Christopher B. Brooke

The paper shows that single-cell heterogeneity in IFN induction potential is heritable and driven by baseline variation in JNK and AP-1 signaling states.

This study analyzes influenza A virus deletion-containing genomes over time, finding that specific mutations enhance their replication and interference while being lethal in wild-type backgrounds.

This study shows TRIM21 acts as a molecular rheostat regulating influenza A virus replication by modulating ubiquitination and innate immune signaling, with PRKDC as a compensatory antiviral factor when TRIM21 is absent.

This study models the fitness effects of coinfection and reassortment in segmented viruses, finding that increased genetic divergence and inter-strain mixing generally reduce viral fitness.

The paper identifies intrinsic OASL expression as a determinant of IFN induction potential in influenza A virus-infected cells using scRNA-seq analysis.

This study uses deep mutational scanning to analyze the functional impact of NEP mutations in influenza A virus, revealing pleiotropic effects on viral replication and host adaptation.

This study compares the ability of seasonal H1N1 and H3N2 influenza A viruses to antagonize interferon induction and signaling at the single-cell level, finding differences in their IFN antagonism potential.

This study measures viral burst sizes in thousands of infected cells using dqPCR, finding significant variation in H3N2 and H1N1 strains with a small fraction of cells producing most viruses.

This study shows that natural variation in neuraminidase activity affects the evolutionary potential of hemagglutinin in seasonal H1N1 influenza viruses.

The paper develops an Illumina-based sequencing framework and pipeline to accurately detect and map influenza virus DIP-associated RNAs, demonstrating its reliability through simulated and experimental data.