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Post-infective fatigue syndrome is not associated with altered cytokine production
Vollmer-Conna U, Cameron B, Hadzi-Pavlovic D, Singletary K, Davenport T, Nisenbaum R, Vernon S, Reeves WC, Hickie I, Wakefield D, Lloyd AR
Clinical Infectious Diseases 2007, 45:732-735.
Summary
This manuscript evaluates the hypothesis that abnormalities in the immune response play a pivotal role in the pathophysiology of CFS. One problem associated with studying CFS involves the fact that most persons with the illness have been sick for many years, which makes it difficult to disentangle comorbidity due to having suffered illness for many years and pathophysiologic processes that cause the illness. In this case we followed 22 subjects who developed CFS following acute infectious mononucleosis (due to EBV), acute Q fever and acute Ross river virus disease and 42 controls who recovered uneventfully. We assessed levels of 8 cytokines at 1, 2, 3, 6 and 12 months. We did not find any differences between cytokine levels among those who developed post-infection CFS and those who recovered uneventfully. This argues against the hypothesis that prolonged fatigue is associated with altered cytokine production. These results also support other findings from this study of post-infection fatigue (see earlier publications on this and other pages) that failed to reveal substantive differences in specific antiviral immune response between subjects with CFS following infection and those who recovered promptly.
Abstract
Peripheral blood specimens and clinical data were obtained over a 12-month period from subjects in the Dubbo Infection Outcomes Study to examine cytokine production in postinfective fatigue syndrome. Ex vivo production of 8 cytokines was examined in 22 case patients and in 42 control subjects who recovered promptly. No significant differences were found. Ongoing production of the cytokines examined does not play a role in postinfective fatigue syndrome.
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