Host Cell and Environmental Factors

The extent and rate of protein synthesis inhibition by VSV also appears to be host cell dependent. Wertz and Youngner (1970) noted considerable differences in susceptibility of chick embryo fibroblasts 

10 cells by 4 hr after mock infection). [ HJuridine incorporation into uninfected cells ranged from 1 x 10 to 5 x 10 cpm per 4 x lO cells. Data from McGowan and Wagner (1981). 

Two other factors that appear to control cell response to protein synthesis inhibition by VSV are ionic environment and co-infection with another virus, each of which is related to preferential translation of competing messenger RNAs. It is of peripheral interest that a hypertonic environment of VSV-infected cells inhibits synthesis of the membrane-associated viral G and M proteins to a greater extent than the nucleocapsid proteins (Nuss and Koch, 1976a). Hypertonic environment appears to favor translation of poliovirus and VSV mRNA 

Superinfection with poliovirus has a striking effect on VSV-in-fected HeLa-Ss cells the evidence in these experiments was quite convincing that preformed VSV mRNA was not translated following infection with poliovirus (Ehrenfeld and Lund, 1977 Trachsel et al., 1980). Of course, the effect of VSV on cellular protein synthesis could not be determined in this experiment because poliovirus itself drastically inhibits cellular protein synthesis. As mentioned above, the ascendency of the mRNAs of two viruses may also depend on the type of cell which is doubly infected with the two competing viruses (Otto and Lucas-Lenard, 1980). 

Specific proteins synthesized by undifferentiated cells appear to be quite susceptible to inhibition by VSV infection. We have found that actin synthesis by L cells following VSV infection is inhibited to about the same extent as most other cell proteins (Thomas and Wagner, unpublished experiments). In fact, McAllister and Wagner (1976) did not detect, by polyacrylamide gel electrophoresis, any specific proteins in undifferentiated L cells that were resistant to the protein synthesis inhibitory activity of VSV. By the same token, all the ribosomal proteins synthesized by L cells were inhibited to about the same extent after VSV infection (Marvaldi and Lucas-Lenard, 1977) in fact, VSV infection had an even greater inhibitory effect on incorporation of ribosomal proteins into newly assembled ribosomes (Jaye et al., 1980). 

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