Abstract
Influenza viruses replicate their single-stranded RNA genomes in the nucleus of infected cells and these replicated genomes (vRNPs) are then exported from the nucleus to the cytoplasm and plasma membrane before budding. To achieve this export, influenza viruses hijack the host cell export machinery. However, the complete mechanisms underlying this hijacking remain not fully understood. We have previously shown that influenza viruses induce a marked alteration of the nucleus during the time-course of infection and notably in the nucleolar compartment. In this study, we discovered that a major nucleolar component, called nucleolin, is required for an efficient export of vRNPs and viral replication. We have notably shown that nucleolin interacts with the viral nucleoprotein (NP) that mainly constitutes vRNPs. Our results suggest that this interaction could allow vRNPs to “catch” the host cell export machinery, a necessary step for viral replication.
Highlights
Influenza A viruses (IAV) are responsible for respiratory diseases that affect millions of people worldwide in recurrent annual epidemics, sometimes fatally
Nucleolin redistributes with IAV ribonucleoprotein complexes to the nuclear periphery of infected cells
In accordance with these observations, we report in this study the differential delocalization through the nucleus of the three major nucleolar components, nucleolin, B23 and fibrillarin during the time-course of IAV infection
Summary
Influenza A viruses (IAV) are responsible for respiratory diseases that affect millions of people worldwide in recurrent annual epidemics, sometimes fatally. Numerous cellular components have been identified as functional interacting partners of IAV proteins and some are subject to different extents of viral “retasking”[3,5,6,7,8,9] In view of their nuclear replication, IAV require the efficient export of their vRNPs from the nucleus towards the cytoplasm and budding regions of the cell membrane for a productive infection[10]. Chase and collaborators showed that the interaction between vRNPs and the nuclear export machinery takes place in dense chromatin domains that allow IAV to “snatch” Crm1-RanGTP nuclear export complexes to the detriment of cellular substrates[13] These results, together with other observations, highlight the involvement of host nuclear compartmentalization and chromatin territories in regulating nuclear traffic of IAV vRNPs14–17. High-throughput RNAi approaches have highlighted the functional requirement of several of these nucleolar components in viral replication[31,32,33]
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