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Journal of Virology, March 2009, p. 2368-2373, Vol. 83, No. 5
0022-538X/09/$08.00+0 doi:10.1128/JVI.02371-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Ana Falcón,2,
Haixia Zhou,1
Jason Netland,3
Luis Enjuanes,4
Pilar Pérez Breña,2 and
Stanley Perlman1,3*
Department of Microbiology,1 Interdisciplinary Program in Immunology, University of Iowa, Iowa City, Iowa 52242,3 Laboratory of Respiratory Viruses, CNM, Instituto de Salud Carlos III, Madrid, Spain,2 Centro Nacional de Biotecnologia, Department of Molecular and Cell Biology, Campus University Autónoma, Cantoblanco, 28049 Madrid, Spain4
Received 14 November 2008/ Accepted 8 December 2008
Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes several accessory proteins of unknown function. One of these proteins, protein 6 (p6), which is encoded by ORF6, enhances virus replication when introduced into a heterologous murine coronavirus (mouse hepatitis virus [MHV]) but is not essential for optimal SARS-CoV replication after infection at a relatively high multiplicity of infection (MOI). Here, we reconcile these apparently conflicting results by showing that p6 enhances SARS-CoV replication to nearly the same extent as when expressed in the context of MHV if cells are infected at a low MOI and accelerates disease in mice transgenic for the human SARS-CoV receptor.
Published ahead of print on 17 December 2008.
Jincun Zhao and Ana Falcón contributed equally to this work.
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