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Published online before print September 2, 2003

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(Journal of Leukocyte Biology. 2003;74:631-634.)
© 2003 by Society for Leukocyte Biology

HIV and cells of macrophage/dendritic lineage and other non-T cell reservoirs: new answers yield new questions

Ronald G. Collman^*, Carlo-Federico Perno, Suzanne M. Crowe, Mario Stevenson and Luis J. Montaner^¶,1

^* Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia;
Department of Experimental Medicine, University of Rome "Tor Vergata," Italy;
Macfarlane Burnet Institute for Medical Research and Public Health, National Centre for HIV Virology Research, Melbourne, Victoria, Australia;
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester; and
^¶ The Wistar Institute, Philadelphia, Pennsylvania

¹ Correspondence: The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104-4268. E-mail: montaner{at}wistar.upenn.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 
Defining how human immunodeficiency virus (HIV) interacts with macrophages, dendritic cells (DC), and other non-T cell reservoirs remains a critical area of research despite widespread use in the developed world of highly active antiretroviral therapy. In fact, as highlighted at the Fifth International Workshop on HIV and Cells of Macrophage/Dendritic Lineage and Other Reservoirs, as viral suppression in T cells becomes increasingly effective, these alternative reservoirs may take on even greater relative importance as sites for viral persistence and as a target for purging. These cells may be especially important reservoirs in several critical settings of clinical relevance, and there are major differences in the molecular mechanisms that regulate HIV replication in these cells compared with T cells. Dysfunction of these cells may also play a major role in particular aspects of pathogenesis. Three broad themes emerged from the workshop regarding areas of recent progress, which also serve to identify current research challenges of (i) determining the role played by macrophages, DC, and other non-T cell viral targets in transmission and dissemination and as viral reservoirs at various stages of disease and in different compartments in vivo; (ii) identifying the molecular mechanisms by which virus–cell interactions affect the inflammatory, immune, and other functions of these cells; and (iii) defining the unique pathways that regulate infection and replication in these cellular compartments. This issue of JLB contains several reviews and original reports resulting from the workshop that address recent progress and highlight the current research questions regarding these cell types.

Key Words: HAART • HIV encephalopathy • nerve growth factor • monocyte

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 
Why should there be an issue of JLB focused on macrophages, dendritic cells (DC), and other non-T cell reservoirs in human immunodeficiency virus (HIV) infection? Is studying how HIV interacts with these cells still a relevant area of research in the era of highly active antiretroviral therapy (HAART)? The answer from the fifth meeting of the International Workshop on HIV and Cells of Macrophage/Dendritic Lineage and Other Reservoirs, held in Rome in October 2002, was a resounding yes for three reasons. First, as discussed in several workshop presentations and articles in this issue, as viral suppression in T cells becomes increasingly effective, the role of alternative reservoirs as sites for viral persistence and as a target for purging takes on even greater relative importance. As discussed below, these cells appear to be particularly important reservoirs in several critical settings of major clinical relevance. Second and also discussed below and in this issue, there are marked differences between T cells and macrophage/DC/other non-T cell reservoirs in the cellular and molecular mechanisms that regulate the effects of HIV replication. Thus, findings in lymphocytes cannot necessarily be extrapolated to the other cell types, which require independent investigation. Finally, it has long been known that macrophages and related cells are the site of infection in several organs and play a critical role in the pathogenesis of HIV encephalopathy (HIVE). Despite widespread use of HAART in the developed world, HIVE remains an important clinical problem. Thus, mechanisms of cellular dysfunction, including inflammatory and neurotoxic consequences, as well as innate-immune dysfunction, remain a critical area for understanding pathogenesis and defining novel targets for intervention.

The workshop, which convenes every 3 years, originally grew out of studies of HIV–macrophage interactions. Macrophages and DC remain the principal recognized non-T cell compartments involved in HIV infection in vivo, and these cells clearly play important and well-established roles in multiple aspects of pathogenesis. An expanding range of other cell types are now also included among potential reservoirs, such as natural killer cells, CD8 cells, B cells, endothelia, glia, and others, although the extent to which they are infected in vivo and what if any roles they might play in pathogenesis remain poorly understood.

The goal of this issue, like the workshop on which it is based, is to focus on progress made over the last few years in understanding the unique molecular, viral, and pathogenesis questions associated with infection of these cell types. Emerging from the presentations were three broad themes reflecting areas of significant progress, which also highlight critical avenues for future research. These areas are defining the role played by macrophages, DC, and other non-T cell viral targets in transmission, dissemination, and as viral reservoirs; determining the mechanisms by which virus–cell interactions affect the inflammatory, immune, and other functions of these cells; and identifying the unique pathways and mechanisms that regulate infection and replication in these cellular compartments.

