This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Saha, K.
Right arrow Articles by Volsky, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Saha, K.
Right arrow Articles by Volsky, D. J.

 Previous Article  |  Next Article 

J Virol, January 1998, p. 876-881, Vol. 72, No. 1
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Endogenous Production of beta -Chemokines by CD4+, but Not CD8+, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro

Kunal Saha,1 Galina Bentsman,1 Leonard Chess,2 and David J. Volsky1,*

Molecular Virology Laboratory, St. Luke's-Roosevelt Hospital Center, College of Physicians & Surgeons, Columbia University, New York, New York 10019,1 and Division of Rheumatology, Department of Medicine, College of Physicians & Surgeons, Columbia University, New York, New York 100322

Received 24 June 1997/Accepted 28 September 1997

Recent studies have demonstrated that the beta -chemokines RANTES, MIP-1alpha , and MIP-1beta suppress human immunodeficiency virus type 1 (HIV-1) replication in vitro and may play an important role in protecting exposed but uninfected individuals from HIV-1 infection. However, levels of beta -chemokines in AIDS patients are comparable to and can exceed levels in nonprogressing individuals, indicating that global beta -chemokine production may have little effect on HIV-1 disease progression. We sought to clarify the role of beta -chemokines in nonprogressors and AIDS patients by examination of beta -chemokine production and HIV-1 infection in patient T-lymphocyte clones established by herpesvirus saimiri immortalization. Both CD4+ and CD8+ clones were established, and they resembled primary T cells in their phenotypes and expression of activated T-cell markers. CD4+ T-cell clones from all patients had normal levels of mRNA-encoding CCR5, a coreceptor for non-syncytium-inducing (NSI) HIV-1. CD4+ clones from nonprogressors and CD8+ clones from AIDS patients secreted high levels of RANTES, MIP1alpha , and MIP-1beta . In contrast, CD4+ clones from AIDS patients produced no RANTES and little or no MIP-1alpha or MIP-1beta . The infection of CD4+ clones with the NSI HIV-1 strain ADA revealed an inverse correlation to beta -chemokine production; clones from nonprogressors were poorly susceptible to ADA replication, but clones from AIDS patients were highly infectable. The resistance to ADA infection in CD4+ clones from nonprogressors could be partially reversed by treatment with anti-beta -chemokine antibodies. These results indicate that CD4+ cells can be protected against NSI-HIV-1 infection in culture through endogenously produced factors, including beta -chemokines, and that beta -chemokine production by CD4+, but not CD8+, T cells may constitute one mechanism of disease-free survival for HIV-1-infected individuals.

* Corresponding author. Mailing address: Molecular Virology Laboratory, 432 W. 58th St., St. Luke's-Roosevelt Hospital Center, New York, NY 10019. Phone: (212) 582-4451. Fax: (212) 582-5027. E-mail: djv4{at}columbia.edu.




This article has been cited by other articles:

