Document 0875
 DOCN  M9470875
 TI    Evolution of a disrupted TAR RNA hairpin structure in the HIV-1 virus.
 DT    9409
 AU    Klaver B; Berkhout B; University of Amsterdam, Department of Virology,
       Academic Medical; Center, The Netherlands.
 SO    EMBO J. 1994 Jun 1;13(11):2650-9. Unique Identifier : AIDSLINE
       MED/94283390
 AB    Human immunodeficiency virus type 1 (HIV-1) RNA contains an extended
       hairpin structure at the 5' end (the TAR element) that is essential for
       viral replication. The upper part of the stem-loop structure binds the
       virally encoded transcriptional activator protein Tat and cellular
       co-factors, but no clear function for the lower stem region has been
       established. Here, we report that mutant HIV-1 viruses with base
       substitutions in the lower stem region are dead, most likely at the
       level of transcription from an integrated provirus. By using large
       amounts of these mutant DNA constructs for transfections, revertant
       viruses with a great variety of genetic changes (point mutations, short
       deletions) could be isolated in prolonged culture experiments that
       lasted over 6 months. The pattern and evolution of these changes
       supported the notion that base-pairing of the lower stem region is
       essential for optimal HIV-1 replication. The functional and genetic
       plasticities of this RNA domain and the HIV-1 long terminal repeat
       promoter are discussed.
 DE    Base Composition  Base Sequence  Cell Line  DNA Mutational Analysis
       DNA, Viral/GENETICS  Evolution  Human  HIV Long Terminal
       Repeat/*GENETICS  HIV-1/GROWTH & DEVELOPMENT/*GENETICS/PHYSIOLOGY
       Kinetics  Molecular Sequence Data  *Nucleic Acid Conformation  Point
       Mutation/*GENETICS  Proviruses  RNA, Viral/ANALYSIS/*CHEMISTRY  Support,
       Non-U.S. Gov't  Transcription, Genetic  Virus Replication/GENETICS
       JOURNAL ARTICLE

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