Source:http://linkedlifedata.com/resource/pubmed/id/18312467
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2008-4-2
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pubmed:abstractText |
Human T-cell lymphotropic virus type 1 (HTLV-1) causes adult T-cell leukemia and inflammatory disorders. Aberrant activation of nuclear factor-kappaB (NF-kappaB) has been linked to HTLV-1 pathogenesis and to various kinds of cancers, including adult T-cell leukemia. NF-kappaB-inducing kinase (NIK) is critical for non-canonical activation of NF-kappaB and for the development of lymphoid organs. HTLV-1 activates NF-kappaB by the non-canonical pathway, but examination of the role of NIK in proliferation of HTLV-1-infected cells in vivo has been hindered by lack of a suitable animal model. Alymphoplasia (aly/aly) mice bear a mutation of NIK, resulting in defects in the development of lymphoid organs and severe deficiencies in both humoral and cell-mediated immunity. In the present study we therefore used a mouse model of HTLV-1 infection with aly/aly mice. The number of HTLV-1-infected cells in the reservoir organs in aly/aly mice was significantly smaller than in the control group 1 month after infection. In addition, aly/aly mice did not maintain provirus for 1 year and antibodies against HTLV-1 were undetectable. These results demonstrate that the absence of functional NIK impairs primary HTLV-1 proliferation and abolishes the maintenance of provirus. Interestingly, clonal proliferation of HTLV-1-infected mouse cells was not detected in aly/aly mice, which is consistent with the lack of HTLV-1 persistence. These observations imply that the clonal proliferation of HTLV-1-infected cells in secondary lymphoid organs might be important for HTLV-1 persistence.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1349-7006
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pubmed:author |
pubmed-author:FujisawaJun-ichiJ,
pubmed-author:HanaiShujiS,
pubmed-author:JiangShi-WenSW,
pubmed-author:KamadaYuheiY,
pubmed-author:KimuraMakoM,
pubmed-author:MiwaMasanaoM,
pubmed-author:NittaTakayukiT,
pubmed-author:SugiharaEijiE,
pubmed-author:SunBinlianB,
pubmed-author:TakahashiHidetoH,
pubmed-author:TanakaMasakazuM
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pubmed:issnType |
Electronic
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pubmed:volume |
99
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
872-8
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:18312467-Animals,
pubmed-meshheading:18312467-Cell Proliferation,
pubmed-meshheading:18312467-Cell Transformation, Viral,
pubmed-meshheading:18312467-HTLV-I Infections,
pubmed-meshheading:18312467-Human T-lymphotropic virus 1,
pubmed-meshheading:18312467-Humans,
pubmed-meshheading:18312467-Lymph Nodes,
pubmed-meshheading:18312467-Mice,
pubmed-meshheading:18312467-Models, Animal,
pubmed-meshheading:18312467-Protein-Serine-Threonine Kinases,
pubmed-meshheading:18312467-RNA, Viral
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pubmed:year |
2008
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pubmed:articleTitle |
Reduction of human T-cell leukemia virus type-1 infection in mice lacking nuclear factor-kappaB-inducing kinase.
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pubmed:affiliation |
Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki 305-8575, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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