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.
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).
Tumor necrosis factor (TNF)-α and interferon (IFN)-γ, the pro-inflammatory Th1 cytokines are the indispensable coordinators of the inflammatory responses involved in hepatitis B virus (HBV) pathogenesis.
Tumor necrosis factor receptor superfamily member 10 (TNFRSF10) is a death domain-containing receptor for the apoptotic ligand TNFSF10, which involves multiple processes, including hepatocarcinogenesis and immune response against HBV infection.
A multiple logistic regression analysis revealed that TNF-alpha-238GA and -857CC were independently associated with chronic HB after gender and age were adjusted.
A search strategy was developed for each database using the following inclusion criteria: for participants, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and resolved or chronic HBV infection; for intervention, tumor necrosis factor (TNF) inhibitors or non-TNF biologic or nonbiologic DMARDs; and for outcome, HBV reactivation.
A20, a ubiquitin-editing protein encoded by tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) gene, is complicated in HBV infection and liver injury.
Carriers of TNF-α -1031C and -863A variant alleles had lower baseline levels of serum HBV DNA and lower liver necroinflammatory activity than dominant homozygotes.
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.
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.
Fas receptor/ligand (Fas/FasL) and the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) system plays a key role in hepatic death during HBV infection.