scholarly journals Role of tumor necrosis factor-.ALPHA. in acute hepatitis B virus infection

2010 ◽  
Vol 30 (5) ◽  
pp. 445-450
Author(s):  
Hiroyasu Ito ◽  
Kazuki Ando ◽  
Tetsuya Ishikawa ◽  
Mitsuru Seishima
Keyword(s):  
Hepatitis B Virus ◽  
Virus Infection ◽  
Tumor Necrosis ◽  
Hepatitis B Virus Infection ◽  
Necrosis Factor Alpha ◽  
B Virus ◽  
Acute Hepatitis B ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor receptors in patients with chronic hepatitis B virus infection

1995 ◽  
Vol 108 (5) ◽  
pp. 1453-1463 ◽  
Author(s):  
George Marinos ◽  
Nikolai V. Naoumov ◽  
Siegbert Rossol ◽  
Francesco Torre ◽  
Philip Y.N. Wong ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Tumor Necrosis ◽  
Hepatitis B Virus Infection ◽  
Tumor Necrosis Factor Receptors ◽  
Chronic Hepatitis B Virus ◽  
B Virus ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor Alpha Inhibition of Hepatitis B Virus Replication Involves Disruption of Capsid Integrity through Activation of NF-κB

2003 ◽  
Vol 77 (7) ◽  
pp. 4033-4042 ◽  
Author(s):  
Michael Biermer ◽  
Robyn Puro ◽  
Robert J. Schneider
Keyword(s):  
Hepatitis B Virus ◽  
Tumor Necrosis Factor ◽  
Hepatitis B ◽  
Virus Replication ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
B Virus ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Chronic infection by hepatitis B virus results from an inability to clear the virus, which is associated with liver disease and liver cancer. Tumor necrosis factor alpha (TNF-α) is associated with noncytopathic clearance of hepatitis B virus in animal models. Here we demonstrate that the nuclear factor κB (NF-κB) signaling pathway is a central mediator of inhibition of hepatitis B virus by TNF-α and we describe the molecular mechanism. TNF-α is shown to suppress hepatitis B virus DNA replication without cell killing by disrupting the formation or stability of cytoplasmic viral capsids through a pathway requiring the NF-κB-activating inhibitor of κB kinase complex IKK-α/β and active transcription factor NF-κB. Hepatitis B virus replication could also be inhibited and viral capsid formation could be disrupted in the absence of TNF-α solely by overexpression of IKK-α/β or strong activation of NF-κB. In contrast, inhibition of NF-κB signaling stimulated viral replication, demonstrating that HBV replication is both positively and negatively regulated by the level of activity of the NF-κB pathway. Studies are presented that exclude the possibility that HBV inhibition by NF-κB is carried out by secondary production of gamma interferon or alpha/beta interferon. These results identify a novel mechanism for noncytopathic suppression of hepatitis B virus replication that is mediated by the NF-κB signaling pathway and activated by TNF-α.

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