Document 3315
 DOCN  M94A3315
 TI    Distinct mechanisms of HIV-1 latency in the two cell line models U1 and
       ACH-2.
 DT    9412
 AU    Cannon P; Kim SH; Ulich C; Kim S; Seoul National University, Korea.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):104 (abstract no. PA0035). Unique
       Identifier : AIDSLINE ICA10/94369260
 AB    The U1 and ACH-2 cell lines are human monocytic and T-lymphoid cells
       respectively, persistently infected with HIV-1. These cell lines express
       viral RNA and proteins at very low levels, but can be induced to produce
       larger amounts virion particles. For this reason, they have been used
       extensively as in vitro models of HIV latency. In order to examine the
       basis for the latent state of HIV in these cell lines, we have
       investigated the roles of the essential viral regulatory factor Tat.
       First, we transiently transfected the HIV LTR as a reporter plasmid for
       Tat function. Second, purified Tat protein was added to the culture to
       test whether HIV production could be increased. Third, we constructed U1
       and ACH-2 derivatives constitutively expressing Tat. Results obtained
       from these analyses indicated that the provirus in the U1 cell line is
       latent because of suboptimal levels of Tat, while Tat is not limiting
       for viral production in ACH-2 cells. A different mechanism therefore
       underlies the latent state of HIV in U1 and ACH-2 cells. This result
       also argues against a model of HIV latency based simply on suboptimal
       levels of the Rev protein. We are currently studying the role(s) of Rev
       using experimental schemes similar to those employed for the analysis of
       Tat.
 DE    Cell Line  Gene Expression  Gene Products, rev/GENETICS/PHYSIOLOGY  Gene
       Products, tat/GENETICS/PHYSIOLOGY  Genes, tat  Human  HIV
       Infections/ETIOLOGY  HIV Long Terminal Repeat
       HIV-1/GENETICS/*PHYSIOLOGY/PATHOGENICITY  Models, Biological
       Monocytes/MICROBIOLOGY  T-Lymphocytes/MICROBIOLOGY  Transfection  Virus
       Replication/GENETICS/PHYSIOLOGY  MEETING ABSTRACT

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       protected by Copyright Law (Title 17, U.S.Code).