Interleukin-1 and Tumor Necrosis Factor-α Trigger Restriction of Hepatitis B Virus Infection via a Cytidine Deaminase Activation-induced Cytidine Deaminase (AID)*

@article{Watashi2013Interleukin1AT,
  title={Interleukin-1 and Tumor Necrosis Factor-$\alpha$ Trigger Restriction of Hepatitis B Virus Infection via a Cytidine Deaminase Activation-induced Cytidine Deaminase (AID)*},
  author={Koichi Watashi and Guoxin Liang and Masashi Iwamoto and Hiroyuki Marusawa and Nanako Uchida and Takuji Daito and Kouichi Kitamura and Masamichi Muramatsu and Hirofumi Ohashi and Tomoko Kiyohara and Ryosuke Suzuki and Jisu Li and Shuping Tong and Yasuhito Tanaka and Kazumoto Murata and Hideki Aizaki and Takaji Wakita},
  journal={The Journal of Biological Chemistry},
  year={2013},
  volume={288},
  pages={31715 - 31727}
}
Background: Cytokines and host factors triggering innate immunity against hepatitis B virus (HBV) are not well understood. Results: IL-1 and TNFα induced cytidine deaminase AID, an anti-HBV host factor, and reduced HBV infection into hepatocytes. Conclusion: IL-1/TNFα reduced host susceptibility to HBV infection through AID up-regulation. Significance: Proinflammatory cytokines modulate HBV infection through a novel innate immune pathway involving AID. Virus infection is restricted by… Expand
Role of tumor necrosis factor-α, interleukin-1β, interleukin-6 in liver inflammation in chronic hepatitis B and chronic hepatitis C
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