Document 0292
 DOCN  M9590292
 TI    Human immunodeficiency virus-1 induces increased activity of cellular
       topoisomerases.
 DT    9509
 AU    Jardine D; Tachedjian G; Locarnini S; Birch C; Antiviral Laboratory,
       Victorian Infectious Diseases Reference; Laboratory, Fairfield Hospital.
 SO    Annu Conf Australas Soc HIV Med. 1994 Nov 3-6;6:217 (unnumbered
       abstract). Unique Identifier : AIDSLINE ASHM6/95291807
 AB    The presence of HIV supercoiled DNA in cells infected with this virus
       suggests a role for topoisomerases in the replication cycle of HIV-1.
       Previously we have demonstrated topoisomerase I activity in sucrose
       gradient purified HIV-1 virions from several isolates. By comparing the
       ionic requirements and inhibition by various drugs of the
       virus-associated enzyme with a mammalian topoisomerase I, we have
       concluded that the topoisomerase activity associated with the purified
       virus particles is of cellular origin. In MT-2 cells infected with
       HIV-1, inhibitors of both eukaryotic topoisomerase I and II failed to
       exhibit an antiviral effect at non-toxic levels. Topoisomerase I and II
       were extracted at various times after infection with HIV-1 and placed
       into in vitro assays designed to detect topoisomerase activity.
       Quantitation of human topoisomerase I and II activity levels revealed
       that HIV-1 induces an increase in both topoisomerase I and II activity
       during infection. The increase in topoisomerase I activity occurs almost
       immediately post-infection whilst the increase in topoisomerase II
       occurs late in infection. These increases in intracellular enzymatic
       activity are not reflected in Western Blot profiles, possibly indicating
       phosphorylation of the enzymes to an active form.
 DE    Cell Line, Transformed  DNA Topoisomerase/*BIOSYNTHESIS  DNA
       Topoisomerase (ATP-Hydrolysing)/*BIOSYNTHESIS  Enzyme
       Induction/PHYSIOLOGY  Human  HIV-1/*PATHOGENICITY  Virus
       Integration/*PHYSIOLOGY  Virus Replication/*PHYSIOLOGY  MEETING ABSTRACT

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