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• W1586891419 endingPage "6585" @default.
• W1586891419 startingPage "6577" @default.
• W1586891419 abstract "Following primary infection, human cytomegalovirus (HCMV) establishes a latent infection in hematopoietic cells from which it reactivates to cause serious disease in immunosuppressed patients such as allograft recipients. HCMV is a common cause of disease in newborns and transplant patients and has also been linked with vascular diseases such as primary and post-transplant arteriosclerosis. A major factor in the pathogenesis of vascular disease is the CC chemokine MCP-1. In this study, we demonstrate that granulocyte macrophage progenitors (GMPs) latently infected with HCMV significantly increased expression of MCP-1 and that this phenotype was dependent on infection with viable virus. Inhibitors of a subset of G(alpha) proteins and PI3K inhibited the up-regulation of MCP-1 in latently infected cultures, suggesting that the mechanism underlying this phenotype involves signaling through a G-protein coupled receptor. In GMPs infected with the low passage viral strain Toledo, up-regulated MCP-1 was restricted to a subset of myeloid progenitor cells expressing CD33, HLA-DR, and CD14 but not CD1a, CD15, or CD16, and the increase in MCP-1 was sufficient to enhance migration of CD14(+) monocytes to latently infected cells. Latent HCMV-mediated up-regulation of MCP-1 provides a mechanism by which HCMV may contribute to vascular disease during the latent phase of infection or facilitate dissemination of virus upon reactivation from latency." @default.
• W1586891419 created "2016-06-24" @default.
• W1586891419 creator A5021071538 @default.
• W1586891419 creator A5039861279 @default.
• W1586891419 date "2008-05-15" @default.
• W1586891419 modified "2023-10-16" @default.
• W1586891419 title "Human Cytomegalovirus Latent Infection of Myeloid Cells Directs Monocyte Migration by Up-Regulating Monocyte Chemotactic Protein-1" @default.
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• W1586891419 doi "https://doi.org/10.4049/jimmunol.180.10.6577" @default.
• W1586891419 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18453576" @default.
• W1586891419 hasPublicationYear "2008" @default.
• W1586891419 type Work @default.
• W1586891419 sameAs 1586891419 @default.

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