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Journal of Virology, March 2002, p. 2585-2594, Vol. 76, No. 6
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.6.2585-2594.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Reovirus-Induced Alterations in Gene Expression Related to Cell Cycle Regulation

George J. Poggioli,1 Roberta L. DeBiasi,2,3 Ryan Bickel,3 Robert Jotte,4,5 Aaron Spalding,4 Gary L. Johnson,4,6,7 and Kenneth L. Tyler1,3,8,9,10*

Departments of Neurology,3 Pediatrics,2 Medicine,8 Hematology and Oncology,5 Microbiology,1 Pharmacology,4 Immunology, University of Colorado Health Sciences Center,9 Neurology Service, Denver Veterans Affairs Medical Center, Denver, Colorado 80220,10 Program in Molecular Signal Transduction,6 Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 802067

Received 9 July 2001/ Accepted 30 November 2001

Mammalian reovirus infection results in perturbation of host cell cycle progression. Since reovirus infection is known to activate cellular transcription factors, we investigated alterations in cell cycle-related gene expression following HEK293 cell infection by using the Affymetrix U95A microarray. Serotype 3 reovirus infection results in differential expression of 10 genes classified as encoding proteins that function at the G1-to-S transition, 11 genes classified as encoding proteins that function at G2-to-M transition, and 4 genes classified as encoding proteins that function at the mitotic spindle checkpoint. Serotype 1 reovirus infection results in differential expression of four genes classified as encoding proteins that function at the G1-to-S transition and three genes classified as encoding proteins that function at G2-to-M transition but does not alter any genes classified as encoding proteins that function at the mitotic spindle checkpoint. We have previously shown that serotype 3, but not serotype 1, reovirus infection induces a G2-to-M transition arrest resulting from an inhibition of cdc2 kinase activity. Of the differentially expressed genes encoding proteins regulating the G2-to-M transition, chk1, wee1, and GADD45 are known to inhibit cdc2 kinase activity. A hypothetical model describing serotype 3 reovirus-induced inhibition of cdc2 kinase is presented, and reovirus-induced perturbations of the G1-to-S, G2-to-M, and mitotic spindle checkpoints are discussed.

* Corresponding author. Mailing address: Department of Neurology (B-182), University of Colorado Health Sciences Center, 4200 E. 9th Ave., Denver, CO 80262. Phone: (303) 393-2874. Fax: (303) 393-4686. E-mail: Ken.Tyler{at}UCHSC.edu.

Journal of Virology, March 2002, p. 2585-2594, Vol. 76, No. 6
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.6.2585-2594.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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