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J Virol. 1992 March; 66(3): 1354-1360
Biological phenotype of human immunodeficiency virus type 1 clones at different stages of infection: progression of disease is associated with a shift from monocytotropic to T-cell-tropic virus population.
H Schuitemaker,
M Koot,
N A Kootstra,
M W Dercksen,
R E de Goede,
R P van Steenwijk,
J M Lange,
J K Schattenkerk,
F Miedema and
M Tersmette
Central Laboratory, Netherlands Red Cross Blood Transfusion Service, Amsterdam.
ABSTRACT
The composition of human immunodeficiency virus type 1 (HIV-1) clonal populations at different stages of infection and in different compartments was analyzed. Biological HIV-1 clones were obtained by primary isolation from patient peripheral blood mononuclear cells under limiting dilution conditions, with either blood donor peripheral blood lymphocytes or monocyte-derived macrophages (MDM) as target cells, and the biological phenotype of the clones was analyzed. In asymptomatic individuals, low frequencies of HIV-1 clones were observed. These clones were non-syncytium inducing and preferentially monocytotropic. In individuals progressing to disease, a 100-fold increase in frequencies of productively HIV-1-infected cells was observed as a result of a selective expansion of nonmonocytotropic clones. In a person progressing to AIDS within 19 months after infection, only syncytium-inducing clones were detected, shifting from MDM-tropic to non-MDM-tropic over time. From his virus donor, a patient with wasting syndrome, only syncytium-inducing clones, mostly non-MDM-tropic, were recovered. Parallel clonal analysis of HIV-1 populations in cells present in bronchoalveolar lavage fluid and peripheral blood from an AIDS patient revealed a qualitatively and quantitatively more monocytotropic virus population in the lung compartment than in peripheral blood at the same time point. These findings indicate that monocytotropic HIV-1 clones, probably generated in the tissues, are responsible for the persistence of HIV-1 infection and that progression of HIV-1 infection is associated with a selective increase of T-cell-tropic, nonmonocytotropic HIV-1 variants in peripheral blood.
J Virol. 1992 March; 66(3): 1354-1360
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(2003). Cytolysis by CCR5-Using Human Immunodeficiency Virus Type 1 Envelope Glycoproteins Is Dependent on Membrane Fusion and Can Be Inhibited by High Levels of CD4 Expression. J. Virol.
77: 6645-6659
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Schmitt, N., Chene, L., Boutolleau, D., Nugeyre, M.-T., Guillemard, E., Versmisse, P., Jacquemot, C., Barre-Sinoussi, F., Israel, N.
(2003). Positive Regulation of CXCR4 Expression and Signaling by Interleukin-7 in CD4+ Mature Thymocytes Correlates with Their Capacity To Favor Human Immunodeficiency X4 Virus Replication. J. Virol.
77: 5784-5793
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Jekle, A., Keppler, O. T., De Clercq, E., Schols, D., Weinstein, M., Goldsmith, M. A.
(2003). In Vivo Evolution of Human Immunodeficiency Virus Type 1 toward Increased Pathogenicity through CXCR4-Mediated Killing of Uninfected CD4 T Cells. J. Virol.
77: 5846-5854
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Ito, Y., Grivel, J.-C., Margolis, L.
(2003). Real-Time PCR Assay of Individual Human Immunodeficiency Virus Type 1 Variants in Coinfected Human Lymphoid Tissues. J. Clin. Microbiol.
41: 2126-2131
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Heredia, A., Davis, C., Amoroso, A., Dominique, J. K., Le, N., Klingebiel, E., Reardon, E., Zella, D., Redfield, R. R.
(2003). Induction of G1 cycle arrest in T lymphocytes results in increased extracellular levels of beta -chemokines: A strategy to inhibit R5 HIV-1. Proc. Natl. Acad. Sci. USA
100: 4179-4184
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Olivetta, E., Percario, Z., Fiorucci, G., Mattia, G., Schiavoni, I., Dennis, C., Jager, J., Harris, M., Romeo, G., Affabris, E., Federico, M.
(2003). HIV-1 Nef Induces the Release of Inflammatory Factors from Human Monocyte/Macrophages: Involvement of Nef Endocytotic Signals and NF-{kappa}B Activation. J. Immunol.
