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Archetype JC virus efficiently propagates in kidney‐derived cells stably expressing HIV‐1 Tat

Identifieur interne : 000972 ( Istex/Curation ); précédent : 000971; suivant : 000973

Archetype JC virus efficiently propagates in kidney‐derived cells stably expressing HIV‐1 Tat

Auteurs : Souichi Nukuzuma ; Masanori Kameoka [Japon] ; Shigeki Sugiura ; Kazuo Nakamichi ; Chiyoko Nukuzuma ; Isao Miyoshi ; Tsutomu Takegami [Japon]

Source :

RBID : ISTEX:F30EF4F1A9397D40091BFCD2352C95DBDC607939

English descriptors

Abstract

Pathogenic JCV with rearranged regulatory regions (PML‐type) causes PML, a demyelinating disease, in the brains of immunocompromised patients. On the other hand, archetype JCV persistently infecting the kidney is thought to be converted to PML‐type virus during JCV replication in the infected host under immunosuppressed conditions. In addition, Tat protein, encoded by HIV‐1, markedly enhances the expression of a reporter gene under control of the JCV late promoter. In order to examine the influence of Tat on JCV propagation, we used kidney‐derived COS‐7 cells, which only permit archetype JCV, and established COS‐tat cells, which express HIV‐1 Tat stably. We found that the extent of archetype JCV propagation in COS‐tat cells is significantly greater than in COS‐7 cells. On the other hand, COS‐7 cells express SV40 T antigen, which is a strong stimulator of archetype JCV replication. The expression of SV40 T antigen was enhanced by HIV‐1 Tat slightly according to real‐time RT‐PCR, this was not closely related to JCV replication in COS‐tat cells. The efficiency of JCV propagation depended on the extent of expression of functional Tat. To our knowledge, this is the first report of increased production of archetype JCV in a culture system using cell lines stably expressing HIV‐1 Tat. We propose here that COS‐tat cells are a useful tool for studying the role of Tat in archetype JCV replication in the development of PML.

Url:
DOI: 10.1111/j.1348-0421.2009.00166.x

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ISTEX:F30EF4F1A9397D40091BFCD2352C95DBDC607939

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Souichi Nukuzuma
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Shigeki Sugiura
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Kazuo Nakamichi
<affiliation>
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Chiyoko Nukuzuma
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<mods:affiliation>Department of Microbiology, Kobe Institute of Health, 4‐6, Minatojima‐Nakamachi, Chuo‐ku, Kobe, Hyogo 650‐0046</mods:affiliation>
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Isao Miyoshi
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<term>Archetype</term>
<term>Assay</term>
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<term>Cell clones</term>
<term>Cell lines</term>
<term>Cell lines stably</term>
<term>Cell monolayer</term>
<term>Cells stably</term>
<term>Cells transfected</term>
<term>Cells untransfected</term>
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<term>Copy numbers</term>
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<term>Culture system</term>
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<term>Detectable level</term>
<term>Epithelial cells</term>
<term>Etiologic agent</term>
<term>Expression vector</term>
<term>Galactosidase activity</term>
<term>Genome replication</term>
<term>Glial cells</term>
<term>High incidence</term>
<term>Human polyomavirus</term>
<term>Human virus type</term>
<term>Hypervariable sequences</term>
<term>Immunocompromised patients</term>
<term>Immunocytochemical staining</term>
<term>Jurkat cells</term>
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<term>Lipofectamine reagent</term>
<term>Luciferase</term>
<term>Luciferase activity</term>
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<term>Mrna</term>
<term>Mrna expression</term>
<term>National center</term>
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<term>Other hand</term>
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<term>Persistent infection</term>
<term>Plasmid</term>
<term>Previous report</term>
<term>Primer</term>
<term>Proc natl acad</term>
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<term>Progressive multifocal leukoencephalopathy</term>
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<term>Regulatory region</term>
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<term>Reporter gene</term>
<term>Reporter gene assay</term>
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<term>Simian virus</term>
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<term>Blackwell publishing asia</term>
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<term>Human polyomavirus</term>
<term>Human virus type</term>
<term>Hypervariable sequences</term>
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<term>Lipofectamine reagent</term>
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<term>Other hand</term>
<term>Parental cells</term>
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<term>Plasmid</term>
<term>Previous report</term>
<term>Primer</term>
<term>Proc natl acad</term>
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<term>Simian virus</term>
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<front>
<div type="abstract" xml:lang="en">Pathogenic JCV with rearranged regulatory regions (PML‐type) causes PML, a demyelinating disease, in the brains of immunocompromised patients. On the other hand, archetype JCV persistently infecting the kidney is thought to be converted to PML‐type virus during JCV replication in the infected host under immunosuppressed conditions. In addition, Tat protein, encoded by HIV‐1, markedly enhances the expression of a reporter gene under control of the JCV late promoter. In order to examine the influence of Tat on JCV propagation, we used kidney‐derived COS‐7 cells, which only permit archetype JCV, and established COS‐tat cells, which express HIV‐1 Tat stably. We found that the extent of archetype JCV propagation in COS‐tat cells is significantly greater than in COS‐7 cells. On the other hand, COS‐7 cells express SV40 T antigen, which is a strong stimulator of archetype JCV replication. The expression of SV40 T antigen was enhanced by HIV‐1 Tat slightly according to real‐time RT‐PCR, this was not closely related to JCV replication in COS‐tat cells. The efficiency of JCV propagation depended on the extent of expression of functional Tat. To our knowledge, this is the first report of increased production of archetype JCV in a culture system using cell lines stably expressing HIV‐1 Tat. We propose here that COS‐tat cells are a useful tool for studying the role of Tat in archetype JCV replication in the development of PML.</div>
</front>
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