What is it about?
In this study we evidenced that microtubule-stabilization negatively interferes with influenza A/NWS/33 virus replication in LLC-MK2 but not in MDCK cells. Conversely, microtubule-depolymerization improves NWS growth in LLC-MK2 but not in the MDCK model. The occurrence of alpha-tubulin hyperacetylation - a post-translational modified form suggestive of stable microtubules - was significantly delayed in infected LLC-MK2 cells when compared to MDCK cells. Furthermore, mock-infected LLC-MK2 cells were shown to have higher levels of both acetylated alpha-tubulin and microtubule-associated protein 4, the latter being essential for the maintenance of normal microtubule polymer levels in interphase epithelial cells. We evidenced that MAP4 silencing improves NWS growth in LLC-MK2 cells. By evidencing the cell type-dependent regulatory role of microtubule dynamics on NWS replication in mammalian kidney cells, we demonstrated that microtubule-stabilization represents a restriction factor for the initiation of NWS infection in LLC-MK2 but not in MDCK cells.
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Why is it important?
This study contributes to improve the understanding on the differential behaviour of NWS influenza strain in two mammalian cell models. Very important, here we provide new insights into the cell type-dependent regulatory role of microtubule dynamics during the initiation of NWS infection.
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This page is a summary of: Highly Dynamic Microtubules Improve the Effectiveness of Early Stages of Human Influenza A/NWS/33 Virus Infection in LLC-MK2 Cells, PLoS ONE, July 2012, PLOS,
DOI: 10.1371/journal.pone.0041207.
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