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(Journal of Leukocyte Biology. 2000;68:303-310.)
© 2000 by Society for Leukocyte Biology

Permissive factors for HIV-1 infection of macrophages

Sharon M. Wahl, Teresa Greenwell-Wild, Hollie Hale-Donze, Niki Moutsopoulos and Jan M. Orenstein

Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland; and Department of Pathology, George Washington University Medical Center, Washington, DC

Correspondence: Sharon M. Wahl, PhD, NIDCR, NIH, 30 Convent Drive, MSC 4352, Building 30, Room 332, Bethesda, MD 20892-4352. E-mail: smwahl{at}dir.nidcr.nih.gov


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ABSTRACT
 
Immunodeficiency, the consequence of HIV-1 infection, predisposes the host to opportunistic infections. In turn, opportunistic pathogens influence target cell susceptibility to HIV-1 infection and replication. Although the advent of highly active antiretroviral therapy (HAART) has altered these sequelae, co-infections may prevail in some parts of the world and in failed HAART regimens. Moreover, immune activation as occurs in tonsil and non-infectious mucosal inflammatory lesions may also be associated with proximal sites of viral replication. These connections between enhancement of HIV-1 infection and activation/inflammation warrant further elucidation of the factors promoting permissiveness to HIV-1 infection. Using the opportunistic pathogen Mycobacterium avium as an in vitro model, we demonstrated that co-infection facilitated HIV-1 infection of monocyte-macrophages by multiple pathways. M. avium activated NF-{kappa}B, the downstream consequences of which included augmented expression of tumor necrosis factor {alpha} and CCR5 receptors, both permissive for sustaining HIV-1 infection. Pronounced viral replication in lymph nodes co-infected with M. avium and HIV-1 paralleled these in vitro findings. Furthermore, reduction in viral burden is associated with treatment of infected or inflamed tissues, underscoring the link between immune activation and viral replication.

Key Words: Mycobacterium avium • nuclear factor {kappa}ß • viral replication


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INTRODUCTION
 
The human immunodeficiency virus (HIV-1) infects its human hosts through cells expressing CD4 and a coreceptor belonging to the seven-transmembrane G-protein-coupled chemokine receptor superfamily [1 ]. Macrophage-tropic (M-tropic or R5) HIV-1 variants preferentially target CC chemokine receptor 5 (CCR5)-expressing cells, whereas cells with membrane CXC chemokine receptor 4 (CXCR4) are commonly infected by T- or dual-tropic isolates (T-tropic or X4). Initial transmission, infection, and viral isolates are typically represented by M-tropic HIV-1 variants [2 3 4 ], thought to target macrophages and/or dendritic cells [1 ]. Small numbers of antigen-presenting cells interacting with receptive CD4+ T cells likely initiate the infective process [5 , 6 ], and early stages of infection are then represented by CD4+ T cell viral replication in the tissues [7 8 9 ]. Later in the infection process with developing immune incompetency and, particularly in the context of co-infections [7 8 9 10 11 ] or tissue immune activation [12 13 14 ], the numbers of HIV-1-positive macrophages can become quite pronounced (Fig. 1 ). Paradoxically, in this context, the viral phenotype often [2 , 3 ], but not always [15 ], shifts to an X4 T or dual tropism, and plasma viral burden may escalate [16 17 18 ]. Treatment of the inflammatory disease, opportunistic and/or bacterial infections can reverse plasma viral load to pre-co-infection levels [12 , 16 17 18 ].



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  		Figure 1. HIV-1 and M. avium infection of macrophages. In mucosa of HIV-1 immunosuppressed subjects, M. avium recruits and infects large numbers of macrophages (A, acid-fast stain). (B) At the electron microscopic level, individual macrophages contain numerous mycobacteria. (C, D) In situ hybridization for HIV-1 RNA in a lymph node infected with HIV-1 only (C) and in a lymph node infected with both HIV-1 and M. avium (D) reveals greatly augmented viral replication in co-infected tissue [7 , 10 ].

