<15> Phosphatidylserine vesicles enable efficient en bloc transmission of enteroviruses
Phosphatidylserine
vesicles enable efficient en bloc transmission of
enteroviruses
Chen et
al., 2015, Cell 160, 619–630
Speaker: Yu-Lun Chen
(陳昱倫) Time: 13:00~14:00, Oct. 21, 2015
Commentator: Dr. Guey-Chuen Perng (彭貴春老師) Place: Room 601
Abstract:
Enteroviruses are
a genus of positive-sense single-stranded RNA, non-enveloped
viruses, which include polioviruses (PV), coxsackie
A and B viruses (CA, CB) and human rhinovirus. The cell-to-cell
spread of nonenveloped viruses usually requires cell
lysis. However, there are reports that extracellular coxsackie
viruses B3 (CVB3) are present in vesicles (Robinson et al., 2014) and
poliovirus (PV) are able to spread non-lytically
among the host cells (Bird, Maynard, Covert, & Kirkegaard, 2014). These
findings raised the important questions regarding the extracellular nature of enteroviral particles and the significance of non-lytic
release of the virus particles. In this study, the authors investigated the
assembly, release and subsequent infection processes of enteroviral
particles. Their findings showed that multiple infectious enteroviral
particles were clustered within individual phosphatidylserine (PS)
lipid-enriched vesicles and non-lytically secreted
out of cells. These viral particles in the vesicles are more efficient in
establishing infection than free viral particles. They also demonstrated that
the vesicles encapsulate and traffic large numbers of mature infectious viral
particles between cells and enable the transfer of multiple viral RNA genomes
collectively into the new host cells by a mechanism that is dependent on both
the virus-specific receptor of the recipient host cell as well as the vesicular
PS lipids. This study reveals a novel mode of viral transmission, where enteroviral genomes are transmitted from cell-to-cell en bloc in membrane-bound PS vesicles
instead of as single independent genomes.
References:
1.
Bird, S. W., Maynard, N. D., Covert, M. W., &
Kirkegaard, K. (2014). Nonlytic viral spread enhanced by autophagy components. Proc Natl Acad Sci U S A, 111(36),
13081-13086. doi: 0.1073/pnas.1401437111
2.
Robinson,
S. M., Tsueng, G., Sin, J., Mangale, V., Rahawi, S., McIntyre, L. L., Feuer, R.
(2014). Coxsackievirus B exits the host cell in shed microvesicles displaying
autophagosomal markers. PLoS Pathog, 10(4),
e1004045. doi: 10.1371/journal.ppat.1004045