Replication of Vesicular Stomatitis Virus Facilitated in Nonpermissive Cells by Early Functions of Shope Fibroma Virus (original) (raw)

Restricted Replication of Vesicular Stomatitis Virus in Human Lymphoblastoid Cells

Journal of Virology, 1973

Replication of' vesicular stomatitis virus (VSV) is restricted in one human lymphoblastoid cell line (Raji), but not in another similar cell line (Wil-2), compared with growth in HeLa cells. This restriction is characterized by a low proportion of cells yielding infectious virus and is associated with limited production of 42S virion RNA. Primary transcription of' 13S and 26S VSVspecific RNA is not restricted in Raji cells, and the 13S RNA produced contains adenylate-rich sequences. This suggests that the block in Raji cells involves some step required for the replication of virion RNA.

Host Cell Functions in Vesicular Stomatitis Virus Replication

WORLD SCIENTIFIC eBooks, 2014

Vesicular stomatitis virus (VSV), the prototypic rhabdovirus, has been used as an excellent paradigm for understanding the mechanisms of virus replication, pathogenesis, host response to virus infection and also for myriads of studies on cellular and molecular biology. Biochemical studies as well as high-throughput genomics, proteomics, and chemical approaches have revealed a plethora of cellular factors and pathways that regulate replication of VSV. These factors include those that support virus replication and also those that restrict its replication. This chapter discusses the role(s) of many of these host cell factors and pathways involved in VSV replication. Although mechanistic understanding of the roles of some of these factors in VSV replication has been obtained, the roles of many others need to be investigated for a better understanding of the virus-host cell interactions.

Normal replication of vesicular stomatitis virus without C proteins

1996

The expression of two small basic proteins (C and C) encoded by a second open reading frame of the New Jersey serotype of vesicular stomatitis virus (VSV) P gene was reported previously (Spiropoulou and Nichol, J. Virol., 67, 3103-3110, 1993). Here we found that the Indiana serotype virus also expressed C and C proteins from this reading frame. We eliminated C and C expression by making a single base change that introduced a stop codon in the C and C coding sequence, but left the P-protein sequence unchanged. This mutated P gene supported normal replication and packaging of VSV minigenomes encoding G and M proteins. The mutated P gene was also recombined into an infectious clone of VSV that was used to recover virus. The mutant virus no longer expressed the C and C proteins but showed growth kinetics identical to wild-type virus. The amounts of viral mRNAs and proteins synthesized were indistinguishable in mutant and wild-type virus infected cells as were the yields and composition of mutant and wild-type virus particles. The kinetics of host protein-synthesis shut-off were also identical for both viruses. Although the C and C proteins were dispensable for VSV growth in tissue culture, they are known to be conserved in all vesiculoviruses, and thus perhaps play a role in viral pathogenesis or transmission by insect vectors.