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Journal of Virology, April 2007, p. 4286-4297, Vol. 81, No. 8
0022-538X/07/$08.00+0     doi:10.1128/JVI.01623-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Fusogenic Variants of a Noncytopathic Paramyxovirus

Shaguna Seth,^1, Ioanna Skountzou,¹ Kim M. Gernert,² and Richard W. Compans^1*

Department of Microbiology and Immunology,¹ BIMCORE (Biomolecular Computing Resource), Emory University School of Medicine, Atlanta, Georgia 30322²

Received 28 July 2006/ Accepted 31 January 2007

SER virus is a type 5 parainfluenza virus that does not exhibit syncytium formation, in contrast to most other paramyxoviruses. This property has been attributed, at least in part, to the presence of an extension of the cytoplasmic tail (CT) of the SER F protein, as truncations or mutations of this region resulted in enhanced fusion. In this study we used repeated passage to select for mutant SER viruses, which were found to be fusogenic. The mutant viruses replicated at levels comparable to or higher than the wild-type SER virus and caused plaque formation, in contrast to the wild-type virus which does not form plaques. The mutants differed strikingly in their plaque sizes. The F genes of mutant viruses were cloned and sequenced and shared some mutations, including a proline-to-leucine change at position 22 and an isoleucine-to-leucine substitution at position 191; other changes that were specific to each mutant were also found. The HN proteins of mutant viruses also showed mutations spanning the length of the protein whereas the M protein showed a consistent mutation, threonine to isoleucine, at position 129. The structure of the F protein was used to identify residues involved in the mutant phenotypes in terms of their location and proximity to heptad repeat domains.

Published ahead of print on 7 February 2007.

Present address: Nastech Pharmaceutical Company Inc., Research and Development, Bothell, WA 98021-8906.