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Journal of Virology, November 2009, p. 11090-11101, Vol. 83, No. 21
0022-538X/09/$08.00+0     doi:10.1128/JVI.01239-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Mammalian Orthoreovirus Particles Induce and Are Recruited into Stress Granules at Early Times Postinfection{triangledown}

Qingsong Qin, Craig Hastings, and Cathy L. Miller*

Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa 50011

Received 15 June 2009/ Accepted 19 August 2009

Infection with many mammalian orthoreovirus (MRV) strains results in shutoff of host, but not viral, protein synthesis via protein kinase R (PKR) activation and phosphorylation of translation initiation factor eIF2{alpha}. Following inhibition of protein synthesis, cellular mRNAs localize to discrete structures in the cytoplasm called stress granules (SGs), where they are held in a translationally inactive state. We examined MRV-infected cells to characterize SG formation in response to MRV infection. We found that SGs formed at early times following infection (2 to 6 h postinfection) in a manner dependent on phosphorylation of eIF2{alpha}. MRV induced SG formation in all four eIF2{alpha} kinase knockout cell lines, suggesting that at least two kinases are involved in induction of SGs. Inhibitors of MRV disassembly prevented MRV-induced SG formation, indicating that viral uncoating is a required step for SG formation. Neither inactivation of MRV virions by UV light nor treatment of MRV-infected cells with the translational inhibitor puromycin prevented SG formation, suggesting that viral transcription and translation are not required for SG formation. Viral cores were found to colocalize with SGs; however, cores from UV-inactivated virions did not associate with SGs, suggesting that viral core particles are recruited into SGs in a process that requires the synthesis of viral mRNA. These results demonstrate that MRV particles induce SGs in a step following viral disassembly but preceding viral mRNA transcription and that core particles are themselves recruited to SGs, suggesting that the cellular stress response may play a role in the MRV replication cycle.

* Corresponding author. Mailing address: Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, 1802 University Boulevard, VMRI Building 3, Ames, IA 50011. Phone: (515) 294-4797. Fax: (515) 294-1401. E-mail: clm{at}iastate.edu

{triangledown} Published ahead of print on 26 August 2009.

Journal of Virology, November 2009, p. 11090-11101, Vol. 83, No. 21
0022-538X/09/$08.00+0     doi:10.1128/JVI.01239-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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