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Babcock, G. J., Farzan, M., Sodroski, J.
(2003). Ligand-independent Dimerization of CXCR4, a Principal HIV-1 Coreceptor. J. Biol. Chem.
278: 3378-3385
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Qin, X.-F., An, D. S., Chen, I. S. Y., Baltimore, D.
(2003). Inhibiting HIV-1 infection in human T cells by lentiviral-mediated delivery of small interfering RNA against CCR5. Proc. Natl. Acad. Sci. USA
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Hsu, M., Harouse, J. M., Gettie, A., Buckner, C., Blanchard, J., Cheng-Mayer, C.
(2002). Increased Mucosal Transmission but Not Enhanced Pathogenicity of the CCR5-Tropic, Simian AIDS-Inducing Simian/Human Immunodeficiency Virus SHIVSF162P3 Maps to Envelope gp120. J. Virol.
77: 989-998
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Basmaciogullari, S., Babcock, G. J., Van Ryk, D., Wojtowicz, W., Sodroski, J.
(2002). Identification of Conserved and Variable Structures in the Human Immunodeficiency Virus gp120 Glycoprotein of Importance for CXCR4 Binding. J. Virol.
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Fuller, C. L., Choi, Y. K., Fallert, B. A., Capuano, S. III, Rajakumar, P., Murphey-Corb, M., Reinhart, T. A.
(2002). Restricted SIV Replication in Rhesus Macaque Lung Tissues During the Acute Phase of Infection. Am. J. Pathol.
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Zhang, L., Rowe, L., He, T., Chung, C., Yu, J., Yu, W., Talal, A., Markowitz, M., Ho, D. D.
(2002). Compartmentalization of Surface Envelope Glycoprotein of Human Immunodeficiency Virus Type 1 during Acute and Chronic Infection. J. Virol.
76: 9465-9473
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Jekle, A., Schramm, B., Jayakumar, P., Trautner, V., Schols, D., De Clercq, E., Mills, J., Crowe, S. M., Goldsmith, M. A.
(2002). Coreceptor Phenotype of Natural Human Immunodeficiency Virus with Nef Deleted Evolves In Vivo, Leading to Increased Virulence. J. Virol.
76: 6966-6973
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Kijak, G. H., Simon, V., Balfe, P., Vanderhoeven, J., Pampuro, S. E., Zala, C., Ochoa, C., Cahn, P., Markowitz, M., Salomon, H.
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Patel, P. G., Yu Kimata, M. T., Biggins, J. E., Wilson, J. M., Kimata, J. T.
(2002). Highly Pathogenic Simian Immunodeficiency Virus mne Variants That Emerge during the Course of Infection Evolve Enhanced Infectivity and the Ability To Downregulate CD4 but Not Class I Major Histocompatibility Complex Antigens. J. Virol.
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Zheng, N. N., Vella, C., Easterbrook, P. J., Daniels, R. S.
(2002). Selection following isolation of human immunodeficiency virus type 1 in peripheral blood mononuclear cells and herpesvirus saimiri-transformed T cells is comparable. J. Gen. Virol.
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Hoffman, N. G., Seillier-Moiseiwitsch, F., Ahn, J., Walker, J. M., Swanstrom, R.
(2002). Variability in the Human Immunodeficiency Virus Type 1 gp120 Env Protein Linked to Phenotype-Associated Changes in the V3 Loop. J. Virol.
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CRISTILLO, A. D., HIGHBARGER, H. C., DEWAR, R. L., DIMITROV, D. S., GOLDING, H., BIERER, B. E.
(2002). Up-regulation of HIV coreceptor CXCR4 expression in human T lymphocytes is mediated in part by a cAMP-responsive element. FASEB J.
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Zhao, X.-Q., Huang, X.-L., Gupta, P., Borowski, L., Fan, Z., Watkins, S. C., Thomas, E. K., Rinaldo, C. R. Jr.
(2002). Induction of Anti-Human Immunodeficiency Virus Type 1 (HIV-1) CD8+ and CD4+ T-Cell Reactivity by Dendritic Cells Loaded with HIV-1 X4-Infected Apoptotic Cells. J. Virol.
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Suzuki, J.-i., Miyano-Kurosaki, N., Kuwasaki, T., Takeuchi, H., Kawai, G., Takaku, H.
