Literature DB >> 8122376

Tat and rev differentially affect restricted replication of human immunodeficiency virus type 1 in various cells.

L Duan1, J W Oakes, A Ferraro, O Bagasra, R J Pomerantz.   

Abstract

Human immunodeficiency virus type 1 (HIV-1) can infect various cell lines in culture and be maintained in a chronic state of restricted replication. These states of proviral latency are characterized by a predominance of spliced compared to unspliced viral RNA species. The proximate molecular mechanisms leading to restricted HIV-1 replication may differ in various cell lines. Importantly, recent studies have demonstrated that the site of integration is the critical parameter leading to proviral latency in ACH-2 cells. Utilizing murine retroviral shuttle vectors, the HIV-1 Tat protein was demonstrated to dramatically increase HIV-1 expression in the restrictively infected U1 monocytic cell line but not in the ACH-2 T-lymphocytic line. The HIV-1 Rev protein only modestly increased viral expression in both of these cell types. Thus, these data support the hypothesis that the mechanisms which initiate and/or maintain restricted HIV-1 expression may differ in various cell types in cell culture, and possibly in vivo.

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Year:  1994        PMID: 8122376     DOI: 10.1006/viro.1994.1148

Source DB:  PubMed          Journal:  Virology        ISSN: 0042-6822            Impact factor:   3.616


  9 in total

1.  A point mutation in the HIV-1 Tat responsive element is associated with postintegration latency.

Authors:  S Emiliani; C Van Lint; W Fischle; P Paras; M Ott; J Brady; E Verdin
Journal:  Proc Natl Acad Sci U S A       Date:  1996-06-25       Impact factor: 11.205

2.  Binding of intracellular anti-Rev single chain variable fragments to different epitopes of human immunodeficiency virus type 1 rev: variations in viral inhibition.

Authors:  Y Wu; L Duan; M Zhu; B Hu; S Kubota; O Bagasra; R J Pomerantz
Journal:  J Virol       Date:  1996-05       Impact factor: 5.103

3.  Permanent occupancy of the human immunodeficiency virus type 1 enhancer by NF-kappa B is needed for persistent viral replication in monocytes.

Authors:  J M Jacqué; B Fernández; F Arenzana-Seisdedos; D Thomas; F Baleux; J L Virelizier; F Bachelerie
Journal:  J Virol       Date:  1996-05       Impact factor: 5.103

4.  Inhibition of human immunodeficiency virus type 1 Rev function by a dominant-negative mutant of Sam68 through sequestration of unspliced RNA at perinuclear bundles.

Authors:  V B Soros; H V Carvajal; S Richard; A W Cochrane
Journal:  J Virol       Date:  2001-09       Impact factor: 5.103

5.  Mutations in the tat gene are responsible for human immunodeficiency virus type 1 postintegration latency in the U1 cell line.

Authors:  S Emiliani; W Fischle; M Ott; C Van Lint; C A Amella; E Verdin
Journal:  J Virol       Date:  1998-02       Impact factor: 5.103

6.  The tumor suppressor protein p53 strongly alters human immunodeficiency virus type 1 replication.

Authors:  L Duan; I Ozaki; J W Oakes; J P Taylor; K Khalili; R J Pomerantz
Journal:  J Virol       Date:  1994-07       Impact factor: 5.103

7.  Regulation of macrophage activation and human immunodeficiency virus production by invasive Salmonella strains.

Authors:  S B Mizel; L S Kucera; S H Richardson; F Ciacci; N P Iyer
Journal:  Infect Immun       Date:  1995-05       Impact factor: 3.441

8.  Elimination of endogenous aberrant kappa chain transcripts from sp2/0-derived hybridoma cells by specific ribozyme cleavage: utility in genetic therapy of HIV-1 infections.

Authors:  L Duan; R J Pomerantz
Journal:  Nucleic Acids Res       Date:  1994-12-11       Impact factor: 16.971

9.  Increasing transduction efficiency of recombinant murine retrovirus vectors by initiation of endogenous reverse transcription: potential utility for genetic therapies.

Authors:  H Zhang; L X Duan; G Dornadula; R J Pomerantz
Journal:  J Virol       Date:  1995-06       Impact factor: 5.103

  9 in total

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