Considerable interest remains in identifying the permissive factors that promote HIV-1 replication within the central nervous system (CNS), lymphoid tissues, and various sites of immune activation [19 ]. In recent investigations, multiple factors have been characterized that contribute to the recruitment and sensitization of monocyte/macrophage populations as hosts for HIV-1 replication. Although many of the predisposing influences of opportunistic infections (OI) may appear less relevant in the aftermath of current antiretroviral therapies targeting HIV-1 reverse transcriptase and protease, many of the extenuating pathways initiated by OI are also engendered by inflammatory lesions [12 ] and in antigenically challenged lymphoid tissues [13 , 20 ]. Moreover, although highly active antiretroviral therapy (HAART) has reduced the incidence of OI dramatically, HAART is not available universally, HAART failures occur, and OI may experience a burst early after onset of HAART therapy [21 22 23 ]. Persistent latent virus [24 ] and viral rebound after withdrawal of HAART [25 , 26 ] also underscore the need for further delineation of the linkage between infection and immune activation with the mechanisms of enhanced HIV-1 permissiveness of target cells to virus replication. Understanding the cellular, molecular, and immunological factors that enhance or suppress virus replication is fundamental to controlling and/or eradicating this pathogen.


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IMPACT OF COINFECTION ON HIV-1
 
Early in infection, HIV-1 can be identified in lymphoid tissues, typically associated with but not necessarily infecting follicular dendritic cells, and replicating in CD4+ T lymphocytes [7 8 9 , 27 28 29 ]. Although resting CD4+ cells are not impervious to infection [8 ], virus replication favors a prepared (activated) host [5 , 30 ]. The acute response to HIV-1 may control infection, but seeding of the lymphoid tissues with chronic and latently infected cells provides a smoldering source of virus which may be re-ignited by an OI, inflammation, or other antigenic challenge.

Over the evolution of infection, virus production and target cell depletion may disrupt the architecture of lymphoid tissues [7 ]. As the immune system is compromised, susceptibility to opportunistic pathogens increases. Deposition of these additional pathogens within this malfunctioning system results in co-dependence with not only uncontrolled bacterial, fungal, or parasitic infection, but exacerbated viral replication. The failure of the host to contain an OI due to lost immunocompetency may trigger a chain reaction of activation and infection which, if persistent, spills out into the circulation, resulting in an enhanced viral load and long-range transmission [5 , 16 17 18 ]. To understand the underlying basis for these devastating sequelae, we have focused on dissecting the mechanisms whereby co-infection, using Mycobacterium avium complex (MAC) as a model, as well as tissue sites of nonspecific inflammation, can drive HIV-1 replication, but also provide a permissive environment under which macrophages emerge as susceptible viral hosts. In the normal host, M. avium is unable to establish persistent infection and is cleared, whereas in immunocompromised individuals, M. avium, an intracellular organism, enters macrophages and replicates without control and may disseminate widely [31 , 32 ] (Fig. 1) . Accumulation of bacteria-laden macrophages precipitates a granulomatous-like lesion replete with multinucleated giant cells (MNGC), activated macrophages, and newly recruited mononuclear cells [7 , 10 , 11 , 31 ].


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RECRUITMENT OF VIRAL HOSTS
 
Perhaps one of the earliest contributing factors to HIV-1 infection and replication associated with co-infection and/or sites of immune activation is recruitment and localization of susceptible hosts, both CD4+ T lymphocytes and monocyte/macrophages. Macrophages infected in vitro with only HIV-1 up-regulate the expression of recruitment factors including transforming growth factor ß (TGF-ß) [33 , 34 ] and the chemokines, macrophage inflammatory protein-1{alpha} (MIP-1{alpha}), MIP-1ß [35 , 36 ], monocyte chemotactic protein-1 (MCP-1), and RANTES [37 ], that are potent chemoattractants for T cells and monocytes. Together with HIV-1-induced vascular permeability factors, such as vascular endothelial growth factor (VEGF) [37 ], recruitment factors released by local HIV-1 infection may call in a supply of host cells. This ability to recruit susceptible hosts represents a key virulence factor in establishing a foothold and propagating the virus.

