       Document 3267
 DOCN  M94A3267
 TI    Possible role of dUTPase analog in compositional divergency in evolution
       of retriviruses.
 DT    9412
 AU    Blinov VM; Resenchuk SM; Chirikova GB; Denisov SI; Zverev VV; Institute
       of Molecular Biology, Koltsovo, Novosibirsk, Russia.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):115 (abstract no. PA0081). Unique
       Identifier : AIDSLINE ICA10/94369308
 AB    HIV, unlike other lentiviruses, has high evolutionary rate in the
       accumulation of mutations. Earlier we have revealed a new enzymatic
       activity (dUTPase EC 3.6.4.23) in the subfamily of lentiviruses, which
       includes VISNA, EIAV, FIV, and CAEV. However, in the subfamily of
       lentiviruses including HIV1, HIV2, SIV, and HTLV of type 1 and 2 the
       dUTPase-analogous fragment is deleted. As this enzyme takes part in DNA
       reparation and nucleotide metabolism, we suggest that the loss of
       dUTPase is responsible for the extraordinary variability of the
       representatives of the latter subfamily. The significant differences in
       the content of C and T pairs between the subfamilies of lentiviruses is
       suggested to be due to the absense of dUTPase in HIV1, HIV2, and SIV on
       one hand, and the presence of the enzyme in the subfamily of latent
       lentiviruses. The role of dUTPase in virus cycle--integration of the
       genomes of different lentiviruses in a host chromosome, and the
       influence of this process on the pathogenesis of slow (FIV, EIAV, VISNA)
       and fast (HIV1, HIV2, SIV) viruses is discussed.
 DE    Animal  Base Composition  DNA, Viral/CHEMISTRY/GENETICS  *Evolution
       Gene Deletion  Genes, Viral  Human  HIV-1/ENZYMOLOGY/GENETICS
       HIV-2/ENZYMOLOGY/GENETICS  Lentivirus/CLASSIFICATION/ENZYMOLOGY/GENETICS
       Mutation  Pyrophosphatases/*GENETICS  Retroviridae/*ENZYMOLOGY/*GENETICS
       Retroviridae Infections/ETIOLOGY  MEETING ABSTRACT

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

