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Purification of High Yield Extracellular Vesicle Preparations Away from Virus
Published on: September 12, 2019
Poliovirus infection transiently increases COPII vesicle budding
Meg Trahey1, Hyung Suk Oh, Craig E Cameron
1Division of Biological Sciences and Center for Structural and Functional Neuroscience, The University of Montana, Missoula, Montana, USA.
Abstract:
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.
Insights
Poliovirus infection initially boosts COPII vesicle production, a key part of the host cell
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Poliovirus (PV) utilizes host cell secretory pathway membranes for viral RNA replication.
- Previous studies identified the intermediate compartment and Golgi apparatus as PV replication organelle precursors.
Purpose of the Study:
- To investigate the impact of poliovirus infection on COPII vesicle biogenesis.
- To understand the role of COPII vesicles in PV replication complex formation.
Main Methods:
- Examined the effect of PV infection on COPII vesicle formation in host cells.
- Assessed the membrane-associated levels of Sec16A, a COPII biogenesis regulator.
Main Results:
- PV infection induced a biphasic response in COPII vesicle biogenesis: early enhancement followed by inhibition.
- An increase in membrane-bound Sec16A correlated with the early rise in COPII vesicle production.
Conclusions:
- The early enhancement of COPII vesicle formation likely benefits poliovirus by providing necessary membrane precursors for replication complexes.
- Poliovirus manipulates host cell COPII vesicle dynamics to facilitate its replication cycle.
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