Table 5.
Estimates of correlationsa (standard error) of response to infection with PRRSV isolate NVSL
| Trait | VL | WG | TP | PV | Tmax | Vmax |
|---|---|---|---|---|---|---|
| VL | −0.33 (0.03) | 0.10 (0.03) | 0.66 (0.02) | 0.36 (0.03) | −0.27 (0.03) | |
| WG | −0.74 (0.10) | −0.02 (0.03) | −0.22 (0.03) | −0.16 (0.03) | 0.12 (0.03) | |
| TP | 0.31 (0.15) | 0.27 (0.16) | −0.09 (0.03) | 0.72 (0.01) | 0.12 (0.03) | |
| PV | 0.85 (0.07) | −0.73 (0.13) | 0.05 (0.19) | −0.23 (0.03) | 0.40 (0.03) | |
| Tmax | 0.81 (0.10) | −0.11 (0.16) | 0.83 (0.07) | 0.50 (0.21) | −0.51 (0.02) | |
| Vmax | −0.72 (0.21) | 0.45 (0.22) | −0.11 (0.26) | −0.27 (0.33) | −0.57 (0.19) |
WG weight gain (kg), VL viral load (area under the Wood’s curve of log10 serum viremia from 0 to 21 days post infection; viremia * days), TP time to peak viremia (days), PV peak viremia (log10 serum viremia), Tmax time to maximal rate of viremia decay (days), Vmax maximal rate of viremia decay (log10 serum viremia/day)
aPhenotypic correlations (above diagonal) and genetic correlations (below diagonal) were estimated using an animal model in ASReml and the full G-matrix