Maximal interferon induction by influenza lacking NS1 is infrequent owing to requirements for replication and export.

ABSTRACT: Influenza A virus exhibits high rates of replicative failure due to a variety of genetic defects. Most influenza virions cannot, when acting as individual particles, complete the entire viral life cycle. Nevertheless influenza is incredibly successful in the suppression of innate immune detection and the production of interferons, remaining undetected in >99% of cells in tissue-culture models of infection. Notably, the same variation that leads to replication failure can, by chance, inactivate the major innate immune antagonist in influenza A virus, NS1. What explains the observed rarity of interferon production in spite of the frequent loss of this, critical, antagonist? By studying how genetic and phenotypic variation in a viral population lacking NS1 correlates with interferon productio

SUBMITTER: Vicary AC 

PROVIDER: S-EPMC10138204 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature