Use of a human immunodeficiency virus type 1 Rev mutant without nucleolar dysfunction as a candidate for potential AIDS therapy

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Published in:	Journal of Virology Vol. 69; no. 3; pp. 1591 - 1599
Main Authors:	Furuta, R A, Kubota, S, Maki, M, Miyazaki, Y, Hattori, T, Hatanaka, M
Format:	Journal Article
Language:	English
Published:	United States American Society for Microbiology 01-03-1995
Subjects:	Acquired Immunodeficiency Syndrome - therapy AIDS/HIV Amino Acid Sequence Base Sequence Cell Line Cell Nucleolus - pathology DNA Primers - chemistry Gene Expression Regulation, Viral Genes, Dominant Genes, rev Genetic Therapy HeLa Cells HIV-1 - genetics HIV-1 - growth & development Humans Molecular Sequence Data Mutation RNA, Viral - genetics Virus Replication
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Abstract	Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI
AbstractList	Applications of transdominant mutants of human immunodeficiency virus type 1 (HIV-1) regulatory proteins, especially Rev mutant, have been attempted for gene therapy against AIDS, because the Rev protein is essential for viral replication. We have previously reported that a mutant Rev protein (dRev) lacking its nucleolar targeting signal remained out of nuclei in expressed cells and strongly inhibited the function of Rev. To investigate the effects of dRev on HIV-1 replication, we established several dRev-expressing human cell lines with two different vector systems and examined virus production in these cells. An HIV-1-derived vector containing drev cDNA was constructed and introduced into CD4-positive HeLa cells and cells of the human T-cell line CCRF-CEM (CEM). In dRev-expressing HeLa cells, virus replication, syncytium formation, and cell death caused by HIV-1 infection were remarkably suppressed, and the same vector also conferred a resistant phenotype on CEM cells. The production was also suppressed in CEM cells containing the drev gene driven by a cytomegalovirus promoter. In addition, we found that dRev did not cause nucleolar dysfunction in a transient assay, in contrast to other transdominant mutants and wild-type Rev. Since dRev cannot migrate into the nuclei, it is expected not to interfere with nuclear/nucleolar functions of the host cell. We conclude that dRev is one promising candidate as an antiviral molecule for gene therapy against AIDS. Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI
Author	M Hatanaka T Hattori Y Miyazaki M Maki S Kubota R A Furuta
AuthorAffiliation	Department of Molecular Virology, Kyoto University, Japan
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SubjectTerms	Acquired Immunodeficiency Syndrome - therapy AIDS/HIV Amino Acid Sequence Base Sequence Cell Line Cell Nucleolus - pathology DNA Primers - chemistry Gene Expression Regulation, Viral Genes, Dominant Genes, rev Genetic Therapy HeLa Cells HIV-1 - genetics HIV-1 - growth & development Humans Molecular Sequence Data Mutation RNA, Viral - genetics Virus Replication
Title	Use of a human immunodeficiency virus type 1 Rev mutant without nucleolar dysfunction as a candidate for potential AIDS therapy
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