Ultrastructural Characterization of Membrane Rearrangements Induced by Porcine Epidemic Diarrhea Virus InfectionZhou, X., Cong, Y., Veenendaal, T., Klumperman, J., Shi, D., Mari, M. & Reggiori, F., 5-Sep-2017, In : Viruses. 9, 9, 18 p., 251.
Research output: Contribution to journal › Article › Academic › peer-review
The porcine epidemic diarrhea virus (PEDV) is a coronavirus (CoV) belonging to the alpha-CoV genus and it causes high mortality in infected sucking piglets, resulting in substantial losses in the farming industry. CoV trigger a drastic reorganization of host cell membranes to promote their replication and egression, but a detailed description of the intracellular remodeling induced by PEDV is still missing. In this study, we examined qualitatively and quantitatively, using electron microscopy, the intracellular membrane reorganization induced by PEDV over the course of an infection. With our ultrastructural approach, we reveal that, as most of CoV, PEDV initially forms double-membrane vesicles (DMVs) and convoluted membranes (CMs), which probably serve as replication/transcription platforms. Interestingly, we also found that viral particles start to form almost simultaneously in both the endoplasmic reticulum and the large virion-containing vacuoles (LVCVs), which are compartments originating from the Golgi, confirming that alpha-CoV assemble indistinguishably in two different organelles of the secretory pathway. Moreover, PEDV virons appear to have an immature and a mature form, similar to another alpha-CoV the transmissible gastroenteritis coronavirus (TGEV). Altogether, our study underlies the similarities and differences between the lifecycle of alpha-CoV and that of viruses belonging to other CoV subfamilies.
|Number of pages||18|
|Publication status||Published - 5-Sep-2017|
- PEDV, alpha-coronavirus, lifecycle, electron microscopy, membrane rearrangement, CORONAVIRUS NUCLEOCAPSID PROTEIN, SARS-CORONAVIRUS, ENDOPLASMIC-RETICULUM, MOUSE HEPATITIS, CELL-CULTURE, REPLICATION, MORPHOGENESIS, PROLIFERATION, PATHOGENESIS, INHIBITION