The presence of a co-infection and/or an inflammatory response in the context of HIV-1 exacerbates this accumulation of CD4+ targets. The sometimes massive accumulation of mononuclear phagocytes (Fig. 2 , CD68+ cells) in HIV-1 and OI co-infected lymphoid tissue is indicative of an active recruitment process [7 , 10 , 38 , 39 ]. Although macrophages, once infected with HIV-1 or exposed to gp120, exhibit diminished chemotaxis to certain stimuli due to receptor down-regulation [40 , 41 ], the activated cells release recruitment factors to attract new host cells. Morphologically, relatively immature monocytic cells as well as differentiated macrophages and MNGCs are found in co-infected lymphoid tissues consistent with a process of chemotactic attraction of monocytes from the circulation and/or of tissue macrophages in proximal tissue followed by their activation and differentiation. In assessing potential recruitment pathways engendered by the presence of OI, which might preferentially recruit mononuclear phagocytes, we identified both {alpha} and ß chemokine expression. By cDNA microarray and ribonuclease protection assay (RPA) analysis, M. avium infection induced expression of mRNA for multiple chemokines, which may be responsible for the impressive recruitment of mononuclear phagocytes into a localized site of infection, including MCP-1, interleukin (IL)-8, MIP-1ß, and MIP-1{alpha} [39 ]. Exposure of macrophages to mycobacterial antigens (MAg) or purified cell wall lipoarabinomannan (LAM) also rapidly up-regulated chemokine mRNA expression [39 ]. In parallel, chemokine protein levels were elevated in the supernatants of MAC-infected or MAg-stimulated cultures. Not only is there a rapid expression of chemotactic factors [39 ], but also a biphasic response, since MCP-1 and MIP-1{alpha} are also evident 7–10 days after M. avium infection and replication in vitro (Fig. 2C) . The pronounced levels of viral replication within a localized tissue depend on continuing recruitment and/or generation of CD4+ hosts. Moreover, localized release of chemokines may influence trafficking of already infected cells, in addition to naive hosts.



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  		Figure 2. Accumulation of macrophages in M. avium and HIV-1-infected tissue. CD68 staining for macrophages in HIV-1-infected lymphoid tissue (A) is enhanced in HIV-1 plus M. avium co-infected (B) lymph node. (C) Expression of chemokines in macrophage supernatants 7 days after infection with M. avium [39 ].

Supplemental to these recruitment factors, enhanced adhesion molecule expression was associated with the perivascular localization of mononuclear cells in co-infected lymphoid tissues. M. avium infection or exposure to MAg rapidly up-regulated mRNA expression for adhesion molecules such as {alpha}5 integrin and ICAM-1 [39 ]. Increased cell-cell and cell-matrix interactions likely facilitate not only transendothelial migration to sites of HIV-1 and/or MAC infection, but also transmission of virus from cell to cell, underlying the process of proximal activation and transmission [5 ]. M. avium infection of macrophages triggers the synthesis and/or release of multiple molecules, which may initiate recruitment and activation and therefore, vulnerability of CD4+ HIV-1 target cells.


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CO-INFECTION PROMOTES VIRUS SUSCEPTIBILITY
 
Our initial studies demonstrated that within M. avium- and HIV-1-coinfected lymph nodes, a markedly increased representation of HIV-1-positive macrophages was apparent [7 , 10 , 11 ] (Fig. 1) . Disruption of the structure of the lymphoid tissue was evident and the cellular constitution was characterized by reduced numbers of CD4+ T cells, but increased numbers of macrophages and MNGCs. Most of these phagocytic cells contained acid-fast bacilli and, within the regions of M. avium infection, HIV-1 detection by in situ hybridization was striking. Besides co-expression of HIV-1 and acid-fast bacilli, double-labeling with in situ hybridization and immunohistochemistry confirmed the macrophage lineage (CD68+, HAM56+, lysozyme+) of the viral hosts, in addition to the residual infected CD4+ T cell populations. This enhanced recruitment and infection with HIV-1 associated with co-infection was not limited to MAC, but also observed with other OI [7 , 10 ]. Subsequent studies have confirmed the association between co-infections and enhanced susceptibility of macrophages to HIV-1 [42 43 44 45 ].

