Journal Article

Cytokine Polymorphisms Have a Synergistic Effect on Severity of the Acute Sickness Response to Infection

Uté Vollmer-Conna, Barbara F. Piraino, Barbara Cameron, Tracey Davenport, Ian Hickie, Denis Wakefield and Andrew R. Lloyd

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 47, issue 11, pages 1418-1425
Published in print December 2008 | ISSN: 1058-4838
Published online December 2008 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/592967
Cytokine Polymorphisms Have a Synergistic Effect on Severity of the Acute Sickness Response to Infection

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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–α, interleukin-6, interleukin-10, and interferon-γ) 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-γ +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.

Journal Article.  4889 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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