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CUTTING EDGE |
,§
Units of
*
Molecular Immunoregulation,
Human Virology, and
Immunobiology of HIV, DIBIT, San Raffaele Scientific Institute, Milan, Italy; and
§
Department of Biology and Genetics, University of Milan, Milan, Italy
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResults and DiscussionReferences |
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) express CXCR4, this coreceptor is assumed to be nonfunctional
for HIV-1 infection. We addressed this apparent paradox by infecting
human monocyte-derived M with primary and TCLA isolates that were
rigorously characterized for coreceptor usage and by adding the natural
CXCR4 ligand, stem cell differentiation factor-1, to specifically block
CXCR4-mediated entry. Our results show that primary HIV-1 isolates that
selectively use CXCR4 productively infected both normal and C-C
chemokine receptor-5-null M. By contrast, M supported the entry
of CXCR4-dependent TCLA strains with variable efficiency but were not
productively infected. Thus, the tropism of HIV isolates results from
complex virus/host cell interactions both at the entry and postentry
levels. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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)3-tropic (M-tropic),
slow/low, or non-syncytia-inducing (NSI) infect both monocyte-derived
M (MDMs) and primary CD4+ T lymphocytes but do not
usually infect established T cell lines such as MT-2. By contrast, T
cell line-tropic (T-tropic), rapid/high, or syncytia-inducing (SI)
strains grow in T cell lines and form syncytia in MT-2 cells and in
PBMCs. The ability of SI isolates to infect M productively is
controversial. Indeed, while T cell line-adapted (TCLA) strains usually
fail to replicate in MDMs (4), conflicting results have been reported
when primary isolates were used (5, 6, 7, 8, 9, 10).
The recent identification of several chemokine receptors as HIV
coreceptors has provided a molecular basis for the difference in
tropism of different HIV-1 strains. In particular, C-C chemokine
receptor (CCR)5, which is the RANTES, MIP-1
, and MIP-1ß receptor,
has been shown to serve as the main coreceptor for NSI viruses
(11, 12, 13, 14); CXC chemokine receptor-4 (CXCR4)/fusin, which is the natural
receptor for stem cell differentiation factor (SDF)-1 (15, 16),
mediates the entry of both primary and TCLA SI HIV-1 strains (17).
CCR2b and CCR3 can also serve as entry cofactors for certain virus
strains (14, 18). More recently, Bob and Bonzo (19), which are two
orphan seven-transmembrane domain G protein-coupled receptors that are
expressed in T cells but weakly, if at all, in M, were reported as
potential new coreceptors for fusion by M-tropic and T-tropic HIV-1
strains as well as by SIV.
While the lack of CCR5 expression on most T cell lines (20) has
provided a rationale for the inability of NSI strains to infect these
cells, the issue of MDM infection by HIV-1 strains with an SI phenotype
remains unresolved. Although M express significant levels of CXCR4
on their membranes (21), this coreceptor is assumed to be nonfunctional
for infection (22). Because of the critical role of M in the
pathogenesis of HIV-1 infection, we addressed this apparent paradox by
infecting normal human MDMs in vitro with a panel of primary HIV-1
isolates and TCLA strains that had been rigorously characterized for
coreceptor usage. Furthermore, we added the natural CXCR4 ligand,
SDF-1, to specifically block CXCR4-mediated viral entry. Our results
show that primary HIV-1 isolates can productively infect human MDMs
using CXCR4 as a coreceptor. By contrast, productive infection was not
observed with CXCR4-dependent TCLA HIV-1 strains, even though viral
entry occurred with variable efficiency.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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mAbs that were specific for human CXCR4 (12G5) (21) and CCR5 (2D7) were kindly provided by J. Hoxie (University of Pennsylvania, Philadelphia, PA) and C. Mackay (Leukosite, Cambridge, MA), respectively. Anti-CD14 mAb P9, FITC-conjugated goat anti-mouse IgG, and isotype controls were purchased from Becton Dickinson (Mountain View, CA). SDF-1 and RANTES were obtained from Upstate Biotechnology (Lake Placid, NY) and R&D Systems (Minneapolis, MN), respectively. The endotoxin content of the cell culture reagents was assessed by the Limulus amebocyte lysate assay (BioWhittaker, Walkersville, MD) and was <0.125 Eu/ml.
