Vesicular stomatitis virus, detection

Vandenbroeck et al.7 used an ELISA to determine the recovery of immu-noreactive porcine interferon-gamma (IFN-y) from E. coli inclusion bodies. The ELISA used a polyclonal coating antibody with detection by a MAb. The inclusion bodies were solubilized in diluted 6 M guanidine/HCl and IFN subsequently refolded by its removal. The antiviral activity of the interferon was measured with a bioassay using the cytopathic effect (CPE) of vesicular stomatitis virus (VSV) on bovine kidney cells. The results of this study showed that the immu-noreactivity measured by ELISA matched the biological activity measured by bioassay. 

In discussing the mechanism of antiviral protection and stimulation of interferon production in the mouse, DeClercq and Merigan46 concluded that there was a direct relationship between the extent of protection against vesicular stomatitis virus, the titers of interferon produced and the doses of tilorone. Giron et al.47, however, found no correlation between interferon induction and protection against MM virus in mice. Protection was achieved at doses far below the doses at which detectable interferon was found in the serum. Both findings may be consistent with differing mechanisms of viral inactivation for the two viruses under study. 

As a transport marker we use the temperature-sensitive membrane protein ts-045-G from the vesicular stomatitis virus (ZUberstein etal., 1980). This transmembrane protein has the feature of accumulating in the ER at 39.5°, but moves vectoriaUy through the secretory pathway to the plasma membrane (PM) at the permissive temperature of 32°, where an antibody recognizing an external epitope can be used to detect it. This has the principal advantage that transport in individual cells is highly synchronized. 

It has been realized for some time that viral multiplication can occur with only minimal cytopathic effects (Choppin, 1964). Conversely, considerable cytopathology can result from infection with a virus, the multiplication of which is restricted in that host. Cantell et al. (1962) were perhaps the first to describe that L cells could be destroyed by large doses of a UV-irradiated virus, vesicular stomatitis virus, in the absence of a detectable synthesis of viral antigen this toxic activity could not be separated from the viral particle. We shall discuss in a later chapter why this does not prove the absence of viral replicative functions or that preformed virion components are necessarily cytotoxic. However, it is quite clear that early interactions... 

Doyle and Holland, 1973) in the case of these DI particles of vesicular stomatitis virus, the only replicative event detectable is transcription of a 46-nucleotide leader sequence from the 3 end of the remaining segment of the viral genome (Emerson et al., 1977). 

Emerson, S. U., 1982, Reconstitution studies detect a single polymerase entry site on the vesicular stomatitis virus genome. Cell 31 635. 

Significant antiviral ejfectivity was shown in vitro for titanocene dichloride (I) against numerous DNA and RNA viruses in the extracellular phase Typical examples of viruses, which were inhibited by direct contact with I and lost infectivity up to 100%, were orthopoxvirus (vaccinia) and herpes virus (pseudorabies) as DNA viruses, and rhabdovirus (vesicular stomatitis), paramyxovirus (Newcastle disease) and diverse orthomyxoviruses (e.g. influenza A and B) as RNA viruses. A comparable antiviral effect against herpes viruses was detectable after application of the ferricenium salt whereas, on the other hand, vanadocene dichloride (11) and molybdenocene dichloride (V) failed to show antiviral activity under the same experimental conditions. 

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