Enhanced virus susceptibility is related to the ability of MAC to up-regulate NF-{kappa}B [10 ] (Fig. 3 ), which has multiple downstream consequences [46 ], including enhanced expression of the HIV-1 coreceptor CCR5 [8 , 10 ]. The necessity of CCR5 for HIV-1 infection in vivo has been documented in humans homozygous for an inactive mutant CCR5 allele who are markedly less susceptible to HIV-1 infection [1 , 47 48 49 50 ]. CCR5 also represents the natural receptor for the CC chemokines, MIP-1{alpha}, MIP-1ß, and RANTES [1 , 51 ], likely influencing both migration and susceptibility to infection by HIV-1. It might be anticipated that augmented expression of MIP-1{alpha} and MIP-1ß by MAC would suppress/block HIV-1 infection [52 ]. However, under some circumstances, these chemokines reportedly enhance HIV-1 replication in macrophages [53 ] and in a subset of tonsil cultures [54 ], consistent with our in vitro and in vivo findings in MAC co-infected lymph nodes [7 , 10 , 11 , 38 ]. The impact of the chemokines on both recruitment and viral infection are likely dependent on concentration and other additional factors. Activation of NF-{kappa}B drives both the transcription of CCR5 through a binding site in the CCR5 promoter [51 ] and TNF-{alpha} to further promote HIV-1 replication (Fig. 3) [55 , 56 ]. HIV-1 infection itself also increases CCR5 expression [Peng et al., unpublished results]. In the context of co-pathogens, enhancement of CCR5 may occur by multiple mechanisms, both direct and indirect. In addition to direct enhancement via MAC activation of NF-{kappa}B, both TNF-{alpha} [10 ] and IFN-{gamma} [10, 57, Peng et al., unpublished results] enhance CCR5 levels in vitro, consistent with high CCR5 expression in co-infected tissues [10 ]. TNF-{alpha} is not typically detected in HIV-1-infected lymphoid tissue in the absence of OI or inflammation [10 , 58 ], but is induced by M. avium and other antigenic stimuli [10 ]. Although in a recent study analysis of two lymph nodes co-infected with HIV-1 and MAC revealed only occasional HIV-1 RNA+, CD45+, CD68+, lysozyme+ cells [59 ], multiple other studies document that OI promote HIV-1 production in macrophage hosts [42 43 44 45 ].



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  		Figure 3. M. avium induces macrophage activation to promote viral replication. Mycobacterial antigens activate NF-{kappa}B as shown by electrophoretic mobility shift assay (EMSA; A), which drives TNF-{alpha} and CCR5 mRNA expression (B, Northern analysis) and enhances HIV-1 replication (C). P24 antigen levels were determined in the supernatants of macrophage cultures infected with HIV-1BaL (TCID50 = 2.5 x 103) after 11, 14, and 18 days (solid bars, HIV only; hatched bars, HIV + MAg).