Chemotaxis assay
Cell migration was assayed in 48-well transwell chambers using a 5-mm pore size polycarbonate membrane (Costar, Cambridge, MA). Chemokines diluted in RPMI 1640/0.3% human serum albumin were added to the lower chamber. Cells (3 x 106/ml, 100 µl) were added to the upper chamber. The filter was removed after a 2-h incubation at 37°C, and the cells that migrated in the lower chamber were counted using a FACScan (Becton Dickinson) at 60 µl/min for 30 s. Specific cell types were selected by gating on the appropriate forward and side scatter. Cell migration was assessed in duplicate and expressed as a chemotactic index (the ratio between the number of cells that migrated in the presence of chemokines and spontaneous migration).
Isolation of MDMs and HIV-1 infection
MDMs were isolated as described previously (23). MDM
preparations contained 
90% CD14+ cells as assessed by
immunofluorescence. To obtain monocytes, nonadherent cells were removed
after 1 h, and the remaining adherent cells were cultured for
24 h.
MDMs were infected with three primary CCR5-dependent HIV-1 isolates (HIV-15508, HIV-16088, and HIV-110005), one primary isolate (HIV-157) that uses both CCR5 and CXCR4, three primary CXCR4-dependent HIV-1 isolates (HIV-127, HIV-134, and HIV-1130), and the TCLA strains HIV-1IIIB and HIV-1MN that were continuously grown in MOLT-3 and PM1 cells, respectively. All isolates were characterized for coreceptor usage by infecting U87.CD4 glioma cells that coexpressed CCR1, CCR2B, CCR3, CCR5, and CXCR4 (9) and osteosarcoma GHOST34.CD4 cells that had been transfected with the Bob or Bonzo genes (kindly provided by D.R. Littman, Skirball Institute, New York, NY). MDMs were infected with DNase-treated virus (tissue culture ID50: 50/106 cells). The p24 Ag concentrations in the culture supernatants were determined by ELISA (23).
Semiquantitative PCR for HIV-1 proviral DNA
DNA was extracted from MDMs at 14 h postinfection by salting-out. PCR was performed using primers 1 and 2II (24) that amplify a 218-base pair (bp) fragment from the HIV-1 gag gene. Samples were subjected to 50 cycles of amplification (95°C for 1 min, 63°C for 1 min, and 72°C for 1 min). The PCR products were separated on a 1.8% agarose gel, transferred to a nylon membrane, and hybridized with a gag-specific, 32P-labeled oligonucleotide (5'-AGGCGACTGGTGAGTACGCCAAAA). To normalize for the quantity of DNA in each sample, a 441-bp region of the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene was amplified using primers 5'-GGGAAGGTGAAGGTCGGAGTC and 5'-GCTGATGATCTTGAGGCTGTTGTC. The results are expressed as the ratio between the intensities of the HIV-1 and GAPDH bands as assessed by scanning densitometry. Each sample was amplified in duplicate or triplicate.
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Results and Discussion |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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As a first step in assessing the role of CXCR4 in MDM infection by
SI HIV-1 isolates, we analyzed CXCR4 expression on monocytes and MDMs
from normal donors. Figure 1
shows that
immunofluorescence with mAb 12G5 detected variable but significant
levels of CXCR4 protein on monocytes at 1 day postisolation as assessed
by the percentage of positive cells and by mean fluorescence intensity
(MFI). Although culture-induced differentiation resulted in a
progressive decrease of CXCR4, the receptor was expressed at a
comparable intensity on MDMs at the time of infection (day 5 of
culture, MFI = 20–29) and on MOLT-3 cells, which are a T cell
line that is widely used to expand SI HIV-1 strains (MFI = 24).
The expression of the other major HIV-1 coreceptor, CCR5, followed a
similar pattern in all of the donors examined (n = 3).
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).
RANTES-induced chemotaxis was in a comparable range. Taken together,
these results show that, at the time of exposure to the virus, CXCR4 is
expressed on MDMs at substantial levels and is functional.
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To define the role of CXCR4 in MDM infection by HIV-1, we selected
from a panel of 33 primary HIV-1 isolates that had been rigorously
characterized for coreceptor usage (9), 3 isolates that exclusively use
CXCR4, together with a control group of 3 CCR5-dependent isolates. As
expected, MDMs were efficiently infected by primary NSI HIV-1 isolates.
In a representative experiment, p24 Ag levels at 9 days after the
infection of cultures with HIV-15508,
HIV-16088, and HIV-110005 were 5.6, 2.3, and
7.2 ng/ml, respectively. Notably, MDMs were also efficiently infected
by all of the CXCR4-dependent primary SI strains, with p24 Ag release
rapidly reaching substantial levels (Fig. 3A). The source of HIV in our
cultures was most likely MDMs rather than contaminating T cells.
Indeed, no p24 Ag secretion was ever detected despite an intense
surface expression of CXCR4 when nonadherent
CD3+/CD14- cells were infected with the same
isolates at 5 days after purification (data not shown).
