Bovine enterovirus

Poliovirus (Type 1) Coxsackie Virus (Type B3) Bovine Enterovirus ME Mengo Rhinovirus (Type lA) FMDV (Type 0)... 

When added to whole cells, non-infectious bovine enterovirus ds RNA is cytotoxic (64). The cytotoxicity occurred in the presence of inhibitors of protein synthesis, suggesting that translation is not necessaiy for the effect. The ds RNA appeared to be selective, since it inhibited only cellular protein synthesis and not mengovirus protein synthesis (65). These findings are contrary to those found in extracts, where no selectivity of ds RNA was observed. No explanation for this difference is available at this time. 

Perhaps one of the more fascinating studies of virus resistance, and changes in cell surface that affects viral adsorption, is the observation (11 ) that viral transformed cells are much more sensitive to bovine enterovirus-1 infection than the parental non-transformed cell (Table 1). Thus t 3mor-virus (or spontaneous) transformation results in modifications of the cell surface that allows for virus adsorption. Further analysis demonstrates that the resistance to bovine enterovirus-1 of 5 5 and primary kidney is due to a lack of receptor sites. 

As indicated above, these data do not tell us whether a function" is lacking in MDBK which is essential for viral protein or RNA synthesis, or whether a macromolecule is synthesized which prevents the translation of viral proteins or viral RNA synthesis. Since MDBK can be infected productively by other viruses (Bovine enterovirus, influenza), it must be a molecule specific for the mengo-MDBK cell interaction. The greatest enigma in our data is the origin of the early ENA replicase, since very little (or no) protein synthesis occurs. 

Stoner GD, Williams B, Kniazeff A, Shimkin MB (1973) Effect of neuraminidase pretreatment on the susceptibility of normal and transformed mammalian cells to bovine enterovirus 261. Nature 245 319-320... 

The feature common to the cytotoxic effects brought on by nonreplicating influenza virus, poxvirus, and defective-interfering vesicular stomatitis virus is the high multiplicity of infection required. This has led to the assumption that the toxic effect is caused by one or more components of the parental input virion, most likely protein in origin. However, Cordell-Stewart and Taylor (1971, 1973) have provided evidence that the double-stranded viral RNA isolated from cells infected with bovine enterovirus causes a rapid cytopathic effect as determined by trypan-blue uptake or Cr release from affected Ehrlich ascites tumor cells or L1210 cells toxic effects are reduced or do not occur in cells exposed to single-stranded or heat-denatured double-stranded viral RNA and the toxic effect of bovine enteroviral double-stranded RNA is not abolished by inhibitors of protein synthesis such as puromycin or cycloheximide. 

Vibrio cholerae Normal and transformed tissue culture cells Removal of bovine enterovirus receptors Stoner et al., 1973... 

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