Hepatitis B e antigen was negative in 25% of the children who belonged to groups 1 and 3 and in 27% of the children treated with interferon gamma only.
The effect of interferon-alpha and interferon-gamma on hepatocyte HLA antigen expression was also evaluated using primary hepatocyte culture in eight patients with chronic HBV infection.
We examined the effect of recombinant human interferon-gamma on duck hepatitis B virus replication in human hepatoma cells (Huh 7) transiently transfected with cloned duck hepatitis B virus DNA.
We have previously demonstrated that hepatitis B virus (HBV) replication and gene expression are abolished in the livers of HBV transgenic mice by cytotoxic T lymphocytes (CTLs) and during lymphocytic choriomeningitis virus (LCMV) infection, stimuli that trigger the production of alpha/beta interferon, gamma interferon, and tumor necrosis factor alpha in the liver.
Cytokines such as TNF-alpha and interferon gamma (IFN-gamma) are important for the elimination of infected hepatocytes during acute hepatitis B virus (HBV) infection.
To explore the relationship between cytokines (tumor necrosis factor-alpha, interferon-gamma, interleukin-4 and interleukin-10), which expressed abnormal quantity in the peripheral blood to intrauterine hepatitis B virus infectious children, gene single nucleotide polymorphism (SNP) and susceptibility to hepatitis B virus intrauterine infection.
Our data suggest that the polymorphism at position -183 of the IFN-gamma gene promoter may be associated with susceptibility to HBV infection, and age and gender factors are coordinative risk factors.
On the basis of unconditional logistic regression analysis with adjustment for age and sex, no statistically significant association with susceptibility to persistent HBV infection was observed with the IFN-gamma, IFNGR-1 and 2, and IRF-1 gene polymorphisms under the codominant, dominant, and recessive models.
The aim of this study was to evaluate whether IFN-gamma gene polymorphisms or its haplotypes might be associated with predisposition to hepatitis B virus (HBV) infection in the Chinese population.
In summary, high-IFNG-producing alleles in intron 1 of the IFNG locus are associated with high [tsIgE] in asthmatic children from Niue and with natural immunity to the HBV in Polynesian women.
There was no difference in the HBV DNA levels during hepatitis flares between patients with genotypes B and C. Patients with genotype B had a significantly higher number of IFN-gamma producing cells [with hepatitis B core antigen (HBcAg) stimulation] and lower number of IL-10 producing cells (with HBcAg and HBeAg stimulation) compared with patients with genotype C (P = 0.011, =0.043, <0.001 respectively).
Interferon-gamma sensitizes hepatitis B virus-expressing hepatocarcinoma cells to 5-fluorouracil through inhibition of hepatitis B virus-mediated nuclear factor-kappaB activation.
PD-1 expression was assessed by (1) flow cytometry and (2) quantitative real-time polymerase chain reaction; hepatitis B virus (HBV)-specific CD8+ T-cells were quantitated by pentamer staining; T-cell reactivity to HBV antigens was determined by interferon gamma (IFNgamma) and interleukin 10 (IL-10) enzyme-linked immunosorbent spot (ELISPOT) assays; and central/effector memory phenotypes were defined by phenotypic markers.
The antiviral cascade triggered by interferon-gamma (IFN-gamma) represents a vital event for eradicating hepatitis B virus (HBV) in experimental animals.
CTLA4 +49GG genotype was associated to lower TNF-α and IFN-γ levels in patients with chronic HBV infection but this association was diminished by haplotype formation with -318C/T alleles, indicating that the influence of CTLA4 -318C/T and +49A/G polymorphisms on the susceptibility and disease progress of chronic HBV infection may not be effectuated by affecting TNF-α and IFN-γ secretion.