Gene expression pattern in Caco-2 cells following rotavirus infection

被引:73
作者
Cuadras, MA
Feigelstock, DA
An, SW
Greenberg, HB
机构
[1] VAPAHCS, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Dept Med, Stanford, CA 94305 USA
[3] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
关键词
D O I
10.1128/JVI.76.9.4467-4482.2002
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Rotaviruses are recognized as the leading cause of severe dehydrating diarrhea in infants and young children worldwide. Preventive and therapeutic strategies are urgently needed to fight this pathogen. In tissue culture and in vivo, rotavirus induces structural and functional alterations in the host cell. In order to better understand the molecular mechanisms involved in the events after rotavirus infection, we identified host cellular genes whose mRNA levels changed after infection. For this analysis, we used microarrays containing more than 38,000 human cDNAs to study the transcriptional response of the human intestinal cell line Caco-2 to rotavirus infection. We found that 508 genes were differentially regulated >2-fold at 16 h after rotavirus infection, and only one gene was similarly regulated at 1 h postinfection. Of these transcriptional changes, 73% corresponded to the upregulation of genes, with the majority of them occurring late, at 12 or more hours postinfection. Some of the regulated genes were classified according to known biological function and included genes encoding integral membrane proteins, interferon-regulated genes, transcriptional and translational regulators, and calcium metabolism-related genes. A new picture of global transcriptional regulation in the infected cell is presented and families of genes which may be involved in viral pathogenesis are discussed.
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收藏
页码:4467 / 4482
页数:16
相关论文
共 65 条
[21]   COMPARISON OF HUMAN, SIMIAN, AND BOVINE ROTAVIRUSES FOR REQUIREMENT OF SIALIC-ACID IN HEMAGGLUTINATION AND CELL ADSORPTION [J].
FUKUDOME, K ;
YOSHIE, O ;
KONNO, T .
VIROLOGY, 1989, 172 (01) :196-205
[22]   Molecular mechanisms of interferon resistance mediated by viral-directed inhibition of PKR, the interferon-induced protein kinase [J].
Gale, M ;
Katze, MG .
PHARMACOLOGY & THERAPEUTICS, 1998, 78 (01) :29-46
[23]   Large-scale monitoring of host cell gene expression during HIV-1 infection using cDNA microarrays [J].
Geiss, GK ;
Bumgarner, RE ;
An, MC ;
Agy, MB ;
van't Wout, AB ;
Hammersmark, E ;
Carter, VS ;
Upchurch, D ;
Mullins, JI ;
Katze, MG .
VIROLOGY, 2000, 266 (01) :8-16
[24]   Global impact of influenza virus on cellular pathways is mediated by both replication-dependent and -independent events [J].
Geiss, GK ;
An, MC ;
Bumgarner, RE ;
Hammersmark, E ;
Cunningham, D ;
Katze, MG .
JOURNAL OF VIROLOGY, 2001, 75 (09) :4321-4331
[25]   New lessons for rotavirus vaccines [J].
Glass, RI ;
Gentsch, JR ;
Ivanoff, B .
SCIENCE, 1996, 272 (5258) :46-48
[26]   Heat shock cognate protein 70 is involved in rotavirus cell entry [J].
Guerrero, CA ;
Bouyssounade, D ;
Zárate, S ;
Isa, P ;
López, T ;
Espinosa, R ;
Romero, P ;
Méndez, E ;
López, S ;
Arias, CF .
JOURNAL OF VIROLOGY, 2002, 76 (08) :4096-4102
[27]   Integrin αvβ3 mediates rotavirus cell entry [J].
Guerrero, CA ;
Méndez, E ;
Zárate, S ;
Isa, P ;
López, S ;
Arias, CF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (26) :14644-14649
[28]   SYNTHESIS OF HUMAN ROTAVIRUS POLYPEPTIDES IN CELL-CULTURE [J].
HEATH, RL ;
BIRCH, CJ .
JOURNAL OF MEDICAL VIROLOGY, 1988, 25 (01) :91-103
[29]   Integrins α2β1 and α4β1 can mediate SA11 rotavirus attachment and entry into cells [J].
Hewish, MJ ;
Takada, Y ;
Coulson, BS .
JOURNAL OF VIROLOGY, 2000, 74 (01) :228-236
[30]   The transcriptional program in the response of human fibroblasts to serum [J].
Iyer, VR ;
Eisen, MB ;
Ross, DT ;
Schuler, G ;
Moore, T ;
Lee, JCF ;
Trent, JM ;
Staudt, LM ;
Hudson, J ;
Boguski, MS ;
Lashkari, D ;
Shalon, D ;
Botstein, D ;
Brown, PO .
SCIENCE, 1999, 283 (5398) :83-87