	MACROPHAGES, DC, AND OTHER NON-T CELL RESERVOIRS IN HIV INFECTION

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 
A major theme of the workshop was understanding what role these cells play as a reservoir for infection in vivo and in sustaining replication during different phases of infection. In this area, there have been significant, recent developments. In contrast to previously held dogma, Crowe (Fairfield, Australia) and Zhu (Seattle, WA) [¹ ] demonstrated substantial infection of blood monocytes in infected individuals. Crowe demonstrated that the CD14^lo/CD16^high monocyte subpopulation represents the susceptible target in vitro and principal reservoir in vivo, and Zhu showed that monocytes are a principal site of ongoing, subclinical viral replication in subjects who are "completely" suppressed on HAART therapy.

Addressing tissue sites of infection, Smith (Birmingham, AL) et al. [² ] provide evidence for macrophage infection in the gut. Although the prevalence of HIV-1-infected macrophages is low (0.06%) in the gastrointestinal mucosa, the size of the overall anatomical compartment argues for a prominent role of this reservoir in vivo. Infection of perivascular macrophages in the central nervous system (CNS) has been well established in HIV and simian immunodeficiency virus (SIV), and Williams (Boston, MA) and co-workers [³ ] discussed the relationship between bone marrow macrophages, blood monocytes, and cellular trafficking in CNS viral entry. In contrast, Dejucq (Rennes, France) reported that Leydig cells, testicular cells not belonging to a macrophage line, cannot serve as a reservoir for HIV.

Investigating late-stage disease, Martin (Bethesda, MD) and co-workers [⁴ ] discussed his SIV/HIV chimeric virus (SHIV) model showing that once T cells are extensively depleted, continued, high-level viremia is supported by infected macrophages, and furthermore, specific mutations, which confer in vitro macrophage tropism, arise in the env V2 region at this stage. Also relevant to later stages of infection, Goodenow (Gainesville, FL) and co-workers [⁵ ] presented evidence that drug-resistant viruses have a selective fitness advantage in macrophages compared with T cells, in which they exhibit markedly reduced fitness, suggesting that macrophages may serve as a particularly important reservoir in subjects who harbor drug-resistant virus.

Taken together, these data indicate that monocytes and macrophages are sites of infection in vivo and may be especially important in specific circumstances, including sustaining low-level replication and genetic evolution during HAART (perhaps contributing to the emergence of resistant virus) and maintaining viral replication in the setting of drug resistance, late in disease when few T cell targets remain and in specific organs, such as brain (contributing to the pathogenesis of HIVE) and gut (perhaps playing a role in transmission).

Given the importance of this reservoir, several investigators presented novel approaches that might be used for selective targeting and elimination of the macrophage reservoir. Magnani (Urbino, Italy) and co-workers [⁶ ] showed that infected macrophages express activated signal transducer and activator of transcription (STAT)1 and are particularly sensitive to the nucleoside analog fludarabine. He used this approach in combination with red blood cell ghost loading to specifically target these phagocytic cells to eliminate infected macrophages. Perno (Rome, Italy) reported that nerve growth factor (NGF) functions as an autocrine trophic factor for survival of infected macrophages and that NGF neutralization can be used to kill infected macrophages: Scid-hu mice reconstituted with human lymphocytes and infected macrophages showed complete loss of CD4 lymphocytes, and treatment with neutralizing NGF antibody leads to undetectable viremia and complete rescue of CD4 lymphocytes. McGrath (San Francisco, CA), who described that HIV infection can alter macrophage phenotype through insertional activation, presented evidence that this subset may also be selectively susceptible to killing by polyamine analogs. Aquaro (Rome, Italy) showed that inhibiting superoxide blocks HIV replication in macrophages and neural cell apoptosis triggered by infected macrophages, and Schols (Leuven, Belgium) and co-workers [⁷ ] discussed a new compound with anti-HIV activity in macrophages and lymphocytes that is mediated by CD4 down-modulation. Thus, a number of strategies may be available that have the potential to specifically target this reservoir for viral suppression and/or infected cell purging.

These findings suggest several avenues of research that are critical to pursue: defining the site and timing of monocyte/macrophage infection in vivo and how cellular trafficking relates bone marrow, blood, and tissue reservoirs; determining the relative importance of each of these reservoirs in different phases of disease, tissue compartments, and treatment circumstances; and developing effective strategies designed to specifically target this reservoir, to achieve complete viral suppression, and to purge latently or persistently infected elements in this long-lived cell population.

	HIV ALTERATIONS ON CELLULAR FUNCTION

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 
Although monocytes, macrophages, and other non-T cell reservoirs are not substantially depleted in HIV infection, alterations of function have been recognized for many years. It is well established that these functional effects play important roles in neurological disease, in AIDS, and in defective innate immunity, but exactly how HIV elicits these effects has remained elusive. A new theme at this workshop was the identification of specific cellular and molecular mechanisms by which HIV alters macrophage or DC functions.

Focusing on aberrant activation, Collman (Philadelphia, PA) and co-workers [⁸ ] showed that in addition to mediating entry and infection, engagement of macrophage chemokine receptors by gp120 as free protein or on noninfectious virus activates a range of intracellular pathways including ionic and protein kinase signaling, with consequent secretion of soluble mediators. Stevenson (Worcester, MA) discussed mechanisms by which intracellular Nef in infected macrophages hijacks the CD40/CD40 ligand-activation pathway, induces B cells to activate T cells, and thereby enhances permissiveness to infection. Nef was also the focus of Olivetta (Rome, Italy), who showed that exogenous and intracellular Nef elicit inflammatory cytokine secretion by macrophages through nuclear factor-B-dependent pathways and STAT1/STAT3 activation. Pope (New York, NY) and co-workers [⁹ ] described how HIV exploits activation pathways in DC to enhance viral expansion by stimulating soluble products that activate T cells during DC–T cell interactions and also identified a role for Nef. Each of these mechanisms may contribute to aspects of disease in which inappropriate activation occurs, including HIVE, in which macrophage/microglia activation plays a critical role, and viral dissemination, where T cell activation associated with infection serves as an especially effective mechanism of viral expansion. Finally, the complex interactions between HIV-infected macrophages and neuronal injury were discussed by Persidsky (Omaha, NE), who provides an overview in this issue of these complex interactions, and Gendelman (Omaha, NE) [¹⁰ ], who reported that the transcriptional activator OTK18 is up-regulated in macrophages following HIV infection in vitro and is elevated in HIVE brain in vivo.

Mechanisms underlying defective immune function were also the focus of significant new findings. Kedzerska (Melbourne, Australia) presented data on specific intracellular pathways by which HIV infection suppresses FcR and complement-mediated macrophage phagocytosis. Montaner (Philadelphia, PA) and co-workers reported the selective loss of CD123⁺ plasmacytoid DC in vivo, which correlated closely with viral load, and this issue also describes the association between cytokine regulation of DC-specific intercellular adhesion molecule-3-grabbing nonintegrin (SIGN) and viral transmission by macrophages [¹¹ ]. Chougnet (Cincinnati, OH) and co-workers [¹² ] discussed evidence that HIV interferes with macrophage antigen presentation by disrupting CD40/CD40L costimulatory pathway, and Di Marzio (Manhasset, NY) used soluble trimeric CD40L to dissect the pathways involved in CD40-mediated macrophage stimulation. Finally, Porcheray (Fontenay aux Roses, France) presented the notion that HIV infection shifts macrophages away from the alternative (anti-inflammatory) pathway of activation and toward the classical (proinflammatory) activation phenotype.

What these reports highlight is that specific molecular mechanisms are now emerging to explain how HIV alters cellular function. In addition to continuing to unravel the molecular interactions responsible, critical avenues for future research will be to define the extent to which these processes operate in vivo and contribute to viral dissemination, organ system dysfunction, and other specific aspects of pathogenesis to identify therapeutic strategies that can interfere with pathways through which HIV induces cell dysfunction.

	UNIQUE MECHANISMS THAT REGULATE HIV REPLICATION IN NON-T CELL RESERVOIRS

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 
Many advances have been made over the past decade in understanding how infection and replication in macrophages and other cell types differ from that in T cells, such as the role of auxiliary genes in nondividing cell infection and the use of distinct chemokine receptors for entry. The cell-specific mechanisms that regulate infection and replication in these cell types continue to be of great interest, and cellular and molecular factors involved in infection and replication in these reservoirs were addressed in this workshop.

