JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lachmi, B
Right arrow Articles by Kääriäinen, L
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lachmi, B
Right arrow Articles by Kääriäinen, L

 Previous Article  |  Next Article 

J Virol. 1977 April; 22(1): 142-149

Control of protein synthesis in Semliki forest virus-infected cells.

B Lachmi and L Kääriäinen

ABSTRACT

Protein synthesis in Semliki forest virus-infected chicken embryo cells was studied by labeling them with [35S]methionine for short periods at different times after infection, with or without synchronization of protein synthesis by the hypertonic block technique. The rate of host-cell protein synthesis declined almost linearly in inverse correlation to the increase in the amount of virus specific RNA. At 5.5 h postinfection, the host-cell protein synthesis was reduced by about 70%. The viral structural proteins were detectable with certainty at 3.5 h postinfection, and their rate of synthesis increased linearly parallel to the amount of their messenger, the 26S RNA. This suggests that the rate of synthesis of the structural proteins is controlled at the level of transcription. The rate of synthesis of the virus-specific nonstructural proteins attained its maximum between 3 and 4 h postinfection and declined thereafter, wheras the amount of their messenger, the 42S RNA, continued to increase linearly in the cells. Thus, the messenger activity of the 42S RNA is reduced in the late phase of infection compared with its activity in the early phase.


J Virol. 1977 April; 22(1): 142-149




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 1977 by the American Society for Microbiology. All rights reserved.