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Viral infection triggers rapid differentiation of human blood monocytes into dendritic cells

tetano

Editor, Senior Moderator
Published online before print February 6, 2012, doi: 10.1182/blood-2011-09-379479 Blood February 6, 2012 blood-2011-09-379479


Viral infection triggers rapid differentiation of human blood monocytes into dendritic cells

Wanqiu Hou1,
James S. Gibbs1,
Xiuju Lu1,
Christopher B. Brooke1,
Devika Roy2,
Robert L. Modlin3,
Jack R. Bennink1, and
Jonathan W. Yewdell1,*

+ Author Affiliations

1 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States;
2 Division of Dermatology, Department of Medicine, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA, United States;
3 Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA, United States

↵* Corresponding author; email: jyewdell@nih.gov

Abstract

Surprisingly little is known about the interaction of human blood mononuclear cells with viruses. Here, we show that monocytes are the predominant cell type infected when peripheral blood mononuclear cells are exposed to viruses ex vivo. Remarkably, infection with vesicular stomatitis virus, vaccinia virus and a variety of influenza A viruses (including circulating swine origin virus) induces monocytes to differentiate within 18 h into CD16-CD83+ mature dendritic cells (DCs) with enhanced capacity to activate T cells. Differentiation into DCs does not require cell division, and occurs despite the synthesis of viral proteins, demonstrating that monocytes counteract the capacity of these highly lytic viruses to hijack host cell biosynthetic capacity. Indeed, differentiation requires infectious virus and viral protein synthesis. These findings demonstrate that monocytes are uniquely susceptible to viral infection among blood mononuclear cells, with the likely purpose of generating cells with enhanced capacity to activate innate and acquired anti-viral immunity.

http://bloodjournal.hematologylibrary.org/content/early/2012/02/06/blood-2011-09-379479.abstract
 
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