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B shows
that the addition of rSDF-1 blocked the replication of all of the
CXCR4-dependent primary HIV-1 strains. The SDF-1-dependent inhibition
of MDM infection was even more efficient than that observed previously
with human PBMCs (9). A semiquantitative PCR analysis (Fig. 3C) revealed an SDF-1-induced decrease in proviral DNA at
14 h postinfection that pointed to a block at the level of viral
entry. By contrast, SDF-1 had no inhibitory effect on infection by
CCR5-dependent HIV-1 isolates (data not shown). Consistent with the
selective use of CXCR4 as a coreceptor for entry, the addition of the
CCR5 ligand RANTES at a concentration (100 ng/ml) that completely
inhibits infection with NSI isolates (23) did not affect the entry or
the replication of CXCR4-dependent HIV-1 isolates (Fig. 3, B
and C). These data demonstrate that CXCR4 is a functional
coreceptor for the entry of primary HIV-1 SI isolates in MDMs.
Further supporting this conclusion, Table I shows that MDMs from a
ccr5
32-homozygous individual were infected by two HIV-1 primary
isolates (HIV-134 and HIV-1130) that
selectively use CXCR4, as well as by a primary isolate
(HIV-157) that uses both CXCR4 and CCR5. The addition of
SDF-1 efficiently blocked HIV infection by all viruses. By contrast,
RANTES had no significant effect (data not shown). Taken together,
these results show that CXCR4 supports CCR5-independent HIV-1 entry in
M.
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We then compared the ability of CXCR4-dependent TCLA strains and
primary isolates to productively infect MDMs. Proviral DNA was assessed
at 14 h postinfection with two TCLA strains (HIV-1IIIB
and HIV-1MN) and three primary isolates
(HIV-127, HIV-134, and HIV-1130).
Table II shows that the level of viral
entry was variable but comparable overall for TCLA strains and primary
isolates. However, productive infection could not be detected with TCLA
strains, even when entry had occurred with substantial efficiency (e.g.
HIV-1IIIB for donor 1 and HIV-1MN for donor 2).
These results suggest that the low or absent viral replication in MDMs
that had been infected with TCLA HIV-1 strains was due to both entry
and postentry defects.
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infectability by primary HIV-1 strains with different biologic
properties. Our data show that human MDMs can be efficiently infected
by primary HIV-1 isolates that selectively use CXCR4 as a coreceptor.
This notion is supported by a rigorous characterization of all of the
relevant viral isolates as selective CXCR4 users, by the demonstration
that CXCR4 is functional in an independent assay (i.e., chemotaxis),
and most importantly, by the ability of SDF-1, the natural ligand of
CXCR4, to prevent HIV-1 infection. We conclude that MDMs support the
entry and replication not only of CCR5-dependent but also of
CXCR4-dependent primary HIV-1 isolates. Our conclusion is consistent
with the recent demonstration that CXCR4 supports the infection of M
by a dual-tropic primary isolate (10). Thus, in addition to their
well-established role in the early stages of disease and in viral
transmission (25), M are both a source of HIV during the
opportunistic infections that mark the progression of HIV-1 disease
(26) and a target for the CXCR4-dependent HIV-1 strains that emerge in
the late stages of HIV infection (9).
Our findings cast some doubt on the traditional definition of HIV-1
tropism based on the infection of cells that have been
manipulated by culture conditions, and more generally, on the
usefulness of thinking about HIV isolates as M- vs T-tropic. In
particular, the results obtained by us and others with
CXCR4-dependent TCLA HIV-1 strains are conflicting, and underline
how the cellular tropism of HIV isolates is determined by multiple
virus/host cell interactions. Blocks have been observed at the entry
step and have been ascribed to limited coreceptor availability (10)
and/or to the intrinsic fusogenic properties of env proteins (27).
Postentry defects have also been shown, implicating the cellular
factors required to activate viral replication (28, 29). In this
respect, the transcription factors NF-ATc (30) and GATA-3 (31)
activate HIV-1 transcription and replication in T cells, whereas the
binding of CCAAT/enhancer-binding proteins to the HIV-1 long terminal
repeat is required for HIV-1 replication in MDMs (32). By the
same token, the HIV-1-encoded protein vpr is important for efficient
viral replication in primary MDMs but not in activated T cells (33). It
is tempting to speculate that HIV-1 strains that are continuously grown
in T cell lines might become highly dependent upon T cell-specific
transcription factors for their replication and/or develop mutations in
the genomic regions that are critical for replication in M. Such
events would remain functionally silent as long as the virus is
passaged in T cells but would be likely to undermine replication in
M.
