New research from the University of New South Wales (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 US 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 Centres 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.