Cytopathic components

Fig. 2. Model of the cytopathic effects of actin ADP-ribosylating toxins. The activated binding component of C. botulinum C2 toxin binds to a receptor of the eukaryotic cell. This induces a binding site for the enzyme component (C2I), Most likely, C2I enters the cell by endocytosis and subsequent translocation. In the cell, G-actin is ADP-ribosylated, which inhibits its polymerization and traps actin in the monomeric form. ADP-ribosylated actin binds in a capping protein-like manner to the barbed ends of filaments to inhibit further polymerization at the fast-growing end of F-acfin. The foxin has no effects on the pointed end of filaments where actin depolymerization takes place. Additionally, ADP-ribosylation may affect functions of complexes of acfin wifh binding proteins as examplified in Fig. 1 (From (Aktories, 1990) with permission)...

Ohishi I, Iwasaki M, Sakaguchi G (1980) Purification and characterization of two components of botulinum C2 toxin. In Infect. Immun. 30 668-73 Ohishi I, Miyake M, Ogura H et al. (1984) Cytopathic effect of botulinum C2 toxin on tissue-culture cells. In FEMS Microbiol. Lett. 23 281 —4 Ohishi I, Yanagimoto A (1992) Visualizations of binding and internalization of two nonlinked protein components of botulinum C2 toxin in tissue culture cells. In Infect. Immun. 60 4648-55... 

Inclusion body (1) An aggregation of reticulate bodies within chlamydias. (2) A form of cytopathic effect consisting of viral components, masses of viruses, or remnants of viruses. 

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... 

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. 

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