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J Virol, April 1998, p. 3037-3044, Vol. 72, No. 4
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Human Immunodeficiency Virus Type 1 (HIV-1) Viral Protein R (Vpr)
Interacts with Lys-tRNA Synthetase: Implications for Priming of
HIV-1 Reverse Transcription
Lesley A.
Stark
and
Ronald T.
Hay*
School of Biomedical Sciences, Irvine
Building, University of St. Andrews, St. Andrews, Fife KY16 9AL,
Scotland
Received 25 July 1997/Accepted 17 December 1997
The vpr gene of human immunodeficiency virus type 1 (HIV-1) encodes a 96-amino-acid 14-kDa protein (viral protein R
[Vpr]), which is produced late in the viral life cycle and is
incorporated into the virion. Although Vpr is not required for viral
replication in transformed cell lines and primary T lymphocytes, it is
essential for productive infection of macrophages and monocytes and
appears to be important for pathogenesis in vivo. To establish the role of Vpr in HIV-1 replication and pathogenesis, we have isolated cellular
proteins with which Vpr interacts. By using the yeast two-hybrid
system, Lys-tRNA synthetase (LysRS) was identified as a
Vpr-interacting protein. The interaction between Vpr and LysRS
was characterized both in vitro and in vivo, and the domains of Vpr
required for the interaction were defined. In the presence of Vpr,
LysRS-mediated aminoacylation of tRNALys is
inhibited. Since tRNALys is the primer for reverse
transcription of the HIV-1 genome, this suggests that the interaction
between Vpr and LysRS may influence the initiation of HIV-1 reverse
transcription.
*
Corresponding author. Mailing address: Division of Cell
and Molecular Biology, School of Biomedical Sciences, University of St.
Andrews, Irvine Building, North St., St. Andrews, Fife KY16 9AL,
Scotland. Phone: 44 1334 463396. Fax: 44 1334 463400. E-mail: rth{at}st-and.ac.uk.

Present address: MRC Human Genetics Unit, Western General Hospital,
Edinburgh EH4 2XU, Scotland.
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