My opinion has always been that the majority of enterovirus CPE is
due to the disruptions in host-cell protein translation due to
cleavage of 4F. As well, the induction and activation of anti-viral
mechanism such as DAI kinanse which further inhibits the
translational machinery and 2'5'-oligo adenylate synthase which
activates RNase L and degrades host and viral RNA. With high
viral burst these mechanism are likely at play very early in
infection, and could all account for the alterations in cytoskeletal
changes (morphological changes, intracellular transport). The
timeframe of all of this I am not sure. I will ask my cytoskeletal
friends.
Dan Anderson
