| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print July 16, 2001
Unidad de Biologia Molecular, Hospital de la Princesa, Madrid, Madrid 28006
Corresponding Author: mlopez{at}hlpr.insalud.es
Co-infection with hepatitis B virus (HBV) and human immunodeficiency virus type-1 (HIV-1) is relatively common. However, the impact of this co-infection on the clinical outcome of HIV infection has not been elucidated. We herein demonstrate that the HBV X protein (HBx) superinduces ongoing HIV-1 replication and HIV-1 LTR transcription by synergizing with Tat protein and with T-cell activation signals. Although HBx cooperated with mitogenic stimuli in the induction of reporter plasmids harboring the HIV-1 B enhancer, both in a NF-B and NF-AT-dependent manner, deletion of this element from the LTR did not affect the HBx-mediated up-regulation in the presence of Tat and/or mitogens. In contrast, mutation of the proximal LTR Sp1-binding sites abolished the HBx-mediated synergistic activation, but only when it was accompanied by deletion of the B enhancer. When HBx was targeted to the nucleus, its ability to synergize with cellular activation stimuli was maintained. Furthermore, mutations of HBx affecting its interaction with the basal transcription machinery abrogated the synergistic activation by HBx, suggesting that this protein exerts its function by acting as a nuclear co-activator. These results indicate that HBx could contribute to a faster progression to AIDS in HBV-HIV co-infected individuals.
J. Biol. Chem, 10.1074/jbc.M103020200
Submitted on April 5, 2001
Revised on June 22, 2001
Accepted on July 13, 2001
The hepatitis B virus X protein induces HIV-1 replication and transcription in synergy with T-cell activation signals. Functional roles of NF-kB/NF-AT and Sp1 binding sites in the HIV-1 LTR promoter
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  J. Nevado, S. P Tenbaum, A. I. Castillo, A. Sanchez-Pacheco, and A. Aranda Activation of the human immunodeficiency virus type I long terminal repeat by 1{alpha},25-dihydroxyvitamin D3 J. Mol. Endocrinol., June 1, 2007; 38(6): 587 - 601. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. van Opijnen, M. C. Boerlijst, and B. Berkhout Effects of random mutations in the human immunodeficiency virus type 1 transcriptional promoter on viral fitness in different host cell environments. J. Virol., July 1, 2006; 80(13): 6678 - 6685. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Sancho, L. de la Vega, A. Macho, G. Appendino, V. Di Marzo, and E. Munoz Mechanisms of HIV-1 Inhibition by the Lipid Mediator N-Arachidonoyldopamine J. Immunol., September 15, 2005; 175(6): 3990 - 3999. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Sancho, N. Marquez, M. Gomez-Gonzalo, M. A. Calzado, G. Bettoni, M. T. Coiras, J. Alcami, M. Lopez-Cabrera, G. Appendino, and E. Munoz Imperatorin Inhibits HIV-1 Replication through an Sp1-dependent Pathway J. Biol. Chem., September 3, 2004; 279(36): 37349 - 37359. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. van Opijnen, R. E. Jeeninga, M. C. Boerlijst, G. P. Pollakis, V. Zetterberg, M. Salminen, and B. Berkhout Human Immunodeficiency Virus Type 1 Subtypes Have a Distinct Long Terminal Repeat That Determines the Replication Rate in a Host-Cell-Specific Manner J. Virol., April 1, 2004; 78(7): 3675 - 3683. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. O. Kim, Y. Liu, B. Y. Zhou, and J. J. He Induction of C Chemokine XCL1 (Lymphotactin/Single C Motif-1{alpha}/Activation-Induced, T Cell-Derived and Chemokine-Related Cytokine) Expression by HIV-1 Tat Protein J. Immunol., February 1, 2004; 172(3): 1888 - 1895. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
