ABSTRACT
Influenza NS1 protein is an important virulence factor that is capable of binding double-stranded (ds) RNA and inhibiting dsRNA-mediated host innate immune responses. Here we show that NS1 can also bind cellular dsDNA. This interaction prevents loading of transcriptional machinery to the DNA, thereby attenuating IAV-mediated expression of antiviral genes. Thus, we identified a previously undescribed strategy, by which RNA virus inhibits cellular transcription to escape antiviral response and secure its replication.
Subject(s)
DNA/metabolism , Transcription, Genetic/physiology , Viral Nonstructural Proteins/metabolism , Animals , Cell Line , Chromatin/metabolism , Humans , Influenza A virus/physiology , Protein Binding , Viral Nonstructural Proteins/physiology , Virus ReplicationABSTRACT
OBJECTIVE: To resolve if TBX22 mutations cause isolated tongue-tie in the Finnish population. DESIGN: Mutation analysis of the coding region of the TBX22 gene in 50 Finnish isolated tongue-tie patients and 61 control samples. RESULTS: One putative sequence variation was identified from two male patients, but whether this represents a polymorphism or causative mutation remains unknown. CONCLUSIONS: Mutations in the coding region of the TBX22 gene are not a major cause of ankyloglossia in the Finnish population and do not explain the sex difference or inheritance of tongue-tie.