Cell-specific factors involved in entry and early stages of infection remain an important focus. Much progress has been made in the past several years defining entry-enhancement factors such as DC-SIGN, and Cunningham (Westmead, Australia) and co-workers [¹³ ] discussed the expanding group of C-type lectins, which serve as virus stabilization and entry-enhancement factors on various subsets of DC. Conversely, Schwartz (Paris, France) discussed an alternative-entry pathway for HIV in myeloid DC, which leads to degradation. Schmidtmayerova (Manhasset, NY; ref. [¹⁴ ]) addressed differences between macrophages and T cells in the ability of regulated on activation, normal T expressed and secreted (RANTES) to suppress CCR5-mediated entry. Those studies demonstrated that macrophages resist the protective effect of RANTES, as unlike T cells, macrophages rapidly clear RANTES from the media and also fail to secrete other CCR5-inhibitory b-chemokines upon RANTES stimulation. The viral genetics that regulate cell- and compartment-specific infection were addressed by Simmons (Edinburgh, UK), who used new approaches to genetic analysis of viral sequences in brain, lung, colon, bone marrow, and lymph node to suggest that organ-specific clustering is not as prominent as had been reported previously.

Regulation of replication in macrophages at post-entry stages were addressed by Gessani (Rome, Italy) and co-workers [¹⁵ ], who described a complex network of reciprocal regulation, whereby HIV stimulates macrophages to secrete several cytokines and chemokines, which then modulate cellular permissiveness to infection and replication. Rizzi (Milan, Italy), who showed that the B oligomer of pertussis toxin suppresses macrophage infection by inhibiting interleukin (IL)-6/IL-8 autocrine pathways needed to maintain basal replication, also addressed complex cytokine-mediated regulation. Wahl (Bethesda, MD) et al. [¹⁶ ] also described reciprocal interactions, whereby infection activates intracellular signals that lead to altered cellular gene expression, including up-regulation of the cell-cycle protein CDKN1A/p21, which is necessary to sustain HIV replication. Finally, Rohr (Strasburg, France) et al. [¹⁷ ] discussed findings that HIV uses a distinct complement of nuclear transcription factors and different mechanisms of transcriptional regulation in microglia compared with T cells.

Poli (Milan, Italy) et al. [¹⁸ ], who showed that urokinase-type plasminogen activator (uPA)/uPA receptor signaling can suppress late stages of viral replication in macrophages, addressed late stages of the replication cycle. Marsh (London, UK) demonstrated that the viral assembly pathway in macrophages has similarities and differences compared with T cells. In macrophages, this leads to the long-recognized phenomenon of intravesicular virus accumulation, which has important implications for how antigen-presenting cells can effectively deliver a burst of virus to T cells during the process of immune activation.

Thus, progress continues to be made in defining the unique mechanisms involved in regulating HIV replication in these reservoirs, yet full details of these pathways have yet to be defined. In addition to further progress in defining the cell-specific mechanisms of viral regulation, the challenges to be faced now are in determining how the complex reciprocal, regulatory pathways identified in vitro operate in vivo; developing ways to modulate these reciprocal, regulatory pathways; and defining targets for cell-specific, therapeutic intervention in the viral replication cycle.

	CONCLUSIONS

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 
Until HIV can be not only controlled but eradicated as well, studies on the interactions among HIV and macrophages, DC, and other non-T cell reservoirs will continue to be relevant. Indeed, as therapeutic approaches to viral suppression continue to improve, these reservoirs may take on an even more important role, alongside resting T cells, as targets that demand novel strategies for intervention. The workshop provides a venue to periodically focus on this specific set of targets, and this issue of JLB highlights areas of progress in the past several years and more important, identifies the questions that emerge in their wake regarding the role these cells play in vivo; the mechanisms by which virus–cell interactions affect their functions of these cells; and the unique pathways and mechanisms that regulate infection and replication in these cellular compartments (Table 1 ).

	ACKNOWLEDGEMENTS

 
The organizers thank the sponsors of the Fifth International Workshop on HIV and Cells of Macrophage/Dendritic Lineage and Other Reservoirs; the Office of AIDS Research, National Institutes of Health (Bethesda, MD); The National Centre for HIV Virology Research, Australia; and the Istituto Superiore di Sanitá, Italy. Additional support was provided by Abbott Diagnostics, Boehringer Ingelheim Italia, Bristol-Myers Squibb, and Merck Sharp and Dhome. The organizers also thank Mr. Angelo Marotta for his work in coordinating the meeting.

Received July 29, 2003; revised August 4, 2003; accepted August 5, 2003.

