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Cytokine Polymorphisms Have a Synergistic Effect on Severity of the Acute Sickness Response to Infection
Vollmer-Conna U, Piraino BF, Cameron B, Davenport T, Hickie I, Wakefield D, Lloyd AR.
Clinical Infectious Disease 47:1418-1425, 2008.
Summary
Many people with CFS describe an acute flu-like illness as apparently triggering their CFS. A variety of studies have shown that around 10% of people with various acute infectious diseases (e.g., Lyme disease, mononucleosis) do not get better but go on the develop CFS and this does not reflect continued activity of the infectious agent. Those who do develop CFS following acute infection in general were more severely ill than those who spontaneously recover without sequelae. Findings of this study suggest that genetically determined variations in intensity of the inflammatory response are responsible for acute sickness response during infection.
Abstract
Background: Functional polymorphisms in immune response genes are increasingly recognized as important contributors to the marked individual differences in susceptibility to and outcomes of infectious disease. The acute sickness response is a stereotypical set of illness manifestations mediated by the proinflammatory cytokines induced by many different pathogens. The genetic determinants of severity of the acute sickness response have not previously been explored.
Methods: We examined the impact of functional polymorphisms in cytokine genes with critical roles in the early immune response (tumor necrosis factor–a, interleukin-6, interleukin-10, and interferon-g) on the severity and duration of illness following acute infection with Epstein-Barr virus, Coxiella burnetii (the causative agent of Q fever), or Ross River virus.
Results: We found that the interferon-g +874T/A and the interleukin-10_592C/A polymorphisms significantly affected illness severity, cytokine protein levels, and the duration of illness. These cytokine genotypes acted in synergy to potentiate their influence on disease outcomes.
Conclusions: These findings suggest that genetically determined variations in the intensity of the inflammatory response underpin the severity of the acute sickness response and predict the recovery time across varied infections.
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