Tumour necrosis factor to treat chronic hepatitis B virus infection

Nick Sheron*, Johnson Y.N. Lau, Helena M. Daniels, Jeff Webster, Adrian L.W.F. Eddleston, Graeme J.M. Alexander, Roger Williams

*Corresponding author for this work

Research output: Contribution to journalLetterpeer-review

24 Citations (Scopus)
Original languageEnglish
Pages (from-to)321-322
Number of pages2
JournalThe Lancet
Issue number8710
Publication statusPublished - 4 Aug 1990
Externally publishedYes

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and to inhibit the release of interferon beta from these cells/ The concomitant rise in HBV DNA and AST while on treatment suggests that the increase in viral replication may have been accompanied by increased lysis of hepatocytes. This study has shown that long-term outpatient treatment with rTNF is possible. There was little evidence of systemic toxicity despite the presence of very high peak plasma TNF. This finding is noteworthy in view of the postulated toxicity of TNF in septic shock, which is associated with much lower serum TNF.8 None of our patients seroconverted to HBeAb despite the initial reduction in HBV DNA. A synergistic antiviral effect has been shown between TNF and interferon alpha in vitro studies 9 The addition of IFN-fx as a more potent direct antiviral agent or a longer duration of therapy might result in complete viral clearance. By simulating natural patterns of cytokine production the effectiveness of therapy for chronic HBV infection might be enhanced. We thank Dr R. Bown, Dr B. McDougall, Dr A. Forbes, and Dr J. L. Thirkettle for their help. N.S. is supported by the Wellcome Trust and J.Y.N.L. by the Croucher Foundation.

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