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Journal of Virology, October 2009, p. 10653-10663, Vol. 83, No. 20
0022-538X/09/$08.00+0     doi:10.1128/JVI.00956-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Spike Protein of Murine Coronavirus Regulates Viral Genome Transport from the Cell Surface to the Endoplasmic Reticulum during Infection{triangledown}

Hongqing Zhu,{dagger} Dongdong Yu,{dagger} and Xuming Zhang*

Departments of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199

Received 13 May 2009/ Accepted 23 June 2009

We observed that the nonfusogenic mouse hepatitis virus (MHV) strain MHV-2 reached a titer of ~2 log10 higher than that of the fusogenic strain A59 in astrocytoma DBT cells. To determine whether the spike protein is responsible for the difference, a recombinant virus, Penn-98-1, that contains the A59 genome with a spike from MHV-2 was used to infect DBT cells. Results showed that Penn-98-1 behaved like MHV-2, thus establishing a role for the spike protein in viral growth. The inverse correlation between viral fusogenicity and growth was further established in four different cell types and with a fusogenic mutant, the S757R mutant, derived from isogenic Penn-98-1. While both A59 and Penn-98-1 entered cells at similar levels, viral RNA and protein syntheses were significantly delayed for A59. Interestingly, when the genomic RNAs were delivered directly into the cells via transfection, the levels of gene expression for these viruses were similar. Furthermore, cell fractionation experiments revealed that significantly more genomic RNAs for the nonfusogenic MHVs were detected in the endoplasmic reticulum (ER) within the first 2 h after infection than for the fusogenic MHVs. Pretreatment of Penn-98-1 with trypsin reversed its properties in syncytium formation, virus production, and genome transport to the ER. These findings identified a novel role for the spike protein in regulating the uncoating and delivery of the viral genome to the ER after internalization.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Slot 511, Little Rock, AR 72205. Phone: (501) 686-7415. Fax: (501) 686-5359. E-mail: zhangxuming{at}uams.edu

{triangledown} Published ahead of print on 1 July 2009.

{dagger} H.Z. and D.Y. contributed equally to the paper.

Journal of Virology, October 2009, p. 10653-10663, Vol. 83, No. 20
0022-538X/09/$08.00+0     doi:10.1128/JVI.00956-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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