Journal of Virology, October 2001, p. 9538-9542, Vol. 75, No. 19
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.19.9538-9542.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Department of Plant Pathology, North Carolina State University, Raleigh, North Carolina 27695-7616
Received 9 April 2001/Accepted 5 July 2001
A Carnation ringspot virus (CRSV) variant (1.26) was
identified that accumulates virions but is incapable of forming a
systemic infection. The 1.26 capsid protein gene possesses a Ser
Pro
mutation at amino acid 282. Conversion of 1.26 amino acid 282 to Ser
restored systemic infection, while the reciprocal mutation in wild-type CRSV abolished systemic infection. Similar mutations introduced into
the related Red clover necrotic mosaic virus capsid
protein gene failed to induce the packaging but nonsystemic movement
phenotype. These results provide additional support for the
theory that virion formation is necessary but not sufficient for
systemic movement with the dianthoviruses.
Present address: Tomen Agro, Inc., San Francisco, CA 94105.
| J. Bacteriol. | Mol. Cell. Biol. | Microbiol. Mol. Biol. Rev. |
|---|
| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
|---|