The present paper investigated possible correlations between the clinical presentation of hepatitis B and the TNF-α-308G/A, IFN-γ +874A/T, TGF-beta1 -509C/T, and IL-10 -1081A/G polymorphisms and associated serum levels of these cytokines.
Genotype frequencies of TNF-alpha gene promoter at position -308 and -238 were not different between the clearance and the persistence group in univariate analysis, but in multivariate analysis after adjusting for age and sex, -308G/-238G homozygotes were associated with HBV persistence (P = 0.005).
Persistent HBV infection susceptibility is associated with the TNF-α-308G/A gene polymorphism in the Chinese population, whereas HBV clearance is associated with the TNF-α-857C/T gene polymorphism.
Receptivity of human choriocarcinoma JEGIII cells and isolated trophoblast cells to hepatitis B virus infection and enhancement by tumor necrosis factor alpha.
Hepatitis B virus (HBV) gene expression is downregulated in the liver of HBV transgenic mice by a posttranscriptional mechanism that is triggered by the local production of gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) during intrahepatic inflammation (hepatitis).
In early onset hepatitis, serum levels of TNF-α, which primarily cause inflammation and hepatocyte apoptosis, were significantly lower in Dcir1<sup>-/-</sup> mice than in WT mice.
More studies on individuals from various ethnic groups will be necessary to determine the role of TNF-<alpha> promoter polymorphisms in the outcome of HBV infection.
Even in an area of previously high HBV endemicity, where occult HBV infection is likely to have a high prevalence, treatment of rheumatological patients with anti-TNF drugs is safe in terms of its potential to reactivate HBV.
Hepatitis B Virus Screening and Reactivation in a National VA Cohort of Patients with Inflammatory Bowel Disease Treated with Tumor Necrosis Factor Antagonists.
Hepatitis B Vaccination Induced TNF-<i>α</i>- and IL-2-Producing T Cell Responses in HIV- Healthy Individuals Higher than in HIV+ Individuals Who Received the Same Vaccination Regimen.
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.
The electronic medical records from October 2009 to December 2015 of patients diagnosed with IBD at 10 years of age or younger and prescribed anti-tumor necrosis factor alpha (anti-TNF-α) therapy were reviewed for clinical history, medication history, vaccination history, and hepatitis B and varicella titers.
To describe and quantify the incidence and morbidity of hepatitis B reactivation (HBVr) secondary to pharmaceutical agents (eg, rituximab, tumor necrosis factor inhibitors, direct-acting antivirals [DAAs] for hepatitis C) among patients with previously resolved hepatitis B infection.
Therefore, Tupaia TNF-α may contribute significantly to the control of HBV infection though it is not able to completely inhibit HBV replication alone.
Our findings suggest that activation of Tnf-Aicda axis and co-inhibitory signals to T cells in coordination with Th1-type immunity has critical roles in the immune response against HBV infection.