A role for endoplasmic reticulum exit sites in foot-and-mouth disease virus infection

摘要: Picornaviruses replicate their genomes in association with cellular membranes. While enteroviruses are believed to utilize membranes of the early secretory pathway, origin used by foot-and-mouth disease virus (FMDV) for replication unknown. Secretory-vesicle traffic through pathway is mediated sequential acquisition two distinct membrane coat complexes, COPII and COPI, requires coordinated actions Sar1, Arf1 Rab proteins. Sar1 essential generating vesicles at endoplasmic reticulum (ER) exit sites (ERESs), while Rab1 required subsequent vesicle transport COPI vesicles. In present study, we have provided evidence that FMDV pre-Golgi infection. Small interfering RNA depletion or expression a dominant-negative (DN) mutant Sar1a inhibited contrast, dominant-active Sar1a, which allowed formation but stabilizing coats, caused major disruption ER–Golgi intermediate compartment (ERGIC) did not inhibit Treatment cells brefeldin A, DN mutants Rab1a, disrupted Golgi enhanced These results show reagents block ERESs an inhibitory effect on infection, immediately after ER before ERGIC make infection more favourable. Together, these observations argue role initial takes place formed ERESs.