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Background & objectives: Clinical outcome after hepatitis B virus (HBV) exposure varies extremely from spontaneous clearance to chronic hepatitis B and often progresses to liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Host genetic factor plays an important role in the regulation of immune response. This study was aimed to investigate whether HLA class II DQA1 and DQB1 gene polymorphism were associated with chronic hepatitis B infection and in the development of HBV-related LC and HCC. Methods: DQA1 and DQB1 allele polymorphism were studied in 187 patients with HBV-related liver diseases (which included 73 chronic hepatitis B, 84 LC and 30 HCC patients) and 109 controls who had spontaneously recovered from HBV infection using polymerase chain reaction amplification with sequence-specific primers. Results: Our data suggested that DQA1*0101/2/4 [odds ratio (OR)=2.78; Pc=0.003], DQA1*0103 (OR=2.64; Pc=0.0007) and DQB1*0302/3 (OR=2.15; Pc=0.01) were associated with the protection from chronic HBV infection, whereas DQB1*0402 (OR=0.25; Pc=0.001) showed susceptible effect on chronic HBV infection. DQB1*0601 (OR=3.73; Pc=0.006) conferred protective effect from developing LC; similarly, DQB1*0302/3 (OR=5.53; Pc=0.05) and DQB1*0402 (OR=0.00; Pc=0.001) conferred protective effect from developing HCC. However, DQA1*0601 and DQB1*0503 showed susceptible effect on chronic HBV infection; these associations were no longer significant after Bonferroni correction. Interpretation & conclusions: Our results revealed HLA-DQA1*0101/2/4 - DQA1*0103 - DQB1*0302/3 and DQB1*0601 as protective and DQB1*0402 as risk alleles. The study suggests that various subtypes of HLA-DQA1 and DQB1 are associated with both HBV clearance and development of chronic HBV infections.

Summary The basis of hepatitis C virus (HCV) evasion of immune system and its response to treatment is still elusive. There have been studies where the level of C4 has been found to be associated with HCV persistence and disease progression. This study aims to find out relationship between levels of C4 in serum, and its functional SNPs with response to treatment. The study included 84 patients with CHC who received treatment and 75 healthy controls. C4 expression, both at mRNA and protein level, was estimated by Real time and ELISA respectively. Its functional SNP's genotyped by AS-PCR. The mean ± SD baseline C4 levels between the disease and healthy cases was significantly different (1075.74 ± 65.25 vs 1593 ± 24.55 ng/mL, P

Background/objective Quantification of serum hepatitis B antigen (HBsAg) is an important test that marks active infection with hepatitis B and helps in the prediction of the clinical outcome and management of hepatitis B virus (HBV) infection. Correlation with HBV DNA quantitative levels may help in developing strategies for antiviral treatment. This study is aimed to evaluate HBsAg titres in various phase of HBV infection in HBsAg positive patients, and its correlation with HBV DNA viral load levels. Methods 976 HBV related patients were analysed in this retrospective cross-sectional study. Patients were categorised on the basis of the phase of HBV infection: immune tolerant phase (IT, n =123), immune clearance phase (IC, n =192), low-replicative phase (LR, n =476), and HBeAg-negative hepatitis (ENH, n =185). HBsAg titres were quantified and correlated with HBV-DNA levels and clinical parameters. Results Median HBsAg titres were different between each phases of HBV infection ( P r =0.694, P r =0.603, P r =0.523, P r =0.362, P r =0.110, P =0.04). No correlation was observed between serum HBsAg levels and biochemical parameters. Conclusion The study demonstrated significant difference in the median baseline values of serum HBsAg titres in different phases of HBV infection and provides additional information in understanding the natural history of HBV-infection.

