Abstract
Permissive infections of BHK cells and nonpermissive infections of Raji cells were probed for the accumulation of vesicular stomatitis virus intracellular RNAs. In Raji cells, the onset of vesicular stomatitis virus transcription and replication was delayed when compared to BHK cells, and the accumulation of plus and minus sense leader RNAs was significantly reduced. In contrast, full length plus and minus strand replicative RNAs accumulated in Raji cells to levels approximately equivalent to those in BHK cells. In both cell types, approximately four times as many minus strands as plus strands were detected late in the infections. At 16 h postinfection, 12% of the total genomic RNA synthesized in BHK cells was packaged and released whereas only 0.8% was released from Raji cells. In addition, of those particles released by Raji cells, only 1% were infectious whereas 77% of those released by BHK cells were infectious. The virions released from both cell types contained similar amounts of the five viral proteins, however. Analysis of virions from Raji cells revealed a faster electrophoretic mobility of the glycoprotein than the glycoprotein in virions released from BHK cells. These results suggest that Raji cells may be restricted in their ability to support a complete infection at the level of virus assembly rather than at the level of RNA replication.
Highlights
Permissive infections of BHK cells and nonpermis- ual protein synthesis [1,2]
Cells (Bl’iK)-We employed dot blot hybridization to quantitate the intracellular amounts of full length plus and minus strand RNAs which accumulate during permissive infections of BHK cells with Vesicular stomatitis virus (VSV)
The electrophoretic mobility of the viral glycoin contrast to 3300 and 3500 pfu/cell released in BHK cells protein (G) in virions released from VSV infected Raji cells at 16and 24 h postinfection,respectively.This large difference was consistently greater than that observed for G protein in in virus production was expected fromearlier reports but was virions released from BHK cells.Whether the altered migrasurprising in light of the fact that the intracellular accumu- tion of G protein is related to thedecreased infectivityof VSV
Summary
Several lines of evidence have suggesteda role for host cell factors in VSV replication. Glycoprotein than the glycoprotein ivnirions released from BHK cells These results suggest that Raji cells may berestricted in theirability to support a complete infection at the level of virus assembly rather thanat the level of RNA replication. La protein has been shownto interactwith small RNAs from adenovirus- and Epstein-Barr virus (EBERs) -infected cells [18, 19] This interaction occursinRajicellswhich express large quantities of EBER RNAs. In permissive hosts, the La protein has been shown to interact with the plus and minus sense leader RNAs [14, 15] that Leppert et al [20]. Howetvrearn,scription and replication quantify the levels of full length plus and minus sense RNAs can be distinguished in that transcription does not require (replicativeRNAs) which accumulate during VSV infections protein synthesis, whereas replication is dependent on contin- of Raji and BHK cells.
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