Mutations within the conserved NS1 nuclear export signal lead to inhibition of influenza A virus replication.

ABSTRACT:

Background

The influenza A virus NS1 protein is a virulence factor and an antagonist of host cell innate immune responses. During virus infection NS1 protein has several functions both in the nucleus and in the cytoplasm and its intracellular localization is regulated by one or two nuclear localization signals (NLS) and a nuclear export signal (NES).

Methods

In order to investigate the role of NS1 NES in intracellular localization, virus life cycle and host interferon responses, we generated recombinant A/Udorn/72 viruses harboring point mutations in the NES sequence.

Results

NS1 NES was found to be inactivated by several of the mutations resulting in nuclear retention of NS1 at late stages of infection confirming that this sequence is a bona fide functional NES. Some

SUBMITTER: Tynell J 

PROVIDER: S-EPMC4112715 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature