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Everett B, Cameron B, Li H, Vollmer-Conna U, Davenport T, Hickie I, Wakefield D, Vernon S, Reeves WC, Lloyd AR.
Genes and Immunity 2007;September: 13.
This publication resulted from studies of post-infection fatigue. Overall the majority of persons with CFS do not have consistent markers pointing to one infectious agent as a unifying cause of the illness. However, many people report their CFS began following an acute febrile illness and our post-infection fatigue studies with collaborators from the University of New South Wales have shown that roughly 10% of individuals with acute infectious mononucleosis, Ross River disease and acute Q fever develop CFS. We have found that acute illness severity is a risk factor for post-infection CFS and that several genetic polymorphisms are associated with increased risk for CFS. Toll-like receptors are part of the body's innate immune system, which helps control the severity of acute illness due to infection. We conducted this analysis to determine if Toll-like receptor genetic polymorphisms were associated with severity of acute Q fever. We found no correlation between the polymorphisms we studied and susceptibility to Q fever, illness severity, or illness course.
Coxiella burnetii is a macrophage-tropic, Gram-negative organism, which causes acute Q fever infection in humans. This zoonotic infection causes illness ranging from asymptomatic seroconversion to severe and protracted disease featuring hepatitis and pneumonia. Interactions between C. burnetii lipopolysaccharide (LPS) and host Toll-like receptors (TLR)-2 and -4 have been implicated in pathogen recognition, phagocytosis and signaling responses. Nonconservative single nucleotide polymorphisms in the coding regions of TLR-2 (Arg677Trp and Arg753Gln) and TLR-4 (Asp299Gly) have been found to correlate with mycobacterial infections and Gram-negative sepsis respectively. Associations between the TLR-2 and -4 polymorphisms, illness characteristics and immune response parameters were examined in subjects with acute Q fever (nž85) and comparison subjects with viral infections (nž162). No correlation was demonstrated between these polymorphisms and susceptibility to Q fever, illness severity or illness course.
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