|
|
||||||||
Published online before print August 31, 2006
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Article |
,
@
*AIDS Immunopathogenesis Unit and
Laboratory of Clinical Immunology, San Raffaele Scientific Institute, Milan, Italy; and
Vita-Salute San Raffaele University, School of Medicine, Milan, Italy
@ To whom correspondence should be addressed. E-mail: poli.guido{at}hsr.i.
| Abstract |
|---|
HIV infection of mononuclear phagocytes (MP), mostly as tissue macrophages, is a dominant feature in the pathogenesis of HIV disease and its progression to AIDS. Although the general mechanism of infection is not dissimilar to that of CD4+ T lymphocytes occurring via interaction of the viral envelope with CD4 and a chemokine receptor (usually CCR5), other features are peculiar to MP infection. Among others, the long-term persistence of productive infection, sustained by the absence of substantial cell death, and the capacity of the virions to bud and accumulate in intracellular multivescicular bodies (MVB), has conferred to MP the role of "Trojan horses" perpetuating the chronic state of infection. Because the investigation of tissue macrophages is often very difficult for both ethical and practical reasons of accessibility, most studies of in vitro infection rely upon monocyte-derived macrophages (MDM), a methodology hampered by inter-patient variability and lack of uniformity of experimental protocols. A number of cell lines, mostly Mono Mac, THP-1, U937, HL-60, and their derivative chronically infected counterparts (such as U1 and OM-10.1 cell lines) have complemented the MDM system of infection providing useful information on the features of HIV replication in MP. This article describes and compares the most salient features of these different cellular models of MP infection by HIV.
Key Words: mononuclear phagocytes latency cytokine differentiation
This article has been cited by other articles:
![]() |
M. Kader, W. M. Hassan, M. Eberly, M. Piatak, J. D. Lifson, M. Roederer, and J. J. Mattapallil Antiretroviral Therapy prior to Acute Viral Replication Preserves CD4 T Cells in the Periphery but Not in Rectal Mucosa during Acute Simian Immunodeficiency Virus Infection J. Virol., November 15, 2008; 82(22): 11467 - 11471. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Noursadeghi, J. Tsang, R. F. Miller, and D. R. Katz Comment on "Transcription Factor FOXO3a Mediates Apoptosis in HIV-1-Infected Macrophages" J. Immunol., June 15, 2008; 180(12): 7783 - 7783. [Full Text] [PDF] |
||||
![]() |
C. Elia, E. Cassol, N. Sidenius, F. Blasi, A. Castagna, G. Poli, and M. Alfano Inhibition of HIV replication by the plasminogen activator is dependent on vitronectin-mediated cell adhesion J. Leukoc. Biol., November 1, 2007; 82(5): 1212 - 1220. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. J. Montaner, S. M. Crowe, S. Aquaro, C.-F. Perno, M. Stevenson, and R. G. Collman Advances in macrophage and dendritic cell biology in HIV-1 infection stress key understudied areas in infection, pathogenesis, and analysis of viral reservoirs J. Leukoc. Biol., November 1, 2006; 80(5): 961 - 964. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |