       Document 0236
 DOCN  M9440236
 TI    Inhibition of human immunodeficiency virus reactivation from latency by
       a tat transdominant negative mutant.
 DT    9404
 AU    Balboni PG; Bozzini R; Zucchini S; Marconi PC; Grossi MP; Caputo A;
       Manservigi R; Barbanti-Brodano G; Institute of Microbiology, School of
       Medicine, University of; Ferrara, Italy.
 SO    J Med Virol. 1993 Dec;41(4):289-95. Unique Identifier : AIDSLINE
       MED/94149441
 AB    A BK virus (BKV) expression vector, specific for human cells, was
       engineered to express antisense human immunodeficiency virus type 1
       (HIV-1) tat cDNA (tat-AS) or a tat mutant in cysteine 22 (tat22).
       Cysteine residues in the cysteine-rich domain of tat are necessary for
       tat transactivation of the HIV-1 long terminal repeat (LTR). Both the AS
       tat and the tat mutant significantly inhibited transactivation by tat
       when assayed in cells cotransfected with an expression vector where the
       reporter gene for chloramphenicol acetyl transferase was driven by the
       HIV-1 LTR. Infection of Jurkat cell clones stably expressing tat22
       (Jurkat/tat22) or tat-AS (Jurkat/tat-AS) with HIV-1 did not show
       differences in virus titer in comparison to HIV-1-infected control
       cells. However, in two Jurkat/tat22 cell clones, entrance of HIV-1 into
       latency was accelerated significantly and reactivation of HIV-1 from
       latency induced by tumor necrosis factor-alpha (TNF-alpha) or tat was
       blocked. These results suggest that, in a combined and integrated
       approach to the treatment of acquired immunodeficiency syndrome (AIDS),
       anti-tat genetic therapy could be successfully applied to maintain virus
       in latency, thereby extending the duration of the asymptomatic phase
       preceding full-blown AIDS.
 DE    Antigens, CD4/ANALYSIS  Blotting, Northern  Cell Line, Transformed  Gene
       Products, tat/GENETICS  Genes, tat/*GENETICS  Genetic Vectors  Human
       HIV-1/*GENETICS/PHYSIOLOGY  Mutagenesis, Site-Directed
       Mutation/GENETICS  Polyomavirus hominis 1  RNA, Antisense/GENETICS  RNA,
       Viral/ANALYSIS  Support, Non-U.S. Gov't  Transcription, Genetic/GENETICS
       *Virus Activation  *Virus Latency  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