(2002). Inhibition of Human Immunodeficiency Virus Type 1 Activity In Vitro by a New Self-Stabilized Oligonucleotide with Guanosine-Thymidine Quadruplex Motifs. J. Virol.
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Bounou, S., Leclerc, J. E., Tremblay, M. J.
(2002). Presence of Host ICAM-1 in Laboratory and Clinical Strains of Human Immunodeficiency Virus Type 1 Increases Virus Infectivity and CD4+-T-Cell Depletion in Human Lymphoid Tissue, a Major Site of Replication In Vivo. J. Virol.
76: 1004-1014
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Curran, R., Jameson, C. L., Craggs, J. K., Grabowska, A. M., Thomson, B. J., Robins, A., Irving, W. L., Ball, J. K.
(2002). Evolutionary trends of the first hypervariable region of the hepatitis C virus E2 protein in individuals with differing liver disease severity. J. Gen. Virol.
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Platt, E. J., Kuhmann, S. E., Rose, P. P., Kabat, D.
(2001). Adaptive Mutations in the V3 Loop of gp120 Enhance Fusogenicity of Human Immunodeficiency Virus Type 1 and Enable Use of a CCR5 Coreceptor That Lacks the Amino-Terminal Sulfated Region. J. Virol.
75: 12266-12278
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Tanaka, R., Yoshida, A., Murakami, T., Baba, E., Lichtenfeld, J., Omori, T., Kimura, T., Tsurutani, N., Fujii, N., Wang, Z.-X., Peiper, S. C., Yamamoto, N., Tanaka, Y.
(2001). Unique Monoclonal Antibody Recognizing the Third Extracellular Loop of CXCR4 Induces Lymphocyte Agglutination and Enhances Human Immunodeficiency Virus Type 1-Mediated Syncytium Formation and Productive Infection. J. Virol.
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Kwa, D., Vingerhoed, J., Boeser-Nunnink, B., Broersen, S., Schuitemaker, H.
(2001). Cytopathic Effects of Non-Syncytium-Inducing and Syncytium-Inducing Human Immunodeficiency Virus Type 1 Variants on Different CD4+-T-Cell Subsets Are Determined Only by Coreceptor Expression. J. Virol.
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Malkevich, N., Womack, C., Pandya, P., Grivel, J.-C., Fauci, A. S., Margolis, L.
(2001). Human Immunodeficiency Virus Type 1 (HIV-1) Non-B Subtypes Are Similar to HIV-1 Subtype B in that Coreceptor Specificity Is a Determinant of Cytopathicity in Human Lymphoid Tissue Infected Ex Vivo. J. Virol.
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Federico, M., Percario, Z., Olivetta, E., Fiorucci, G., Muratori, C., Micheli, A., Romeo, G., Affabris, E.
(2001). HIV-1 Nef activates STAT1 in human monocytes/macrophages through the release of soluble factors. Blood
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Kreisberg, J. F., Kwa, D., Schramm, B., Trautner, V., Connor, R., Schuitemaker, H., Mullins, J. I., van't Wout, A. B., Goldsmith, M. A.
(2001). Cytopathicity of Human Immunodeficiency Virus Type 1 Primary Isolates Depends on Coreceptor Usage and Not Patient Disease Status. J. Virol.
75: 8842-8847
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Koning, F. A., Schols, D., Schuitemaker, H.
(2001). No Selection for CCR5 Coreceptor Usage during Parenteral Transmission of Macrophagetropic Syncytium-Inducing Human Immunodeficiency Virus Type 1. J. Virol.
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Tokunaga, K., Greenberg, M. L., Morse, M. A., Cumming, R. I., Lyerly, H. K., Cullen, B. R.
(2001). Molecular Basis for Cell Tropism of CXCR4-Dependent Human Immunodeficiency Virus Type 1 Isolates. J. Virol.
75: 6776-6785
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Lane, B. R., Strieter, R. M., Coffey, M. J., Markovitz, D. M.
(2001). Human Immunodeficiency Virus Type 1 (HIV-1)-Induced GRO-{alpha} Production Stimulates HIV-1 Replication in Macrophages and T Lymphocytes. J. Virol.
75: 5812-5822
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