|
|
||||||||
Published online before print August 25, 2006
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||




* The Wistar Institute, Philadelphia, Pennsylvania, USA;
Macfarlane Burnet Institute for Medical Research and Public Health, National Centre for HIV Virology Research, Melborne, Victoria, Australia;
Department of Experimental Medicine and Biochemical Sciences, University of Rome "Tor Vergata," Rome, Italy;
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA; and
¶ Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
1 Correspondence: The Wistar Institute, 3601 Spruce St., Philadelphia, PA 19104-4268. E-mail: montaner{at}wistar.org
ABSTRACT
The continued quest to intervene in HIV-1 infection by halting transmission, suppressing replication, or eradicating disease in infected subjects stresses the significance of dendritic cell and macrophage biology as early and persistent players in the relationship between infection and disease. As highlighted by new data and presentations at the Sixth International Workshop on HIV and Cells of Macrophage/Dendritic Lineage and Other Reservoirs, a greater emphasis is currently underway in studying the potential of targeting these cell types by intervention early in infection, better defining viral phenotypes and entry mechanisms with a more precise nomenclature system, identifying new, intrinsic cellular factors that may restrict infection within these cell types, and pursuing novel roles for macrophage activation and trafficking. Other key areas include examination of these cells as sources of viral persistence in patients, their roles in coinfection, and their metabolic function in HIV pathogenesis and drug toxicity. This issue of JLB contains reviews and original research reports from the workshop, which highlight new findings, current research questions, and key areas in need of future investigation as a result of their significance to HIV prevention and pathogenesis.
Key Words: monocyte
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |