HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (Papers in Press[PDF]) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Moi, M. L. Articles by Kurane, I. PubMed PubMed Citation Articles by Moi, M. L. Articles by Kurane, I. Agricola Articles by Moi, M. L. Articles by Kurane, I.

Involvement of the Fc receptor IIA cytoplasmic domain in antibody dependent enhancement of dengue virus infection

Department of Virology I, National Institute of Infectious Diseases

¹ E-mail: kurane{at}nih.go.jp

Subneutralizing concentrations of antibody to dengue virus enhance dengue virus infection of Fc receptor-expressing cells. This phenomenon, referred to as antibody dependent enhancement (ADE), has been hypothesized to be responsible for the severe form of dengue virus infection, including dengue hemorrhagic fever and dengue shock syndrome. To further analyze the mechanisms of ADE in vitro, we introduced a series of cytoplasmic mutants to human FcRIIA. We then expressed the mutated FcRIIA on COS-7 cells and examined whether these mutants could enhance dengue virus infection. Wild type FcRIIA enhanced dengue virus infection, consistent with previous reports using FcR-positive monocytes. Disruption of the immune tyrosine activation motif (ITAM) in the cytoplasmic domain of FcRIIA or removing the sequences between the two ITAM regions abrogated ADE. These findings suggest that the specific structure of the FcRIIA cytoplasmic domain is essential for the ability of FcRIIA to mediate ADE.

Received 10 July 2009; accepted 20 September 2009.