by University of New South Wales
September 26, 2007
Following is a press release issued September 14, 2007 on behalf of the Dubbo (Australia) Infectious Outcomes Study by the University of New South Wales (UNSW). It refers to the study team's report dated September 15, "Postinfective Fatigue Syndrome Is Not Associated with Altered Cytokine Production."
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New research from UNSW has delivered a final blow* to the theory that Chronic Fatigue Syndrome (CFS) is driven by the body’s immune system and in particular by its production of cytokines.
Attention has now turned to the brain and neural-level reactions as the syndrome’s likely source.
The research, led by Dr. Uté Vollmer-Conna at UNSW’s School of Psychiatry, represents the latest findings in the Dubbo Infectious Outcomes Study and is the most comprehensive and definitive of its type. It is published this week in the prestigious U.S. journal Clinical Infectious Diseases.
The study team, including Professor Andrew Lloyd and Ms. Barbara Cameron from UNSW’s Centre for Infection and Inflammation Research, and collaborators from the University of Sydney and the Atlanta-based Centers for Disease Control and Prevention, found that cytokines production in patients suffering from Post Infective Fatigue Syndrome (PIFS) up to a year after the acute viral infection was no different from those in control patients who had promptly recovered.
PIFS is a well-recognized empirically established illness model permitting prospective study of pathophysiological pathways to CFS.
The study results show that while raised production of cytokines – a group of proteins instrumental in the orchestration of the host immune responses - is likely to be an initial trigger for CFS, it is not responsible for the ongoing symptoms.
Dr. Vollmer-Conna says the most reliable predictor of chronic fatigue following from an acute infection is the severity of the initial viral illness.
“Our group has ruled out the ongoing symptoms being related to abnormal antibody responses, differences in viral load and now to cytokines, “ Dr Vollmer-Conna says. “We are now focusing our attention on the brain because these findings suggest a change takes place at neural pathways in the central nervous system.”
But Dr. Vollmer-Conna stresses this is certainly not the same as saying CFS is all in the mind.
“Rather we believe that an immunological stressor, such as a severe acute infection with certain pathogens, promotes prolonged sensitization in neural systems involved in receiving and interpreting information about symptoms from the body. We are now investigating potential changes in the autonomic nervous system and central nervous system circuits that could explain ongoing symptoms in post-infective and chronic fatigue syndromes.”
MEDIA CONTACTS: Dr. Uté Vollmer-Conna (
ute@unsw.edu.au) 9385 2945, 9344 5534. Steve Offner, UNSW Media Office, 9385 1583 or 0424 580 208.
*Note, some observers have objected to the term "final blow" considering the small size of the study.
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