A molecular epidemiology study investigating familial clustering of hepatitis B virus infection in families with unfavorable prognoses in Northwest China.

Hepatitis B virus (HBV) infections and adverse outcome have been demonstrated to show characteristics of familial clustering. The aim of this study was to investigate the prevalence of different HBV genotypes, HBV sub-genotypes, and Pre-S mutations associated with familial HBV infection clusters with unfavorable prognoses. Families presenting with clustered HBV infections and unfavorable prognoses were enrolled in this study.

Natural Killer Group 2A Expressed on Both Peripheral CD3CD56NK Cells and CD3CD8T Cells Plays a Pivotal Negative Regulatory Role in the Progression of Hepatitis B Virus-Related Acute-on-Chronic Liver Failure.

To explore the role of surface receptors natural killer group 2A (NKG2A) and natural killer group 2D (NKG2D) on CD3CD8T cells and CD3CD56NK cells in the progression of hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF), we measured the expression of NKG2A and NKG2D on the surface of these 2 types of circulating cells by flow cytometry in 3 groups. One group consists of 36 patients with chronic hepatitis B (CHB), another one consists of 22 patients with HBV-related ACLF, and the last one has 12 normal controls (NC). The experimental result indicated that there was no significant difference in the proportion of CD3CD8T cells in total lymphocytes between the 3 groups.

Hepatitis B virus whole-X and X protein play distinct roles in HBV-related hepatocellular carcinoma progression.

Background: The role of HBV X protein (HBx) in the development of hepatocellular carcinoma (HCC) has been well studied. However, little is known about the molecular functions of HBV whole-X protein (HBwx), a protein fused with HBx and upstream 56 amino acid, in HCC. In current study, the molecular functions of HBwx in HCC pathogenesis has been investigated, as well as comparison between HBwx and HBx.

Insulin Resistance Predicts Virological Response to Interferon-α in Chronic Hepatitis B Patients.

Goals: To elucidate impact of insulin resistance (IR) on the response to interferon-α (IFN-α) therapy in chronic hepatitis B (CHB) patients.

Background: Metabolic factors influencing the virological response of CHB patients on IFN-α treatment are still unexplored.

Study: Eighty CHB patients were treated with IFN-α for 48 weeks.

With Cytometric Bead Assay, the Interleukin-10/HBV DNA Ratio Is an Early Predictor for Response to Interferon-α Treatment in Chronic Hepatitis B.

Both host immunity and hepatitis B virus (HBV) contribute to the therapeutic response to interferon (IFN)-α treatment in chronic hepatitis B (CHB) based on the immune modulation function to eliminate virus, while neither viral load nor cytokine alone could reflect the complex interaction between host immune response and virus. This study aimed at exploring a parameter of combined immunological and virological indexes to predict the response profile to IFN-α treatment in patients with CHB. Biochemical (alanine transaminase), virological (HBV DNA load, HBsAg, HBeAg), and immunological [IFN-γ, tumor necrosis factor (TNF), interleukin (IL)-2, IL-4, IL-6, and IL-10] indexes were dynamically monitored (at baseline, 2, 4, 8, 12, 24, 36, 48, and 72 weeks) in 41 patients who received a 48-week IFN-α treatment.

Comparative study of the different activities of hepatitis B virus whole-X protein and HBx in hepatocarcinogenesis by proteomics and bioinformatics analysis.

The hepatitis B virus (HBV) whole-X gene comprises the HBV X gene and the 168-bp region immediately upstream. Although the functions of HBx in hepatocarcinogenesis are well known, the activity of the HBV whole-X protein (HBwx), with 56 additional amino acids, has not yet been explored. In this study, proteomic and bioinformatic analysis was done to determine the protein interaction profiles of HBwx and HBx and to describe their functions in carcinogenesis.

Effect of the HBV whole-X gene on the expression of hepatocellular carcinoma associated proteins.

Background: The hepatitis B virus (HBV) pre-X gene resides upstream of the HBV X gene, and together they form the HBV whole-X gene. Although it has been evident that the HBV whole-X protein is involved in the development of hepatocellular carcinoma, its biological role and molecular mechanism remain largely unknown.

Methods: In this study, we subcloned the HBV whole-X gene and constructed a HBV whole-X expressing vector.

Restoring the Treg cell to Th17 cell ratio may alleviate HBV-related acute-on-chronic liver failure.

Aim: To investigate the role of T helper 17 cells (Th17) and regulatory T cells (Treg) in hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF).

Methods: We enrolled 79 patients with HBV infection into the study, 50 patients with HBV-related ACLF and 29 patients with chronic hepatitis B (CHB), from the First Affiliated Hospital of Medical College from January 2009 to June 2012. The ACLF patients were diagnosed according to the criteria recommended by The 19(th) Conference of the Asian Pacific Association for the Study of the Liver in 2009.

[Expression of COX-2 and PPARg in the livers of patients with acute on chronic HBV-related liver failure and their relationship with clinic parameters].

Objective: To study the expressions of cyclooxygenase-2 (COX-2) and Peroxisome proliferator-activated receptor gamma (PPARg) in liver of patients with hepatitis B virus (HBV) related acute-on-chronic liver failure (ACLF) and their correlation with clinical parameters.

Methods: 35 patients with ACLF, 35 patients with HBV related chronic liver failure (CLF), 27 patients with chronic hepatitis B(CHB) and 15 normal control were enrolled to study the expressions of COX-2 and PPARg in the liver tissues by immunohistochemical staining, and to analyze the correlation of the COX-2 and PPARg levels in liver tissues with clinical parameters.

Results: COX-2 was distinctly expressed in the cytoplasm of the hepatocytes, but PPARg was mostly expressed in the nuclei of the hepatocytes and also could be seen in the cytoplasm.

The balance between intrahepatic IL-17(+) T cells and Foxp3(+) regulatory T cells plays an important role in HBV-related end-stage liver disease.

Background: IL-17(+) T helper cells and Foxp3(+) regulatory T cells are CD4(+) T helper cells with reciprocally regulated differentiation and function. Their frequency and function vary in patients with chronic hepatitis B. In this study, we investigated the balance between IL-17(+) T cells and Foxp3(+) regulatory T cells and illustrated their function in the aggravation of chronic hepatitis B (CHB).