	REFERENCES

TOP ABSTRACT INTRODUCTION MACROPHAGES, DC, AND OTHER... HIV ALTERATIONS ON CELLULAR... UNIQUE MECHANISMS THAT REGULATE... CONCLUSIONS REFERENCES

 

1. Crowe, S. (2003) The contribution of monocytes to HIV-1 persistence, the HIV-1 reservoir and HIV-1 pathogenesis J. Leukoc. Biol. 74,635-641[Abstract/Free Full Text]
2. Smith, P. D., Meng, G., Salazar-Gonzalez, J. F., Shaw, G. M. (2003) Macrophage HIV-1 infection and the gastrointestinal tract reservoir J. Leukoc. Biol. 74,642-649[Abstract/Free Full Text]
3. Kim, W-K., Corey, S., Alvarez, X., Williams, K. (2003) Monocyte/macrophage traffic in HIV and SIV encephalitis J. Leukoc. Biol. 74,650-656[Abstract/Free Full Text]
4. Igarashi, T., Imamichi, H., Brown, C. R., Hirsch, V. M., Martin, M. A. (2003) The emergence and characterization of macrophage tropic SIV/HIV chimeric viruses (SHIVs) present in CD4+ T cell-depleted rhesus monkeys J. Leukoc. Biol. 74,772-780[Abstract/Free Full Text]
5. Goodenow, M. (2003) HIV-1 fitness and macrophages J. Leukoc. Biol. 74,657-666[Abstract/Free Full Text]
6. Magnani, M. (2003) Drug-loaded red blood cell-mediated clearance of HIV-1 macrophage reservoir by selective inhibition of STAT1 expression J. Leukoc. Biol. 74,764-771[Abstract/Free Full Text]
7. Schols, D. (2003) Specific CD4 down-modulating compounds with potent anti-HIV activity J. Leukoc. Biol. 74,667-675[Abstract/Free Full Text]
8. Lee, C., Liu, Q-H., Tomkowicz, B., Yi, Y., Freedman, B. D., Collman, R. G. (2003) Macrophage activation through CCR5- and CXCR4-mediated gp120-elicited signaling pathways J. Leukoc. Biol. 74,676-682[Abstract/Free Full Text]
9. Teleshova, N., Frank, I., Pope, M. (2003) Immunodeficiency virus exploitation of dendritic cells in the early steps of infection J. Leukoc. Biol. 74,683-690[Abstract/Free Full Text]
10. Persidsky, Y., Gendelman, H. E. (2003) Mononuclear phagocyte immunity and the neuropathogenesis of HIV-1 infection J. Leukoc. Biol. 74,691-701[Abstract/Free Full Text]
11. Chehimi, J., Luo, Q., Azzoni, L., Shawver, L., Ngoubilly, N., June, R., Jerandi, G., Farabaugh, M., Montaner, L. J. (2003) HIV-1 transmission and cytokine-induced expression of DC-SIGN in human monocyte-derived macrophages J. Leukoc. Biol. 74,757-763[Abstract/Free Full Text]
12. Chougnet, C. (2003) Role of CD40 ligand dysregulation in HIV-associated dysfunction of antigen-presenting cells J. Leukoc. Biol. 74,702-709[Abstract/Free Full Text]
13. Cunningham, A. (2003) The role of dendritic cell C-type lectin receptors in HIV pathogenesis J. Leukoc. Biol. 74,710-718[Abstract/Free Full Text]
14. Schmidtmayerova, H. (2003) Macrophages and lymphocytes differentially modulate the ability of RANTES to inhibit HIV-1 infection J. Leukoc. Biol. 74,781-790[Abstract/Free Full Text]
15. Gessani, S. (2003) Monocyte/macrophage-derived CC chemokines and their modulation by HIV-1 and cytokines: a complex network of interactions influencing viral replication and AIDS pathogenesis J. Leukoc. Biol. 74,719-725[Abstract/Free Full Text]
16. Wahl, S. M., Greenwell-Wild, T., Peng, G., Ma, G., Orenstein, J. M., Vázquez, N. (2003) Viral and host cofactors facilitate HIV-1 replication in macrophages J. Leukoc. Biol. 74,726-735[Abstract/Free Full Text]
17. Rohr, O., Marban, C., Aunis, D., Schaeffer, E. (2003) Regulation of HIV-1 gene transcription: from lymphocytes to microglial cells J. Leukoc. Biol. 74,736-749[Abstract/Free Full Text]
18. Poli, G. (2003) The role of urokinase-type plasminogen activator (uPA)/uPA receptor in HIV-1 infection J. Leukoc. Biol. 74,750-756[Abstract/Free Full Text]

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This Article Abstract Full Text (PDF) All Versions of this Article: jlb.0703357v1 74/5/631    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Collman, R. G. Articles by Montaner, L. J. Search for Related Content PubMed PubMed Citation Articles by Collman, R. G. Articles by Montaner, L. J.