Macrophages appear to die inevitably of apoptosis when infected with influenza virus [26] . The Fas-mediated extrinsic apoptotic pathway is apparently triggered by TNF family ligands. While both FasL and TNF-a were induced vigorously upon the viral infection, induction of TRAIL was rather mild in H1N1pdminfected swine macrophages. We knew previously that FasL and TNF-a were barely detectable, while the level of TRAIL remained high prior to the infection based on our realtime RT-PCR data (Ct) (Xing et al., unpublished data). We can therefore presume that H1N1pdm-induced apoptosis may be mainly attributed to FasL and TNF-a, while pig macrophages could be resistant to TRAIL, since the cells remained intact despite the presence of a high level of TRAIL before infection. Furthermore, we were also able to determine that both ERK1/2 and JNK1/2 were involved in the induction of FasL, TNF-a, and TRAIL. FasL is also regulated by ERK1 in chicken macrophages infected with an H9N2 avian influenza virus [34] .