Channel catfish virus: interaction with the cytoskeleton

Abstract

The infection of channel catfish ovarian cells with channel catfish virus results in the redistribution of all cytoskeletal elements during virus‐induced syncytium formation. Actin filaments are normally arranged as large stress fibres, even during early stages of infection, but become redistributed as densely staining regions near the centre of the syncytium in latent infection. Microtubules and vimentin filaments (easily visible in early infection) lose all visible organization during syncytium formation. Stabilization of microtubules with taxol results in the production of elongate syncytia with regularly organized microtubules. Conversely, disruption of microtubules with nocodazole inhibits cell fusion and causes a reduction in infectious virus production. This reduction upon treatment with nocodazole, and the subsequent rescue of virus production upon addition of taxol indicates that viral replication relies upon the presence of microtubules.

Herpesviruses that Infect Fish

“…The precise processes have not been worked out for IcHV1, but it is known that upon infecting the cell the virus rapidly suppresses host protein synthesis [ 134 ]. Also the virus causes reorganization of the cytoskeleton [ 150 ]. There is a redistribution of actin filaments and a loss of organization of microtubules and vimentin filaments associated with syncytia formatin.…”

“…Disruption of microtubules with nocodazole inhibits cell fusion and virus production. The addition of taxol (a microtubule stabilizer) to the nocodazole treated cells rescues virus production, showing its dependence on microtubules [ 150 ].…”