Background and aim Progression of hepatitis B virus infection (HBV) might be affected by host genetic factors. The present study was undertaken to study the role of glutathione S-transferases (GST)-M1 and T1 gene polymorphisms in different stages of HBV infection: HBV inactive carrier, chronic hepatitis B and cirrhosis, and cryptogenic cirrhosis. Methods The study population comprised of 170 subjects; 120 cases (HBV inactive carrier, n =30; HBV related chronic hepatitis, n =30; HBV related cirrhosis, n =30; cryptogenic cirrhosis, n =30) and 50 unrelated healthy adults without liver disease as controls. Analysis of GSTM1 and GSTT1 gene polymorphisms was done by multiplex polymerase chain reaction. Results The GSTM1 null genotype was seen more commonly in hepatitis B cirrhosis ( n =21; 70%), chronic hepatitis B ( n =19; 63.33%) and cryptogenic cirrhosis ( n =17; 56.67%) as compared with inactive carrier ( n =9; 30%) and controls ( n =13; 26%). The GSTT1 null genotype was seen less frequently in all the groups, the observed frequencies were controls ( n =7; 14%), inactive carrier ( n =5; 16.67%), chronic hepatitis B ( n =8; 26.67%) and hepatitis B cirrhosis ( n =7; 23.33%). The difference of GSTM1 null genotype frequencies was statistically significant for hepatitis B cirrhosis vs. controls ( P =0.0002), chronic hepatitis B vs. controls ( P =0.002) and cryptogenic cirrhosis vs. controls ( P =0.01). The GSTT1 null genotype was not found to vary significantly between the groups. Conclusion The patients with GSTM1 null genotype are at risk of progression of liver disease as the frequency of GSTM1 null genotype was found to be significantly higher in chronic hepatitis B, hepatitis B cirrhosis and cryptogenic cirrhosis as compared with controls.

Interleukine-18 (IL-18) was originally called interferon (INF-γ) inducing factor and plays a critical dual role in Th1 polarization and viral clearance. We aimed to explore whether single-nucleotide promoter polymorphisms (SNPs) are associated with the outcome of hepatitis B virus (HBV) infection. 271 HBV infected patients were recruited in this study out of these 109 were spontaneously recovered and 162 were diagnosed to be having persistent HBV infection which includes 48 chronic hepatitis, 84 liver cirrhosis, 30 HCC cases and were compared with 280 healthy controls. IL-18 promoter genotyping was performed with sequence-specific primers. The results demonstrated the significant involvement of genotype AA at position -607 in healthy controls (38.6%) when compared to cases (26.0%) (OR = 0.54 (0.385–0.797)) and also associated with spontaneous clearance (37.6%) compared to persistent HBV infections (17.9%) (OR = 2.76 (1.582–4.832)). Whereas, genotype CC at position -607 in cases (18.0%) when compared to healthy controls (6.7%) (OR = 3.03 (1.734–5.303)) also associated with persistent HBV infections (24.1%) compared to spontaneous clearance (9.2%) (OR = 0.31 (0.151–0.67)). And genotype GC at position -137 in cases (49.5%) compared to healthy controls (38.5%) (OR = 1.55 (1.11–2.18)). Whereas, genotype GG at position -137 in healthy controls (56.8%) compared to cases (45.4%) (OR = 0.63 (0.451–0.885)). No significant difference at position -137 was observed between spontaneous clearance and persistent HBV infections. These polymorphisms of the IL-18 gene promoter region at position -607 and -137 could be associated with different outcomes of HBV infection. The people with allele A at position -607 may be protected against HBV infection; moreover AA genotype is associated with spontaneous clearance.

Hepatitis E has both a high incidence and severe course in pregnant women in some geographic regions of HEV (Hepatitis E virus) endemic countries. Intrauterine fetal death, preterm delivery, and perinatal mortality are reported to be higher in pregnant women with HEV infection. Alteration in the steroid hormone levels show high incidence of FHF (Fulminant Hepatic Failure) with high mortality in hepatitis E during pregnancy. The present study is designed to look for the association between ESR (Estrogen Receptor)-beta gene polymorphism for Alu I restriction site and pregnancy outcome. The study group comprised of 142 pregnant women with HEV infection in third trimester, 103 AVH (Acute Viral Hepatitis) cases and 39 ALF (Acute Liver Failure) cases. The control group comprised of 142, age and gestation matched healthy pregnant women with no obstetrics and medical complications. The inclusion criteria for the study group are pregnant women in third trimester with positivity to HEV IgM and/or HEV RNA in the age group of 18-40 years. Genomic DNA is extracted from peripheral blood leukocytes using DNA extraction kit according to the manufacturer’s instructions. The polymorphism study is done by using ESR2 specific primers and its genotype is determined by Alu I restriction enzyme. The occurrence of variant A allele for AluI restriction site is significantly higher in mothers with HEV infection who had preterm (25%) than full term delivery (10%) with OR 2.989 (95% CI = 1.265-8.084, p