Virus entry into animal cells permeabilizes the cell membrane to alpha-amanitin, allowing it to rapidly inhibit RNA synthesis.
Indicates virus-induced membrane permeabilization to toxins; leaves open generalizability across viruses and in vivo relevance.
The transcription inhibitor α-amanitin which does not easily pass through the membrane of normal cells, shows a higher inhibition of cellular RNA synthesis in encephalomyocarditis (EMC) virus-infected HeLa cells as compared with uninfected cells. This selective inhibition is observed within minutes of virus addition to the culture medium. It depends on the multiplicity of infection used and the concentration of α-amanitin present. These results indicate that, very early during infection, α-amanitin is able to pass the cell membrane and get into the nucleus, where it blocks RNA synthesis. No effect is observed in the transport of [3H]uridine into the cells, indicating that the increased inhibition by α-amanitin affects RNA synthesis itself. This phenomenon occurs with different animal viruses irrespective of whether they possess a lipid envelope or not. Finally, no inhibition by NH4Cl or chloroquine is observed in the permeabilization induced by encephalomyocarditis virus, indicating that it is not a low-pH requiring process. However, it does require a metabolically active cell, since NaN3 plus 2′-deoxy-glucose blocked this process.
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Castrillo et al. (1985) studied this question.