TNF family members were also induced in response to H1N1pdm infection, which may be attributable to cell death. We found that in pig macrophages the levels of FasL and TNF-a remained undetectable, while TNF-related apoptosis-inducing ligand (TRAIL) seemed to be most abundant before infection, based on Ct values from realtime RT-PCR (data not shown). FasL and TNF-a were induced most robustly, but TRAIL was only mildly induced in response to infection (Fig. 2B) . Among the induced, the level of TNF-a, critical in both cell death and inflammation, was sharply upregulated up to 14-and 162-fold, and FasL up to 43-and 22-fold at 16 and 36 hrs p.i., respectively. FasL and TNF-a may play a major role in H1N1pdm-triggered extrinsic apoptosis.