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Joint Bone Spine. 2017 Mar;84(2):217-219. doi: 10.1016/j.jbspin.2016.09.017. Epub 2016 Nov 8.

Exacerbation of hepatitis E virus infection during anti-TNFα treatment.

Author information

1
TWINCORE, Center for Experimental and Clinical Infection Research, Division of Experimental Virology, 30625 Hannover, Germany; Department for Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, 30625 Hannover, Germany; German Center for Infection Research, 30625 Hannover, Germany. Electronic address: behrendt.patrick@mh-hannover.de.
2
Department of Gastroenterology and Hepatology, Medicine I, University Medical Center Hamburg-Eppendorf, 20038 Hamburg, Germany; Medical School Brandenburg, University Medical Center II, 14770 Brandenburg an der Havel, Germany.
3
Department of Gastroenterology and Hepatology, Medicine I, University Medical Center Hamburg-Eppendorf, 20038 Hamburg, Germany.
4
TWINCORE, Center for Experimental and Clinical Infection Research, Division of Experimental Virology, 30625 Hannover, Germany.
5
Department of Nephrology and Rheumatology, Medicine III, University Medical Center Hamburg-Eppendorf, 20038 Hamburg, Germany.
6
Department for Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, 30625 Hannover, Germany; German Center for Infection Research, 30625 Hannover, Germany.

Abstract

Chronic hepatitis E virus (HEV) infection may occur in immunocompromised patients. Previous studies report that different immunosuppressive agents interfere with viral replication. However, the role of TNFα in HEV infection is currently unknown. Here, we describe a case of severe exacerbation of a chronic HEV infection in a patient undergoing treatment with a TNFα-inhibitor for psoriatic arthritis despite potent anti-HEV T-cell responses. We used state-of-the-art HEV cell culture methods to test antiviral effects of different drugs and a cytokine release assay to assess HEV specific T cell immunity. In addition standard tools of our diagnostics laboratory were employed. In vitro data confirmed inhibition of HEV replication by TNFα, which could be abolished by addition of TNFα inhibitors. Thus, TNFα may play a critical role in the control of HEV replication. We therefore recommend exclusion of HEV infection prior to initiation of TNFα-inhibitor therapy.

KEYWORDS:

Anti-TNFα therapy; Chronic infection; Exacerbation; Hepatitis E

PMID:
27836355
DOI:
10.1016/j.jbspin.2016.09.017
[Indexed for MEDLINE]

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