This Article
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 Herbein, G.
Right arrow Articles by Gordon, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Herbein, G.
Right arrow Articles by Gordon, S.

 Previous Article  |  Next Article 

J. Virol., May 1997, 4150-4156, Vol 71, No. 5
Copyright © 1997, American Society for Microbiology

55- and 75-kilodalton tumor necrosis factor receptors mediate distinct actions in regard to human immunodeficiency virus type 1 replication in primary human macrophages

G Herbein and S Gordon
Virology Institute of the Faculty of Medicine and INSERM Unit 74, Louis Pasteur University, Strasbourg, France.

We report in this study that repeated tumor necrosis factor alpha (TNF- alpha) pretreatment, starting before and continued after infection by human immunodeficiency virus type 1 (HIV-1), inhibits replication of the monocytotropic Ada strain in primary tissue culture-differentiated macrophages (TCDM), as assessed by sixfold lower levels of reverse transcriptase (RT) activity than that in untreated cells and absence of syncytium formation in TCDM cultures. In order to determine the pathways involved in inhibition of HIV-1 replication in primary TCDM pretreated with TNF-alpha, we tested TNF-alpha mutants T55 and T75, which recognize either the 55-kDa (TNF-R1) or the 75-kDa (TNF-R2) TNF receptor, respectively. Pretreatment of TCDM with the T75 mutant decreased the RT activity compared with that in untreated infected control cells fivefold and almost totally inhibited syncytium formation. In contrast, when TCDM were pretreated with the T55 mutant alone, syncytia were observed and RT activity was decreased about one- half. These results suggest that the inhibition of HIV-1 replication in TCDM pretreated with TNF-alpha might be mediated mainly through the 75- kDa TNF receptor (TNF-R2) rather than through the 55-kDa receptor (TNF- R1). Inhibition of HIV-1 replication in TCDM was observed with both T75 mutant pretreatment and posttreatment, starting at 1 h or 3 days after infection, whereas posttreatment with the T55 mutant, but not pretreatment, stimulated HIV-1 growth in primary TCDM. Both pre- and posttreatment with TNF-alpha inhibited HIV-1 replication in primary TCDM. The stimulation of HIV-1 replication by TNF-alpha in a chronically infected promonocytic cell line, U1, which contains two copies of integrated provirus, was mediated through the 55-kDa TNF-R1 alone and not through the 75-kDa TNF-R2. These results demonstrate that the 55-kDa TNF-R1 is involved in postintegration stimulation of HIV-1 while the 75-kDa TNF-R2 is involved in the inhibition of an early step of the viral life cycle in primary human TCDM.


This article has been cited by other articles:

  • Erikstrup, C., Kallestrup, P., Zinyama-Gutsire, R. B. L., Gomo, E., van Dam, G. J., Deelder, A. M., Butterworth, A. E., Pedersen, B. K., Ostrowski, S. R., Gerstoft, J., Ullum, H. (2008). Schistosomiasis and Infection with Human Immunodeficiency Virus 1 in Rural Zimbabwe: Systemic Inflammation during Co-infection and after Treatment for Schistosomiasis. Am J Trop Med Hyg 79: 331-337 [Abstract] [Full Text]  
  • Mangino, G., Percario, Z. A., Fiorucci, G., Vaccari, G., Manrique, S., Romeo, G., Federico, M., Geyer, M., Affabris, E. (2007). In Vitro Treatment of Human Monocytes/Macrophages with Myristoylated Recombinant Nef of Human Immunodeficiency Virus Type 1 Leads to the Activation of Mitogen-Activated Protein Kinases, I{kappa}B Kinases, and Interferon Regulatory Factor 3 and to the Release of Beta Interferon. J. Virol. 81: 2777-2791 [Abstract] [Full Text]  
  • Varin, A., Decrion, A.-Z., Sabbah, E., Quivy, V., Sire, J., Van Lint, C., Roques, B. P., Aggarwal, B. B., Herbein, G. (2005). Synthetic Vpr Protein Activates Activator Protein-1, c-Jun N-terminal Kinase, and NF-{kappa}B and Stimulates HIV-1 Transcription in Promonocytic Cells and Primary Macrophages. J. Biol. Chem. 280: 42557-42567 [Abstract] [Full Text]  
  • Mahlknecht, U., Will, J., Varin, A., Hoelzer, D., Herbein, G. (2004). Histone Deacetylase 3, a Class I Histone Deacetylase, Suppresses MAPK11-Mediated Activating Transcription Factor-2 Activation and Represses TNF Gene Expression. J. Immunol. 173: 3979-3990 [Abstract] [Full Text]  
  • Perez-Bercoff, D., David, A., Sudry, H., Barre-Sinoussi, F., Pancino, G. (2003). Fc{gamma} Receptor-Mediated Suppression of Human Immunodeficiency Virus Type 1 Replication in Primary Human Macrophages. J. Virol. 77: 4081-4094 [Abstract] [Full Text]  
  • Varin, A., Manna, S. K., Quivy, V., Decrion, A.-Z., Van Lint, C., Herbein, G., Aggarwal, B. B. (2003). Exogenous Nef Protein Activates NF-kappa B, AP-1, and c-Jun N-Terminal Kinase and Stimulates HIV Transcription in Promonocytic Cells. ROLE IN AIDS PATHOGENESIS. J. Biol. Chem. 278: 2219-2227 [Abstract] [Full Text]  
  • Kacani, L., Banki, Z., Zwirner, J., Schennach, H., Bajtay, Z., Erdei, A., Stoiber, H., Dierich, M. P. (2001). C5a and C5adesArg Enhance the Susceptibility of Monocyte-Derived Macrophages to HIV Infection. J. Immunol. 166: 3410-3415 [Abstract] [Full Text]  
  • Herbein, G., O'brien, W. A. (2000). Tumor Necrosis Factor (TNF)-{alpha} and TNF Receptors in Viral Pathogenesis. Exp. Biol. Med. 223: 241-257 [Abstract] [Full Text]  
  • Lane, B. R., Markovitz, D. M., Woodford, N. L., Rochford, R., Strieter, R. M., Coffey, M. J. (1999). TNF-{alpha} Inhibits HIV-1 Replication in Peripheral Blood Monocytes and Alveolar Macrophages by Inducing the Production of RANTES and Decreasing C-C Chemokine Receptor 5 (CCR5) Expression. J. Immunol. 163: 3653-3661 [Abstract] [Full Text]  
  • Honda, Y., Rogers, L., Nakata, K., Zhao, B.-Y., Pine, R., Nakai, Y., Kurosu, K., Rom, W. N., Weiden, M. (1998). Type I Interferon Induces Inhibitory 16-kD CCAAT/ Enhancer Binding Protein (C/EBP){beta}, Repressing the HIV-1 Long Terminal Repeat in Macrophages: Pulmonary Tuberculosis Alters C/EBP Expression, Enhancing HIV-1 Replication. JEM 188: 1255-1265 [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»