that genetic and other environmental factors influences the HBV predisposition. Genetic susceptibility to hepatitis has been investigated inIFNA2b,IFNAR1,HLAloci and in many interleukin related genes[3][6]. Our previous study reported the functional role of Mannose-binding lectin (MBL) gene polymorphisms to HBV disease outcome[7]. Similar to MBL, ficolins are pattern-recognition proteins involved in innate immunity that binds to specific pathogen-associated molecular patterns on the microbial surface and trigger the immune response either by binding to collectin receptors or by initiating the complement lectin pathway. Three ficolins were identified in humans: ficolin-1 (M-Ficolin), ficolin-2 (L-Ficolin) and ficolin-3 (H-Ficolin) and are encoded by the ficolin genesFCN1,FCN2andFCN3respectively[8]. The three different proteins have divergent function and are being expressed in different cells and tissues.FCN2gene, located on chromosome 9q34 consists of eight exons and is expressed primarily in liver cells[9]. Single nucleotide polymorphisms (SNPs) in theFCN2gene had been studied in different populations and was demonstrated that SNPs at positions -986G>A, -602G>A and -4A>G in the promoter region and at +6424G>T in exon 8 were significantly associated with varying serum Ficolin-2 levels and contribute towards susceptibility on many clinical infectious diseases[10][12]. Low Ficolin-2 serum levels andFCN2gene polymorphisms were associated to several infectious diseases such as respiratory infections in children and invasive pneumococcal disease in adults[13][15]. MK 886 We had earlier investigated the possible associations betweenFCN2genotypes and haplotypes to Ficolin-2 levels in rheumatic fever, rheumatic heart disease, leprosy and in malaria[16][18]. Ficolin-2 is mainly expressed in the liver where hepatitis B viruses invade, replicate and finally damage liver cells. The functional role of Ficolin-2 in HBV-infections yet remains unclear and is presumed that Ficolin-2 may possibly play role in clearance of viral particles thereby protecting the liver cells from HBV infection. A recent study has reported the functional role of L-ficolins in recognition and binding of HCV envelope glycoprotein and demonstrated serum Ficolin-2 levels were associated to HCV outcome[19]. However, to the best of our knowledge, no studies had investigated the contribution of Ficolin-2 serum levels andFCN2gene polymorphisms in HBV outcome. In this study, we aim to demonstrate the functional role of Ficolin-2 during hepatitis and investigate any possible contribution ofFCN2gene polymorphisms towards clinical progression of the HBV infection. == Materials and Methods == == Ethics statement == The study was approved by the institutional review board of the Tran Hung Dao Hospital, Hanoi. Informed written consent MK 886 was given by all participants. == Patients and controls == Four hundred and twenty three (n.