Document 0200
 DOCN  M9460200
 TI    Cellular and viral specificity of equine infectious anemia virus Tat
       transactivation.
 DT    9408
 AU    Maury WJ; Carpenter S; Graves K; Chesebro B; LPVD, Rocky Mountain
       Laboratories, NIAID, Hamilton, Montana; 59840.
 SO    Virology. 1994 May 1;200(2):632-42. Unique Identifier : AIDSLINE
       MED/94233726
 AB    Lentiviruses vary in their dependence on a functional tat gene during
       their viral life cycle. To begin to understand the viral and cellular
       parameters controlling equine infectious anemia virus (EIAV)
       transactivation, we investigated Tat function and Tat and LTR structural
       requirements necessary for successful transactivation. EIAV Tat
       expression was required for detection of viral antigens from a
       full-length provirus. The level of transactivation by EIAV Tat as
       measured by LTR-CAT assays correlated well with viral antigen
       expression. Using horse/mouse somatic cell hybrids (SCH), a single SCH
       line which supported EIAV transactivation was identified, indicating
       that the presence of specific horse chromosomes provided cellular
       factors required for transactivation. Transformed cell lines from
       several different species were also tested and found to differ in their
       ability to support EIAV transactivation. A canine cell line, Cf2Th,
       which was permissive for EIAV transactivation, and a human cell line,
       HeLa, which was not permissive for EIAV transactivation, were used to
       map regions of the LTR and Tat that were important in cell-specific
       transactivation. As expected, the R region of EIAV LTR was required for
       transactivation by EIAV Tat in all cell lines studied. Similarly, the R
       region of HIV LTR was necessary for transactivation by HIV Tat. However,
       the composition of the U3 region also influenced transactivation in a
       cell-specific manner. In Cf2Th cells, replacement of EIAV U3 sequences
       with HIV U3 sequences resulted in high basal (nontransactivated)
       expression, and as a result, only a twofold increase in expression was
       observed in the presence of EIAV Tat. Similar studies using HIV Tat
       demonstrated that transactivation occurred in Cf2Th cells when either
       EIAV or HIV U3 sequences were present in the LTR. In contrast,
       transactivation by either HIV or EIAV Tat in HeLa cells required the
       presence of HIV enhancer sequences. These findings suggested that the
       ability of transactivation to occur in some cell lines may involve
       interactions between cell-specific transcription factors and the
       activation domain of Tat. For transactivation in other cell lines, Tat
       appeared to require more ubiquitious factors that interact with both
       EIAV and HIV U3 sequences.
 DE    Animal  Antigens, Viral/BIOSYNTHESIS  Base Sequence  Cell Line  Chimeric
       Proteins/METABOLISM  Comparative Study  Enhancer Elements
       (Genetics)/GENETICS  Gene Expression Regulation, Viral  Gene Products,
       tat/GENETICS/*METABOLISM  Genes, tat/*GENETICS  Horses  Human  Hybrid
       Cells  Infectious Anemia Virus, Equine/*GENETICS  Mice  Molecular
       Sequence Data  Proviruses/GENETICS  Repetitive Sequences, Nucleic
       Acid/GENETICS  Species Specificity  Support, U.S. Gov't, P.H.S.
       *Trans-Activation (Genetics)  Transcription Factors/GENETICS/*METABOLISM
       JOURNAL ARTICLE

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