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T cell receptor Vbeta gene usage in Thai children with dengue virus infection.

S J GagnonCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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A LeporatiCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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S GreenCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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S KalayanaroojCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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D W VaughnCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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H A StephensCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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S SuntayakornCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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I KuraneCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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F A EnnisCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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A L RothmanCenter for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester 01655, USA.

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T lymphocyte activation during dengue is thought to contribute to the pathogenesis of dengue hemorrhagic fever (DHF). We examined the T cell receptor Vbeta gene usage by a reverse transcriptase-polymerase chain reaction assay during infection and after recovery in 13 children with DHF and 13 children with dengue fever (DF). There was no deletion of specific Vbeta gene families. We detected significant expansions in usage of single Vbeta families in six subjects with DHF and three subjects with DF over the course of infection, but these did not show an association with clinical diagnosis, viral serotype, or HLA alleles. Differences in Vbeta gene usage between subjects with DHF and subjects with DF were of borderline significance. These data suggest that the differences in T cell activation in DHF and DF are quantitative rather than qualitative and that T cells are activated by conventional antigen(s) and not a viral superantigen.

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