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Journal of Virology, May 2002, p. 4467-4482, Vol. 76, No. 9
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.9.4467-4482.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Gene Expression Pattern in Caco-2 Cells following Rotavirus Infection

Mariela A. Cuadras,1 Dino A. Feigelstock,1,{dagger} Sungwhan An,1,{ddagger} and Harry B. Greenberg1,2,3*

Department of Medicine,1 Department of Microbiology and Immunology,2 Stanford University School of Medicine, Stanford, California 94305, and the VA Palo Alto Health Care System, Palo Alto, California 943043

Received 3 October 2001/ Accepted 11 January 2002

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.

* Corresponding author. Mailing address: VAPAHCS, 3801 Miranda Ave., MC 154C, Palo Alto, CA 94304. Phone: (650) 493-5000, ext. 63124. Fax: (650) 852-3259. E-mail: hbgreen{at}leland.stanford.edu.

{dagger} Present address: Laboratory of Hepatitis and Related Emerging Agents, DETTD/OBRR/CBER/FDA, Bethesda, MD 20892.

{ddagger} Present address: Genomictree, Inc., Daeduk BioCommunity, Jonmin-Dong 461-6, Daejon 305-390, South Korea.

Journal of Virology, May 2002, p. 4467-4482, Vol. 76, No. 9
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.9.4467-4482.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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