Temporal gene regulation during HIV-1 infection of human CD4+ T cells

被引:91
作者
Corbeil, A [1 ]
Sheeter, D
Genini, D
Rought, S
Leoni, L
Du, PY
Ferguson, M
Masys, DR
Welsh, JB
Fink, JL
Sasik, R
Huang, D
Drenkow, J
Richman, DD
Gingeras, T
机构
[1] Univ Calif San Diego, Dept Med, La Jolla, CA 92023 USA
[2] Univ Calif San Diego, Dept Pathol, La Jolla, CA 92023 USA
[3] Univ Calif San Diego, Dept Phys, La Jolla, CA 92023 USA
[4] Vet Adm Med Ctr, San Diego, CA 92161 USA
[5] Vet Med Res Fdn, San Diego, CA 92161 USA
[6] San Diego Supercomp Ctr, La Jolla, CA 92093 USA
[7] Affymetrix, Santa Clara, CA USA
关键词
D O I
10.1101/gr.GR-1802R
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
CD4(+) T-cell depletion is a characteristic of human immunodeficiency virus type 1 (HIV-1) infection. In this study, modulation of mRNA expression of 6800 genes was monitored simultaneously at eight time points in a CD4(+) T-cell line (CEM-GFP) during HIV infection. The responses to infection included: (1) >30% decrease at 72 h after infection in overall host-cell production of monitored mRNA synthesis, with the replacement of host-cell mRNA by viral mRNA, (2) suppression of the expression of selected mitochondrial and DNA repair gene transcripts, (3) increased expression of the proapoptotic gene and its gene p53-induced product Bax, and (4) activation of caspases 2, 3, and 9. The intense HIV-1 transcription resulted in the repression of much cellular RNA expression and was associated with the induction of apoptosis of infected cells but not bystander cells. This choreographed host gene response indicated that the subversion of the cell transcriptional machinery for the purpose of HIV-1 replication is akin to genotoxic stress and represents a major factor leading to HIV-induced apoptosis.
引用
收藏
页码:1198 / 1204
页数:7
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