HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Institute for Genetic Medicine >
Peer-reviewed Journal Articles, etc >

Synergistic effect of human CycT1 and CRM1 on HIV-1 propagation in rat T cells and macrophages

This item is licensed under: Creative Commons Attribution 2.0 Generic

Files in This Item:
6_43.pdf1.41 MBPDFView/Open
Please use this identifier to cite or link to this item:

Title: Synergistic effect of human CycT1 and CRM1 on HIV-1 propagation in rat T cells and macrophages
Authors: Okada, Hiroyuki Browse this author
Zhang, Xianfeng Browse this author
Ben Fofana, Ismael Browse this author
Nagai, Mika Browse this author
Suzuki, Hajime Browse this author
Ohashi, Takashi Browse this author
Shida, Hisatoshi Browse this author →KAKEN DB
Issue Date: 12-May-2009
Publisher: BioMed Central Ltd.
Journal Title: Retrovirology
Volume: 6
Start Page: 43
Publisher DOI: 10.1186/1742-4690-6-43
Abstract: Background: In vivo studies of HIV-1 pathogenesis and testing of antiviral strategies have been hampered by the lack of an immunocompetent small animal model that is highly susceptible to HIV-1 infection. Although transgenic rats that express the HIV-1 receptor complex hCD4 and hCCR5 are susceptible to infection, HIV-1 replicates very poorly in these animals. To demonstrate the molecular basis for developing a better rat model for HIV-1 infection, we evaluated the effect of human CyclinT1 (hCycT1) and CRM1 (hCRM1) on Gag p24 production in rat T cells and macrophages using both established cell lines and primary cells prepared from hCycT1/hCRM1 transgenic rats. Results: Expression of hCycT1 augmented Gag production 20-50 fold in rat T cells, but had little effect in macrophages. Expression of hCRM1 enhanced Gag production 10-15 fold in macrophages, but only marginally in T cells. Expression of both factors synergistically enhanced p24 production to levels approximately 10-40% of those detected in human cells. R5 viruses produced in rat T cells and macrophages were fully infectious. Conclusion: The expression of both hCycT1 and hCRM1 appears to be fundamental to developing a rat model that supports robust propagation of HIV-1.
Rights: © 2009 Okada et al; licensee BioMed Central Ltd.
Type: article
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 志田 壽利

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 - Hokkaido University