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REGULATION OF APOPTOSIS
 
In addition to the powerful recruitment capability of M. avium and its constituents, M. avium appears to foster an accumulation of hosts for itself and HIV-1 through the regulation of cell-survival factors [Hale-Donze et al., unpublished results]. HIV-1 disease is characterized by gradual depletion of CD4+ cells, leading to declining immunocompetency. Most dying lymphoid cells are found in the lymph node, not in the blood [60 , 61 ], yet within this graveyard, virus production continues and is exacerbated during co-infections [7 , 10 ]. In these later stages of disease, following substantial T cell loss [7 , 62 , 63 ], OI-mediated inhibition of apoptosis may preferentially enable maintenance of persistently infected macrophages. The numbers of apoptotic cells evident in HIV-1-only infected lymph nodes are greater than in lymph node tissues coinfected with HIV-1 and M. avium [Hale Donze et al., unpublished results] (Fig. 4 ). In vitro, M. avium infection of macrophages and/or exposure to MAg promotes viability through the enhanced expression of apoptosis inhibitory molecules [Hale-Donze et al., unpublished results], such as TNF-{alpha} [64 ] and bcl-2 family members [65 ]. Because the apoptotic cells in HIV-1 lymph nodes are often "bystander" cells that have homed to the nodes, rather than productively infected cells [60 , 66 , 67 ], cessation of death may contribute to accumulation of HIV-1 host cell candidates. Moreover, long-lived cellular sources of HIV-1 provide a conduit to infect newly activated cells in the vicinity by the process of proximal activation and transmission [5 ]. The massive accumulation of HIV-1-infected cells in M. avium co-infected lymphoid tissues likely represents the outcome of multiple co-pathogen-driven permissive factors including recruitment, replacement, activation with increased NF-{kappa}B, cytokine and co-receptor expression, and enhanced cell viability (Fig. 5 ).



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  		Figure 4. Reduced apoptosis in co-infected tissues. By TUNEL staining, the numbers of apoptotic cells (TUNEL+) in HIV-1 plus M. avium-infected tissues (C) were less than in HIV-1 only infected (B) or uninfected lymph node (A).



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  		Figure 5. Co-infection induces permissive factors for HIV-1 infection of macrophages. Opportunistic pathogens trigger NF-{kappa}B activation, chemokine and cytokine production, CCR5 expression, and suppress cell death. This recruitment and accumulation of viral hosts with enhanced susceptibility to HIV-1 results in persistence of viral replication.


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IMMUNE ACTIVATION IN TONSIL
 
Another lymphoid site in which immune activation, although not necessarily OI-driven, is commonly associated with enhanced HIV-1 replication is the tonsil [13 , 20 ]. The tonsil represents a unique microenvironment possessing a large reservoir of activated and highly susceptible HIV targets. Part of the tonsil mucosal surface resembles that of other mucous membranes in the oral cavity, vagina, and exocervix with a multilayered epithelial barrier overlying a basement membrane and matrix in the lamina propria in which Langerhans cells, macrophages, and lymphocytes traffic [68 ]. This squamous epithelium transitions into the lympho-epithelium, a large uniquely specialized epithelial surface lining the crypts that contain M cells and is permeated by lymphocytes. Within this region, the external environment has access to lymphoid and circulatory systems of the host, representing a site where antigens and infectious agents cross the mucosal surface.

In non-human primate studies, the tonsil can be a site of primary retroviral infection [9 ], seeding other lymphoid tissues, and/or HIV-1 can be transported there from other sites in the body [69 ]. Within human tonsil, prodigious levels of HIV-1 have been found [13 ] and although often hyperplastic, consistent with activation, the tonsils lacked evidence of infectious organisms other than HIV-1, and were likely activated through environmental stimuli. Initially, the HIV-1 host cells were considered dendritic cells (DC) [20 ]. As in lymph node, FDC may capture the virus [29 ]. An interesting cellular distribution was observed in that MNGC were not evident in germinal centers, surface mucosa, mantle zones, paracortex, or interstitium, but rather preferentially near the surface of the lympho-epithelium. Within the lympho-epithelium, subjacent to the crypt epithelial surface, lacunae between keratinocyte borders housed mononuclear cells and MNGCs [13 ]. HIV-1-positive MNGC as determined by HIV-1 in situ hybridization, p24 immunohistochemistry, and transmission electron microscopy were characteristically surrounded by infected CD68+ mononuclear cells in the lympho-epithelium, whereas HIV-1-positive lymphocytes were most abundant in the germinal centers and paracortex. It is important to note that in addition to synthesizing HIV-1 RNA, the MNGC and mononuclear cells were observed to be producing free mature HIV-1 particles [13 ]. The significance of this HIV-1 cell-specific tissue distribution within the tonsil is unknown, and whether there is a corresponding R5 and X4 HIV-1 variant distribution (compartmentalization) is of considerable interest.

