Furthermore, we showed that the Rab1b downstream effector Golgi-specific BFA resistance factor 1 (GBF1), which activates the small GTPase ADP ribosylation factor 1 (ARF1), is required for IBDV replication, since inhibiting its activity by treatment with bre feldin A (BFA) or golgi cide A (GCA) significantly reduces the yield of infectious viral progeny. Rab1b comprises a key regulator of GC transport and we demonstrate that transfecting the negative mutant Rab1b N121I or knocking down Rab1b expression by RNA interference significantly reduces the yield of infectious viral progeny. By analyzing crucial proteins involved in the secretory pathway, we showed the essential requirement of Rab1b for viral replication. Here, we report that IBDV reorganizes the GC to localize the endosome-associated replication complexes without affecting its secretory functionality.

We previously demonstrated that IBDV hijacks the endocytic pathway for establishing the viral replication complexes on endosomes associated with the Golgi complex (GC). Infectious bursal disease virus (IBDV), the prototypic family member, is the etiological agent of Gumboro disease, a highly contagious immunosuppressive disease in the poultry industry worldwide. The family is composed of nonenveloped viruses with a segmented double-stranded RNA (dsRNA) genome. Birnaviruses are members of the Birnaviridae family, responsible for major economic losses to poultry and aquaculture.

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