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Journal of Virology, August 2007, p. 8579-8586, Vol. 81, No. 16
0022-538X/07/$08.00+0 doi:10.1128/JVI.00263-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Jacqueline Cotte-Laffitte,1,2,
Raymonde Amsellem,1,2 and
Alain L. Servin1,2*
INSERM, UMR 756, Châtenay-Malabry, France,1 Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, France2
Received 7 February 2007/ Accepted 24 May 2007
We found that at the tight junctions (TJs) of Caco-2 cell monolayers, rhesus monkey rotavirus (RRV) infection induced the disappearance of occludin. Confocal laser scanning microscopy showed the disappearance of occludin from the cell-cell boundaries without modifying the expression of the other TJ-associated proteins, ZO-1 and ZO-3. Western immunoblot analysis of RRV-infected cells showed a significant fall in the levels of the nonphosphorylated form of occludin in both Triton X-100-insoluble and Triton X-100-soluble fractions, without any change in the levels of the phosphorylated form of occludin. Quantitative reverse transcription-PCRs revealed that the level of transcription of the gene that encodes occludin was significantly reduced in RRV-infected cells. Treatment of RRV-infected cells with Rp-cyclic AMP and protein kinase A inhibitors H89 and KT5720 during the time course of the infection restored the distribution of occludin and a normal level of transcription of the gene that encodes occludin.
Published ahead of print on 6 June 2007.
I. Beau and J. Cotte-Laffitte contributed equally to this work.
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