HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

Enhanced production of p24 Gag protein in HIV-1-infected rat cells fused with uninfected human cells.

Files in This Item:
EMP83-1.pdf307.5 kBPDFView/Open
Please use this identifier to cite or link to this item:

Title: Enhanced production of p24 Gag protein in HIV-1-infected rat cells fused with uninfected human cells.
Authors: Chen, Jing Browse this author
Zhao, Xudong Browse this author
Lai, Yurong Browse this author
Suzuki, Akira Browse this author
Tomaru, Utano Browse this author
Ishizu, Akihiro Browse this author →KAKEN DB
Takada, Akio Browse this author
Ikeda, Hitoshi Browse this author
Kasahara, Masanori Browse this author
Yoshiki, Takashi Browse this author
Keywords: HIV-1
Rat model
Cell fusion
Cyclin T1
Issue Date: Aug-2007
Publisher: Elsevier Inc.
Journal Title: Experimental and Molecular Pathology
Volume: 83
Issue: 1
Start Page: 125
End Page: 130
Publisher DOI: 10.1016/j.yexmp.2006.11.003
PMID: 17222823
Abstract: Although many human molecules have been suggested to affect replication of human immunodeficiency virus type 1 (HIV-1), the distribution of such cofactors in human cell types is not well understood. Rat W31/D4R4 fibroblasts expressing human CD4 and CXCR4 receptors were infected with HIV-1. The provirus was integrated in the host genome, but only a limited amount of p24 Gag protein was produced in the cells and culture supernatants. Here we found that p24 production was significantly increased by fusing HIV-1-infected W31/D4R4 cells with uninfected human cell lines of T-cell, B-cell, or macrophage lineages. These findings suggest that human cellular factors supporting HIV-1 replication are distributed widely in cells of lymphocyte and macrophage lineages. We also examined whether the amount of p24 produced by rat–human hybrid cells was correlated with expression levels of specific human genes. The results suggested that HP68 and MHC class II transactivator (CIITA) might up- and down-regulate p24 production, respectively. It was also suggested that HIV-1 replication is affected by molecules other than those examined in this study, namely, cyclin T1, cyclin-dependent kinase 9, CRM1, HP68, and CIITA.
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 石津 明洋

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 - Hokkaido University