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Journal of Virology, September 2003, p. 9502-9510, Vol. 77, No. 17
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.17.9502-9510.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Complementation of a Deletion in the Rubella Virus P150 Nonstructural Protein by the Viral Capsid Protein

Wen-Pin Tzeng and Teryl K. Frey*

Department of Biology, Georgia State University, Atlanta, Georgia 30302-4010

Received 20 March 2003/ Accepted 9 June 2003

Rubella virus (RUB) replicons with an in-frame deletion of 507 nucleotides between two NotI sites in the P150 nonstructural protein ({Delta}NotI) do not replicate (as detected by expression of a reporter gene encoded by the replicon) but can be amplified by wild-type helper virus (Tzeng et al., Virology 289:63-73, 2001). Surprisingly, virus with {Delta}NotI was viable, and it was hypothesized that this was due to complementation of the NotI deletion by one of the virion structural protein genes. Introduction of the capsid (C) protein gene into {Delta}NotI-containing replicons as an in-frame fusion with a reporter gene or cotransfection with both {Delta}NotI replicons and RUB replicon or plasmid constructs containing the C gene resulted in replication of the {Delta}NotI replicon, confirming the hypothesis that the C gene was the structural protein gene responsible for complementation and demonstrating that complementation could occur either in cis or in trans. Approximately the 5' one-third of the C gene was necessary for complementation. Mutations that prevented translation of the C protein while minimally disturbing the C gene sequence abrogated complementation, while synonymous codon mutations that changed the C gene sequence without affecting the amino acid sequence at the 5' end of the C gene had no effect on complementation, indicating that the C protein, not the C gene RNA, was the moiety responsible for complementation. Complementation occurred at a basic step in the virus replication cycle, because {Delta}NotI replicons failed to accumulate detectable virus-specific RNA.

* Corresponding author. Mailing address: Georgia State University, Biology Department, P.O. Box 4010, Atlanta, GA 30302-4010. Phone and Fax: (404) 651-3105. E-mail: tfrey{at}gsu.edu.

Journal of Virology, September 2003, p. 9502-9510, Vol. 77, No. 17
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.17.9502-9510.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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