Poliovirus infection transiently increases COPII vesicle budding

Meg Trahey, Hyung Suk Oh, Craig E. Cameron, Jesse C. Hay

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


Poliovirus (PV) requires membranes of the host cell's secretory pathway to generate replication complexes (RCs) for viral RNA synthesis. Recent work identified the intermediate compartment and the Golgi apparatus as the precursors of the replication "organelles" of PV (N. Y. Hsu et al., Cell 141:799-811, 2010). In this study, we examined the effect of PV on COPII vesicles, the secretory cargo carriers that bud from the endoplasmic reticulum and homotypically fuse to form the intermediate compartment that matures into the Golgi apparatus. We found that infection by PV results in a biphasic change in functional COPII vesicle biogenesis in cells, with an early enhancement and subsequent inhibition. Concomitant with the early increase in COPII vesicle formation, we found an increase in the membrane fraction of Sec16A, a key regulator of COPII vesicle formation. We suggest that the early burst in COPII vesicle formation detected benefits PV by increasing the precursor pool required for the formation of its RCs.

Original languageEnglish
Pages (from-to)9675-9682
Number of pages8
JournalJournal of Virology
Issue number18
StatePublished - Sep 2012


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