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Donata Vercelli, Molecular Immunoregulation Unit, DIBIT, San Raffaele Scientific Institute, Via Olgettina 58, 20132 Milano, Italy. E-mail address:
3 Abbreviations used in this paper: M, macrophage(s); M-tropic, macrophage-tropic; NSI, non-syncytia-inducing; MDM, monocyte-derived macrophage; T-tropic, T cell line-tropic; SI, syncytia-inducing; TCLA, T cell line-adapted; CCR, CC chemokine receptor; CXCR4, CXC chemokine receptor-4; SDF, stem cell differentiation factor; GADPH, glyceraldehyde-3-phosphate dehydrogenase; MFI, mean fluorescence intensity.
Received for publication January 21, 1998. Accepted for publication June 23, 1998.
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References |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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ccr5 mutation. J. Virol. 71:3219.[Abstract]
, MIP-1ß receptor as a fusion cofactor for macrophage-tropic HIV-1. Science 272:1955.[Abstract]
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S. Li, J. Juarez, M. Alali, D. Dwyer, R. Collman, A. Cunningham, and H. M. Naif Persistent CCR5 Utilization and Enhanced Macrophage Tropism by Primary Blood Human Immunodeficiency Virus Type 1 Isolates from Advanced Stages of Disease and Comparison to Tissue-Derived Isolates J. Virol., December 1, 1999; 73(12): 9741 - 9755. [Abstract] [Full Text]
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M. Honczarenko, R. S. Douglas, C. Mathias, B. Lee, M. Z. Ratajczak, and L. E. Silberstein SDF-1 Responsiveness Does Not Correlate With CXCR4 Expression Levels of Developing Human Bone Marrow B Cells Blood, November 1, 1999; 94(9): 2990 - 2998. [Abstract] [Full Text] [PDF]
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S. Moir, R. Lapointe, A. Malaspina, M. Ostrowski, C. E. Cole, T.-W. Chun, J. Adelsberger, M. Baseler, P. Hwu, and A. S. Fauci CD40-Mediated Induction of CD4 and CXCR4 on B Lymphocytes Correlates with Restricted Susceptibility to Human Immunodeficiency Virus Type 1 Infection: Potential Role of B Lymphocytes as a Viral Reservoir J. Virol., October 1, 1999; 73(10): 7972 - 7980. [Abstract] [Full Text] [PDF]
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Y. Yi, S. N. Isaacs, D. A. Williams, I. Frank, D. Schols, E. De Clercq, D. L. Kolson, and R. G. Collman Role of CXCR4 in Cell-Cell Fusion and Infection of Monocyte-Derived Macrophages by Primary Human Immunodeficiency Virus Type 1 (HIV-1) Strains: Two Distinct Mechanisms of HIV-1 Dual Tropism J. Virol., September 1, 1999; 73(9): 7117 - 7125. [Abstract] [Full Text]
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C. Chelucci, I. Casella, M. Federico, U. Testa, G. Macioce, E. Pelosi, R. Guerriero, G. Mariani, A. Giampaolo, H.J. Hassan, et al. Lineage-Specific Expression of Human Immunodeficiency Virus (HIV) Receptor/Coreceptors in Differentiating Hematopoietic Precursors: Correlation With Susceptibility to T- and M-Tropic HIV and Chemokine-Mediated HIV Resistance Blood, September 1, 1999; 94(5): 1590 - 1600. [Abstract] [Full Text] [PDF]
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D. J. Chabot, P.-F. Zhang, G. V. Quinnan, and C. C. Broder Mutagenesis of CXCR4 Identifies Important Domains for Human Immunodeficiency Virus Type 1 X4 Isolate Envelope-Mediated Membrane Fusion and Virus Entry and Reveals Cryptic Coreceptor Activity for R5 Isolates J. Virol., August 1, 1999; 73(8): 6598 - 6609. [Abstract] [Full Text]
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M.-J. Truong, E. C. A. Darcissac, E. Hermann, J. Dewulf, A. Capron, and G. M. Bahr Interleukin-16 Inhibits Human Immunodeficiency Virus Type 1 Entry and Replication in Macrophages and in Dendritic Cells J. Virol., August 1, 1999; 73(8): 7008 - 7013. [Abstract] [Full Text]
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J. Richardson, G. Pancino, R. Merat, T. Leste-Lasserre, A. Moraillon, J. Schneider-Mergener, M. Alizon, P. Sonigo, and N. Heveker Shared Usage of the Chemokine Receptor CXCR4 by Primary and Laboratory-Adapted Strains of Feline Immunodeficiency Virus J. Virol., May 1, 1999; 73(5): 3661 - 3671. [Abstract] [Full Text]
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