  • Fakruddin, J. M., Lempicki, R. A., Gorelick, R. J., Yang, J., Adelsberger, J. W., Garcia-Pineres, A. J., Pinto, L. A., Lane, H. C., Imamichi, T. (2007). Noninfectious papilloma virus-like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27. Blood 109: 1841-1849 [Abstract] [Full Text]  
  • Barabitskaja, O., Foulke, J. S. Jr., Pati, S., Bodor, J., Reitz, M. S. Jr. (2006). Suppression of MIP-1{beta} transcription in human T cells is regulated by inducible cAMP early repressor (ICER). J. Leukoc. Biol. 79: 378-387 [Abstract] [Full Text]  
  • Zerhouni, B., Nelson, J. A. E., Saha, K. (2004). CXCR4-Dependent Infection of CD8+, but Not CD4+, Lymphocytes by a Primary Human Immunodeficiency Virus Type 1 Isolate. J. Virol. 78: 12288-12296 [Abstract] [Full Text]  
  • Sorokina, E. M., Merlo, J. J. Jr., Tsygankov, A. Y. (2004). Molecular Mechanisms of the Effect of Herpesvirus saimiri Protein StpC on the Signaling Pathway Leading to NF-{kappa}B Activation. J. Biol. Chem. 279: 13469-13477 [Abstract] [Full Text]  
  • Abdelwahab, S. F., Cocchi, F., Bagley, K. C., Kamin-Lewis, R., Gallo, R. C., DeVico, A., Lewis, G. K. (2003). HIV-1-suppressive factors are secreted by CD4+ T cells during primary immune responses. Proc. Natl. Acad. Sci. USA 100: 15006-15010 [Abstract] [Full Text]  
  • Gross, E., Amella, C. A., Pompucci, L., Franchin, G., Sherry, B., Schmidtmayerova, H. (2003). Macrophages and lymphocytes differentially modulate the ability of RANTES to inhibit HIV-1 infection. J. Leukoc. Biol. 74: 781-790 [Abstract] [Full Text]  
  • Alimonti, J. B., Ball, T. B., Fowke, K. R. (2003). Mechanisms of CD4+ T lymphocyte cell death in human immunodeficiency virus infection and AIDS. J. Gen. Virol. 84: 1649-1661 [Abstract] [Full Text]  
  • Llano, A., Barretina, J., Gutierrez, A., Clotet, B., Este, J. A. (2003). Interleukin-7-Dependent Production of RANTES That Correlates with Human Immunodeficiency Virus Disease Progression. J. Virol. 77: 4389-4395 [Abstract] [Full Text]  
  • Clapham, P. R., McKnight, A. (2002). Cell surface receptors, virus entry and tropism of primate lentiviruses. J. Gen. Virol. 83: 1809-1829 [Abstract] [Full Text]  
  • An, P., Nelson, G. W., Wang, L., Donfield, S., Goedert, J. J., Phair, J., Vlahov, D., Buchbinder, S., Farrar, W. L., Modi, W., O'Brien, S. J., Winkler, C. A. (2002). Modulating influence on HIV/AIDS by interacting RANTES gene variants. Proc. Natl. Acad. Sci. USA 99: 10002-10007 [Abstract] [Full Text]  
  • Llano, A., Barretina, J., Gutierrez, A., Blanco, J., Cabrera, C., Clotet, B., Este, J. A. (2001). Interleukin-7 in Plasma Correlates with CD4 T-Cell Depletion and May Be Associated with Emergence of Syncytium-Inducing Variants in Human Immunodeficiency Virus Type 1-Positive Individuals. J. Virol. 75: 10319-10325 [Abstract] [Full Text]  
  • Clapham, P. R, McKnight, A. (2001). HIV-1 receptors and cell tropism. Br Med Bull 58: 43-59 [Abstract] [Full Text]  
  • Zaitseva, M., King, L. R., Manischewitz, J., Dougan, M., Stevan, L., Golding, H., Golding, B. (2001). Human Peripheral Blood T Cells, Monocytes, and Macrophages Secrete Macrophage Inflammatory Proteins 1{alpha} and 1{beta} following Stimulation with Heat-Inactivated Brucella abortus. Infect. Immun. 69: 3817-3826 [Abstract] [Full Text]  
  • Wünschmann, S., Stapleton, J. T. (2000). Fluorescence-Based Quantitative Methods for Detecting Human Immunodeficiency Virus Type 1-Induced Syncytia. J. Clin. Microbiol. 38: 3055-3060 [Abstract] [Full Text]  
  • Saha, K., Volsky, D. J., Matczak, E. (1999). Resistance against Syncytium-Inducing Human Immunodeficiency Virus Type 1 (HIV-1) in Selected CD4+ T Cells from an HIV-1-Infected Nonprogressor: Evidence of a Novel Pathway of Resistance Mediated by a Soluble Factor(s) That Acts after Virus Entry. J. Virol. 73: 7891-7898 [Abstract] [Full Text]  
  • Aiuti, A., Turchetto, L., Cota, M., Cipponi, A., Brambilla, A., Arcelloni, C., Paroni, R., Vicenzi, E., Bordignon, C., Poli, G. (1999). Human CD34+ Cells Express CXCR4 and Its Ligand Stromal Cell-Derived Factor-1. Implications for Infection by T-Cell Tropic Human Immunodeficiency Virus. Blood 94: 62-73 [Abstract] [Full Text]  
  • Liu, H., Chao, D., Nakayama, E. E., Taguchi, H., Goto, M., Xin, X., Takamatsu, J.-k., Saito, H., Ishikawa, Y., Akaza, T., Juji, T., Takebe, Y., Ohishi, T., Fukutake, K., Maruyama, Y., Yashiki, S., Sonoda, S., Nakamura, T., Nagai, Y., Iwamoto, A., Shioda, T. (1999). Polymorphism in chemokine promoter affects HIV-1 disease progression. Proc. Natl. Acad. Sci. USA 96: 4581-4585 [Abstract] [Full Text]  
  • Lee, B., Ratajczak, J., Doms, R. W., Gewirtz, A. M., Ratajczak, M. Z. (1999). Coreceptor/Chemokine Receptor Expression on Human Hematopoietic Cells: Biological Implications for Human Immunodeficiency Virus-Type 1 Infection. Blood 93: 1145-1156 [Abstract] [Full Text]  
  • Greco, G., Fujimura, S. H., Mourich, D. V., Levy, J. A. (1999). Differential Effects of Human Immunodeficiency Virus Isolates on beta -Chemokine and Gamma Interferon Production and on Cell Proliferation. J. Virol. 73: 1528-1534 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»