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Human herpesvirus 7 infection increases the expression levels of CD46 and CD59 in target cells.

作者信息

Takemoto Masaya, Yamanishi Koichi, Mori Yasuko

机构信息

Laboratory of Virology and Vaccinology, Division of Biomedical Research, National Institute of Biomedical Innovation, 7-6-8 Saito-Asagi, Ibaraki, Osaka 567-0085, Japan.

出版信息

J Gen Virol. 2007 May;88(Pt 5):1415-1422. doi: 10.1099/vir.0.82394-0.

Abstract

CD46 (membrane cofactor protein; MCP) is a molecule that functions as either a complement-regulatory protein (CRP) or a receptor for some pathogens, including human herpesvirus 6. DNA microarray analysis suggested that the expression of CD46 was upregulated in T cells infected with human herpesvirus 7 (HHV-7). Northen and Western blot analyses supported this result at both the transcriptional and translational levels. Flow-cytometric analysis revealed that upregulation of CD46 occurred at a late stage of infection in both SupT1 cells and primary CD4+ T cells, and also that expression of another CRP, CD59, was increased at a late stage of infection. Whether these CRPs actually function in HHV-7-infected cells was addressed and it was found that HHV-7-infected cells were more resistant to complement-dependent cytotoxicity than were uninfected cells. This study is the first report demonstrating that HHV-7 infection causes elevation of the CRPs CD46 and CD59, which may be a possible mechanism for HHV-7 to evade humoral immunity via complement.

摘要

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