What is it about?
During the early stages of A/NWS/33 human influenza virus infection, no appreciable association between incoming virions and cortical actin was detectable in the permissive MDCK model by confocal microscopy, while extensive colocalization and a slower infection progression were observed in LLC-MK2 cells. In the latter model, we also demonstrated the inability of the virus to carry out multiple replication cycles. Treatment with the actin-depolymerizing agent cytochalasin D significantly increased the infection efficiency in LLC-MK2 cells, while a detrimental effect was observed in the MDCK cell line.
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Why is it important?
Our data suggest a host-dependent role of the actin network in inducing a restriction to influenza virus replication.
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This page is a summary of: Host-cell-dependent role of actin cytoskeleton during the replication of a human strain of influenza A virus, Archives of Virology, May 2008, Springer Science + Business Media,
DOI: 10.1007/s00705-008-0103-0.
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