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J Cell Sci. 2017 Dec 1;130(23):4038-4050. doi: 10.1242/jcs.210807. Epub 2017 Oct 23.

KIF13A mediates trafficking of influenza A virus ribonucleoproteins.

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Cell Biology of Viral Infection Lab, Instituto Gulbenkian de Ciência (IGC), 2780-156 Oeiras, Portugal.
Institute of Virology, Hannover Medical School, 30625 Hannover, Germany.
Science4U, MARL Espaços CC02 e CC03, São Julião do Tojal, 2660-421, Loures, Portugal.
Institut Curie, PSL Research University, CNRS, UMR144, Structure and Membrane Compartments, 75005 Paris, France.
Cell Biology of Viral Infection Lab, Instituto Gulbenkian de Ciência (IGC), 2780-156 Oeiras, Portugal


Influenza A is a rapidly evolving virus that is successful in provoking periodic epidemics and occasional pandemics in humans. Viral assembly is complex as the virus incorporates an eight-partite genome of RNA (in the form of viral ribonucleoproteins, vRNPs), and viral genome assembly - with its implications to public health - is not completely understood. It has previously been reported that vRNPs are transported to the cell surface on Rab11-containing vesicles by using microtubules but, so far, no molecular motor has been assigned to the process. Here, we have identified KIF13A, a member of the kinesin-3 family, as the first molecular motor to efficiently transport vRNP-Rab11 vesicles during infection with influenza A. Depletion of KIF13A resulted in reduced viral titers and less accumulation of vRNPs at the cell surface, without interfering with the levels of other viral proteins at sites of viral assembly. In addition, when overexpressed and following two separate approaches to displace vRNP-Rab11 vesicles, KIF13A increased levels of vRNP at the plasma membrane. Together, our results show that KIF13A plays an important role in the transport of influenza A vRNPs, a crucial step for viral assembly.This article has an associated First Person interview with the first author of the paper.


Influenza A virus assembly; KIF13A; Molecular motor; Recycling endosome

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