IAV_FITNESS
Scope
Influenza fitness determinants, conserved noncoding RNA elements, segment-specific viral biology, fidelity, packaging, and innate-sensing consequences.
Working Model
IAV fitness is shaped by RNA-level regulatory circuitry, fidelity errors, segment completeness, splicing outcomes, and co-infection complementation, not only polymerase activity or canonical immune antagonism.
Key Concepts
- Conserved viral noncoding RNAs as regulatory determinants.
- Segment completeness and Segment 8/NS1 sufficiency.
- Rare IFN-positive sentinel cells.
- Defective genomes.
- Co-infection rescue of incomplete viral states.
- Early-cycle virus-intrinsic fitness.
- RNA velocity/MOI titration.
- Late-stage barcoding at the M2 3' splice junction.
People
- Fiorella Chacon: HA/membrane project tied to influenza host response.
- Abigail Korenek: NS1 multifunctionality.
- Ben tenOever
Known Outputs
- Remembered 4-figure IAV paper:
- Fig. 1: defective genomes / Segment 8 loss / rare IFN-positive cells / IRF7.
- Fig. 2: late-stage barcoding at M2 3' splice junction.
- Fig. 3: co-infection rescue of segment completeness and boosted transcription.
- Fig. 4: early-cycle virus-intrinsic fitness, host-state independence, RNA velocity/MOI titration, reassortment framing.
- Keystone abstract: “Fidelity Errors as the Nexus of Innate Sensing, Viral Fitness, and Evolution.”
TODO
- Add raw single-cell datasets, barcoded library design, figure drafts, and manuscript status.