CGIG_OSHV1_RNASEQ_PRJNA1329250
Primary-analysis sample count: 42. The counted unit and independent experimental units are described under Biological replication; counts may represent animals, pools or libraries.
Treatment
Experimental challenge with OsHV-1 microvariant (USA, Australia, or France strain)
Control
Unchallenged control spat from the same two lineages
Biological replication
42 RNA-seq libraries: 12 controls (6 Midori, 6 Miyagi) and 30 OsHV-1 microvariant-challenged (15 Midori, 15 Miyagi, split across USA, Australia, and France viral strains at 5 libraries per lineage-strain cell)
Phenotype interpretation
Infection up-regulated antiviral defense transcripts, including RIG-I-like receptors and the interferon-like pathway, similarly in both lineages; AREE records molecular antiviral responsiveness, not an organism-level survival difference
Analysis status
raw_reanalysis_harmonized
Quality control and results
All 1,564,162,034 read pairs quantified with Salmon 2.3.4 against GCF_963853765.1/RS_2024_06; mapping rates 44.24-61.66% (median 55.93%), well below the 73.9-76.0% of PRJNA516762 but uniform across arms (control 57.0% versus challenged 55.4%, Welch p = 0.30) and across both lineages, so it reflects library preparation rather than viral reads displacing host reads; 5,446 of 25,734 tested genes reach FDR < 0.05 (3,237 challenge-higher, 2,209 challenge-lower); PC1 explains 59.1% of variance and orders challenged above control though six control libraries fall inside the challenged range, and PC2 (16.6%) tracks the Midori/Miyagi split that ~ population + condition blocks on
Limitations
- This intake represents the molecular antiviral response to experimental OsHV-1 microvariant challenge, not a measured survival or organism-level disease-resistance difference between the two lineages.
- Challenge dose, exposure duration, and time of sampling after inoculation are not recorded in the public SRA metadata, so exposure intensity and duration are unresolved.
- The challenged and control arms are unequal in size (30 versus 12 libraries), but lineage is balanced within each arm and within every viral strain: 6 Midori and 6 Miyagi controls, and 5 of each lineage for each of the Australia, France, and USA strains. The lineage effect is therefore not confounded with infection status, and AREE blocks on lineage as ~ population + condition.
- The publication contrasts the USA and Australia microvariant strains and reports no marked difference between them; the France-strain libraries are present in the BioProject and are pooled into the challenged arm of the AREE contrast rather than analyzed as a separate strain effect.
- The BioProject carries no author-deposited processed expression matrix, so AREE has no published feature-level effect table to reconcile against.
- Condition, lineage, and viral-strain assignments were reconstructed from NCBI BioSample attribute tags rather than from a supplementary sample table; the source metadata spells the Miyagi lineage ‘Myagi’, which AREE normalized.