Russell, Alice, Hepgul, Nilay, Nikkheslat, Naghmeh, Borsini, Alessandra, Zajkowska, Zuzanna, Moll, Natalie, Forton, Daniel, Agarwal, Kosh, Chalder, Trudie, Mondelli, Valeria, Hotopf, Matthew, Cleare, Anthony, Murphy, Gabrielle, Foster, Graham, Wong, Terry, Schütze, Gregor A., Schwarz, Markus J., Harrison, Neil ORCID: https://orcid.org/0000-0002-9584-3769, Zunszain, Patricia A. and Pariante, Carmine M. 2019. Persistent fatigue induced by interferon-alpha: a novel, inflammation-based, proxy model of chronic fatigue syndrome. Psychoneuroendocrinology 100 , pp. 276-285. 10.1016/j.psyneuen.2018.11.032 |
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Abstract
The role of immune or infective triggers in the pathogenesis of Chronic Fatigue Syndrome (CFS) is not yet fully understood. Barriers to obtaining immune measures at baseline (i.e., before the trigger) in CFS and post-infective fatigue model cohorts have prevented the study of pre-existing immune dysfunction and subsequent immune changes in response to the trigger. This study presents interferon-alpha (IFN-α)-induced persistent fatigue as a model of CFS. IFN-α, which is used in the treatment of chronic Hepatitis C Virus (HCV) infection, induces a persistent fatigue in some individuals, which does not abate post-treatment, that is, once there is no longer immune activation. This model allows for the assessment of patients before and during exposure to the immune trigger, and afterwards when the original trigger is no longer present.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Publisher: | Elsevier |
ISSN: | 0306-4530 |
Date of First Compliant Deposit: | 2 April 2019 |
Date of Acceptance: | 23 November 2018 |
Last Modified: | 05 May 2023 02:02 |
URI: | https://orca.cardiff.ac.uk/id/eprint/121304 |
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