Background: Similar to other viruses, the viral proteins of Ebola virus (EBOV) interact with a variety of host proteins for its replication. Of the 7 structural proteins encoded in the EBOV genome, VP24 is the smallest and is multifunctional.
Methods: To identify host factors that interact with VP24 and are required for EBOV replication, we transfected 293 cells with plasmid expressing FLAG- and HA-tagged VP24, immunoprecipitated the host proteins that bound to VP24, and analyzed the immunoprecipitants with use of mass spectrometry.
Results: Of the 68 candidate host proteins identified, we selected Sec61α because of its similar intracellular localization to that of VP24 (ie, perinuclear region), its involvement in various biological functions, and its roles in pathogenesis, such as type 2 diabetes and hepatosteatosis, and investigated its possible role in the EBOV life cycle. Our results suggest that Sec61α is not involved in EBOV entry, interferon antagonism by VP24, nucleocapsid formation, or budding. However, Sec61α colocalized with VP24 contributed to the ability of VP24 to inhibit EBOV genome transcription and reduced the polymerase activity of EBOV.
Conclusions: The present study indicates that Sec61α is a host protein involved in EBOV replication, specifically in EBOV genome transcription and replication.