       Document 0316
 DOCN  M9590316
 TI    Mutually dependent synthesis and amplification of viral DNA and RNA
       early after cell-to-cell transmission of HIV infection.
 DT    9509
 AU    Kok T; Li P; Burrell CJ; NCHVR, Division of Medical Virology, IMVS,
       Adelaide SA.
 SO    Annu Conf Australas Soc HIV Med. 1994 Nov 3-6;6:187 (unnumbered
       abstract). Unique Identifier : AIDSLINE ASHM6/95291783
 AB    Using a one-step cell-to-cell transmission model of HIV infection it was
       shown that there were two distinct phases of HIV RNA synthesis. The
       first phase (4h-12h pi) was marked by a significant increase in only the
       full-length 9.2 kb RNA and the second phase (24h pi onwards) comprised a
       dramatic increase in the levels of all three species of viral RNA (Kok,
       Li, Burrell, 1993). We further report here that when virus donor H3B
       cells were pre-treated with 50 micrograms/ml of actinomycin D, washed
       and mixed with untreated recipient Hut78 cells, reverse transcription
       was not affected by the pretreatment, as normal amounts of full length
       linear unintegrated viral DNA were produced. In the same experiment, the
       second phase of induced viral RNA transcription was abolished, but the
       first phase of viral RNA induction was largely unaffected by the drug.
       The continual presence of actinomycin D at 50 micrograms/ml abolished
       all detectable viral nucleic acid synthesis in vivo but had little
       impact on reverse transcriptase activity when tested in vitro. When both
       the virus donor cells and recipient cells were arrested in the late G1
       phase of the cell cycle by aphidicolin, only linear unintegrated viral
       DNA was produced and the second phase, but not the first phase of
       induced viral RNA synthesis, was abolished. Taken together, our results
       suggest that the template for the first phase of viral RNA induction is
       likely to be the linear unintegrated viral DNA, and that there exists a
       yet to be fully characterized pathway of mutually dependent, concurrent
       HIV DNA and RNA synthesis and amplification early after cell to cell
       transmission of infection.
 DE    Cell Line  Cell Transformation, Viral/GENETICS  DNA, Viral/*GENETICS
       Gene Amplification/*GENETICS  Human  HIV/*GENETICS  HIV
       Infections/GENETICS/*TRANSMISSION  Models, Genetic  RNA, Viral/*GENETICS
       Templates  Virus Integration/GENETICS  Virus Replication/*GENETICS
       MEETING ABSTRACT

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

