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J Virol, July 1998, p. 5984-5993, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

The Various Sendai Virus C Proteins Are Not Functionally Equivalent and Exert both Positive and Negative Effects on Viral RNA Accumulation during the Course of Infection

Patrizia Latorre,1 Tamarra Cadd,1,dagger Masae Itoh,2 Joseph Curran,1 and Daniel Kolakofsky1,*

Department of Genetics and Microbiology, University of Geneva School of Medicine, CH1211 Geneva, Switzerland,1 and Department of Microbiology, Kobe University School of Medicine, Chuo-ku, Kobe 650, and Osaka Prefectural Institute of Public Health, Higashinari-ku, Osaka 537, Japan2

Received 26 January 1998/Accepted 7 April 1998

Recombinant Sendai viruses were prepared which cannot express their Cprime, C, or Cprime plus C proteins due to mutation of their respective start codons ([Cprime-minus], [C-minus] and [double mutant], respectively). The [Cprime-minus] and [C-minus] stocks were similar to that of wild-type (wt) virus in virus titer and plaque formation, whereas the double-mutant stock had a much-reduced PFU or 50% egg infective dose/particle ratio and produced very small plaques. Relative to the wt virus infection, the [Cprime-minus] and [C-minus] infections of BHK cells resulted in significantly greater accumulation of viral RNAs, consistent with the known inhibitory effects of the Cprime and C proteins. The double-mutant infection, in contrast, was delayed in its accumulation of viral RNAs; however, once accumulation started, overaccumulation quickly occurred, as in the single-mutant infections. Our results suggest that the Cprime and C proteins both provide a common positive function early in infection, so that only the double mutant undergoes delayed RNA accumulation and exhibits the highly debilitated phenotype. Later in infection, the same proteins appear to act as inhibitors of RNA accumulation. In infections of mice, [Cprime-minus] was found to be as virulent as wt virus whereas [C-minus] was highly attenuated. These results suggest that the Cprime and C proteins cannot be functionally equivalent, since C can replace Cprime for virulence in mice whereas Cprime cannot replace C.

* Corresponding author. Mailing address: Department of Genetics and Microbiology, University of Geneva School of Medicine, CMU, 9 Ave. de Champel, CH1211 Geneva, Switzerland. Phone: 41 22 702 5657. Fax: 41 22 702 5702. E-mail: Daniel.Kolakofsky{at}medecine.unige.ch.

dagger Present address: Microbiology and Tumorbiology Center, Karolinska Institutet, S-171 77 Stockholm, Sweden.

J Virol, July 1998, p. 5984-5993, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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