ME/CFS RESEARCH FORUM: 26-27 March 2007
University of Adelaide
Convenor: Alison Hunter Memorial Foundation
Jonathan Kerr invited to present - unable to attend.
Human parvovirus B19-associated Chronic Fatigue Syndrome (CFS); pathogenesis and treatment
Human parvovirus B19 infection is a common human infection and has been associated with various clinical manifestations of a rheumatic nature such as arthritis, fatigue, and chronic fatigue syndrome (CFS), which can persist for years after the acute phase. Development of CFS following acute B19 infection is associated with pre-existing severe emotional stress. Symptomatic B19 infection has been shown to be associated with carriage of HLA-DRB1*01, *04 and *07 alleles, and development of fatigue during the acute phase has been associated with carriage of the shared epitope (SE), a determinant which is associated with susceptibility to and severity of rheumatoid arthritis (RA). It has been demonstrated recently that acute symptomatic B19 infection is accompanied by raised circulating levels of IL-1b, IL-6, TNF-a, and IFN-g and that raised circulating levels of TNF-a and IFN-g persist in those patients who develop CFS. A resolution of both clinical symptoms and cytokine dysregulation occurs in patients with B19-associated CFS after intravenous immunoglobulin (IVIG) therapy, which is recognized to be the only specific treatment for parvovirus B19 infection. Although CFS may be triggered by various microbial infections, that triggered by B19 virus is clinically indistinguishable from idiopathic CFS and exhibits similar cytokine abnormalities and may represent an accessible model for the study of CFS. In addition, there are clear parallels between the pathogenesis of B19-associated CFS and that of Q-fever-associated CFS.
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