It remains uncertain whether the tonsil in human HIV-1 infection is a primary or secondary site of retroviral spread. Evidence continues to implicate transmission of HIV-1 via an oral route [70 , 71 ], albeit at low frequency due to antiretroviral defenses [72 73 74 ]. To address the potential viral selectivity of tonsil lymphocytes, mononuclear phagocytes, and MNGCs, we have cultured cell suspensions from freshly isolated tonsils with T-tropic (X4, HIVIIIB), M-tropic (R5, HIVBAL), and dual-tropic (89.6) HIV-1 in vitro. As reported for tonsil histocultures [54 , 75 ], these cell populations are susceptible to infection by each of these viral variants [Moutsopoulos et al., unpublished results]. In contrast to peripheral blood mononuclear cells, tonsil cells are readily HIV-1 susceptible without phytohemagglutinin stimulation, indicative of some level of constitutive activation/stimulation and permissiveness for viral spread. Nonetheless, typical T cell activation markers (CD25) do not routinely correlate with tonsil permissiveness, implicating more subtle mechanisms of susceptibility as recently demonstrated in acute SIV and HIV-1 infection [8 ]. Although initially demonstrated that binding of HIV-1 to resting T cells results in abortive infection [30 ], new evidence suggests the lack of a requirement for T cell activation according to accepted criteria for productive infection [8 ]. There may be subliminal levels of activation, not detectable by commonly used markers, which enables susceptibility to infection and production of progeny virions. This may be the case in tonsil infections where lack of constitutive expression of IL-2R, cytokines, and proliferative responses may not reflect a permissive milieu. Defining these permissive factors is fundamental to understanding and potentially disarming pathways of infection that are out of the mainstream of proliferating T cells. Whatever the mechanism, this large reservoir of constitutively "activated," highly susceptible CD4+ lymphocyte and macrophage targets may serve as a site of acute HIV-1 infection, amplification, and persistence, but also as a viral reservoir.


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MUCOSAL IMMUNE ACTIVATION AND HIV-1
 
Besides OI-infected lymphoid tissues and immunologically challenged tonsils, macrophages and MNGC have been shown to be HIV-1 hosts in other sites, most notably in the CNS and in sites of inflammation [19 ]. A striking example of the association of tissue inflammation with localization of HIV-1-infected cell populations was reported in a recent case study [12 ]. Whereas the mucosa represents the primary route of HIV-1 transmission [68 ], mucosal macrophages are not typically a preferred host [76 ]. Nonetheless, an individual with ulcerative colitis who was HIV-1 positive with a high systemic viral burden and low CD4+ T cell levels, exhibited an accumulation of HIV-1-infected cells within the inflamed mucosal tissue [12 ]. As shown for tissues dually infected with opportunistic pathogens and HIV-1, the presence of tissue injury provoked an inflammatory response that resulted in recruitment and activation of lymphocytes and macrophages as HIV-1 hosts. Expression of permissive factors converted the site into a virtual HIV-1 incubator, associated with a high viral burden. The linkage between inflammation and viral replication was further established after surgical removal of the pathologically inflamed intestine. The consequences of removal of the lesion included a dramatic reversal of both the high viral burden and low CD4+ lymphocyte levels [12 ]. These data graphically illustrate the impact of immune activation/inflammation on HIV-1 susceptibility by mechanisms similar to those shown for OI, i.e. chemokines, NF-{kappa}B activation, CCR5, and TNF-{alpha}, and importantly, the ability to reverse these virally permissive sequelae by inhibition or removal of the offending antigen/tissue damage.

Evidence that macrophages emerge as susceptible hosts in sites of infection and/or immune activation not only provides insight into the role of macrophages in the pathogenesis of HIV-1 disease, but also identifies this population as a potential therapeutic target [19 , 77 78 79 80 ]. From their initial involvement in selection and propagation of HIV-1 during acute infection, through persistence and chronicity of viral infection, macrophages contribute to transmission and immunopathology. Further elucidation of the multiple permissive factors that render these cells susceptible will suggest interventional strategies.


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