To examine the susceptibility of pig macrophages to H1N1pdm originating from a human host, we infected 3D/4 cells with the A/ Nanjing/108/2009 (H1N1). Typical cytopathic effect (CPE) appeared 16 hrs post infection and the cell monolayer was destroyed 32 hrs post infection (Fig. 1A) . This result demonstrated that H1N1pdm retains the ability to infect and replicate in swine macrophages, and can reach 1.8610 4 PFU/ml as shown in a replicative curve (Fig. 1B) . Apoptosis occurred and proceeded through the course of the infection, as we observed cleaved/ activated caspase-9 as well as the emergence of downstream executioner caspases-6, -7, and -3, which eventually destroyed the infected swine macrophages (Fig. 1C) . Clearly, cytochrome c was released into the cytosol (Fig. 1E) , which activated mitochondriamediated intrinsic apoptosis as early as 3 hrs post infection. Bak, a pro-apoptotic Bcl-2 family member, was upregulated as detected in the infected cells (Fig. 1D) , and may be involved in the release of cytochrome c from mitochondria in swine macrophages.