Interaction of the Influenza Virus Nucleoprotein with the Cellular CRM1-Mediated Nuclear Export Pathway

• DOI: 10.1128/jvi.75.1.408-419.2001
• Publication Date: 2002-07-27T10:06:37Z
• Authors: Debra Elton; Martha Simpson-Ho...; Kate Archer; Liz Medcalf; Roger Hallam; John McCauley; Paul Digard
• Keywords: Nucleoprotein; Nuclear export signal; Nucleoplasm

Influenza virus transcription occurs in the nuclei of infected cells, where viral genomic RNAs are complexed with a nucleoprotein (NP) to form ribonucleoprotein (RNP) structures. Prior assembly into progeny virions, these RNPs exit nucleus and accumulate cytoplasm. The mechanisms responsible for RNP export only partially understood but have been proposed involve M1 NS2 polypeptides. We found that drug leptomycin B (LMB), which specifically inactivates cellular CRM1 polypeptide, caused nuclear retention NP virus-infected indicating role pathway egress. However, no alteration was seen distribution or NS2, even case mutant synthesizes greatly reduced amounts NS2. Furthermore, distributed throughout cells at early times postinfection but, when retained late by LMB treatment, redistributed periphery nucleoplasm. No such change after treatment. Similar behavior NP, treatment expressing each polypeptide isolation not Conversely, overexpression increased cytoplasmic accumulation had little effect on distribution. Consistent this, bound vitro. Overall, data raise possibility is mediated direct interaction between pathway.