These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Homotypic and heterotypic exclusion of vesicular stomatitis virus replication by high levels of recombinant polymerase protein L.
    Author: Meier E, Harmison GG, Schubert M.
    Journal: J Virol; 1987 Oct; 61(10):3133-42. PubMed ID: 3041035.
    Abstract:
    The recombinant polymerase protein L of vesicular stomatitis virus (VSV) expressed in COS cells is able to transcribe and replicate the viral genome, resulting in complementation of temperature-sensitive polymerase mutants of VSV at the restrictive temperature (M. Schubert, G. G. Harmison, C. D. Richardson, and E. Meier, Proc. Natl. Acad. Sci. USA 82:7984-7988, 1985). Here we report that the efficiency of complementation is dependent on the level of L protein expression. Unexpectedly, only cells expressing low levels of recombinant L protein efficiently complemented tsL gene mutants, whereas cells with high levels of L protein did not. In fact, in all cells with high levels of L protein expression, which at 40 h posttransfection represented almost the total number of transfected cells, viral replication not only of the temperature-sensitive mutant but also of wild-type VSV was excluded. The inhibition of VSV appeared to occur at an early stage of the infectious cycle, and wild-type virus of the same serotype (Indiana) as the recombinant L protein as well as wild-type virus of a different serotype (New Jersey) was affected. Measles virus, on the other hand, was not arrested in cells with high levels of recombinant L protein, demonstrating that these cells were still capable of supporting a viral infection. The expression of high levels of only the amino-terminal half of the L protein from a recombinant mutant L gene that contains a small out-of-frame deletion in the middle of the L gene did not inhibit a VSV infection. Since the level of amplification for both L- and truncated L-encoding vectors is similar, we conclude that the arrest of VSV was caused by high levels of functional full-length L protein itself and not by high levels of vector-encoded L mRNA or other vector products or by side effects of vector amplification. These data strongly support the idea that the highly conserved gene order of nonsegmented negative-strand viruses and the sequential and attenuated mode of transcription are important regulatory elements which balance the intracellular concentration of viral proteins. They both assure that the L gene is the last and the least frequently transcribed gene, giving rise to low levels of L protein necessary for efficient replication.
    [Abstract] [Full Text] [Related] [New Search]