Publication: Permeability changes of integrin-containing multivesicular structures triggered by picornavirus entry
Issued Date
2014-10-09
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19326203
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2-s2.0-84907842368
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Mahidol University
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SCOPUS
Bibliographic Citation
PLoS ONE. Vol.9, No.10 (2014)
Suggested Citation
Pan Soonsawad, Lassi Paavolainen, Paula Upla, Wattana Weerachatyanukul, Nina Rintanen, Juan Espinoza, Gregory McNerney, Varpu Marjomäki, R. Holland Cheng Permeability changes of integrin-containing multivesicular structures triggered by picornavirus entry. PLoS ONE. Vol.9, No.10 (2014). doi:10.1371/journal.pone.0108948 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/32977
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Title
Permeability changes of integrin-containing multivesicular structures triggered by picornavirus entry
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Abstract
© 2014 Soonsawad et al. Cellular uptake of clustered a2b1-integrin induces the formation of membrane compartments that subsequently mature into a multivesicular body (MVB). Enhanced internalization mediated by clustered integrins was observed upon infection by the picornavirus echovirus 1 (EVI). We elucidated the structural features of virus-induced MVBs (vMVBs) in comparison to antibody-induced control MVBs (mock infection) by means of high-pressure cryo fixation of cells followed by immuno electron tomography during early entry of the virus. Three-dimensional tomograms revealed a marked increase in the size and complexity of these vMVBs and the intraluminal vesicles (ILVs) at 2 and 3.5 hours post infection (p.i.), in contrast to the control MVBs without virus. Breakages in the membranes of vMVBs were detected from tomograms after 2 and especially after 3.5 h suggesting that these breakages could facilitate the genome release to the cytoplasm. The in situ neutral-red labeling of viral genome showed that virus uncoating starts as early as 30 min p.i., while an increase of permeability was detected in the vMVBs between 1 and 3 hours p.i., based on a confocal microscopy assay. Altogether, the data show marked morphological changes in size and permeability of the endosomes in the infectious entry pathway of this non-enveloped enterovirus and suggest that the formed breakages facilitate the transfer of the genome to the cytoplasm for replication.