In 1998, Albina et al. first reported the failure of PRRSV in inducing the production of interferon- protein in the lung secretions of infected pigs and in the supernatants of PRRSV-infected alveolar macrophages and peripheral blood mononuclear cells [17] . Furthermore, they observed that PRRSV was also capable of blocking the production of interferon- protein in macrophages by a well-characterized and potent interferon- inducer, swine transmissible gastroenteritis virus (TGEV), a member of the coronaviridae family. Virus replication and infectivity is essential to the inhibition of interferon- production since UV-inactivated PRRSV fails to block the induction of interferon- by TGEV. Interestingly, a recent study reported that PRRSV infectivity is not essential to the inhibition of type I interferon in plasmacytoid dendritic cells, which are resistant to PRRSV infection [4] . The observation that PRRSV is a poor inducer of interferon- is further confirmed by Buddaert et al. [18] . In 2004, Chung et al. reported that PRRSV activated the transcription of interferon- and Mx1 in lung tissues at day 1 and peaked at day 7 after infection in acutely infected animals, suggesting that PRRSV does activate the transcription of interferon- and interferon induced genes such as Mx1 [19] . Others have further reported that different PRRSV isolates exhibit different capacities in inducing the production of interferon- in alveolar macrophages [20] . The activation of interferon- transcription in PRRSV-infected monocyte-derived dendritic cells, peripheral blood mononuclear cells, alveolar macrophages and in porcine alveolar macrophages of PRRSV-infected animals has also been reported [3, 21, 22, 23] . Taken together, the existing evidence clearly indicates that PRRSV activates the transcription of type I interferon in its natural susceptible cells. In MARC-145 cells, however, Miller reported that PRRSV not only failed to activate the transcription of interferon- and , but also suppressed the transcription of interferon- activated by Poly I:C [24] . This suggests a cell type dependent difference in activating the transcription of type I interferon by PRRSV. Marked differences in type I interferon induced antiviral activity against PRRSV between porcine alveolar macrophages and MARC-145 cells have also been reported recently [25] . Since MARC-145 cells are not the natural susceptible cells for PRRSV, the implication of the results in understanding the pathogenesis of PRRSV is debatable. Overall, the existing evidence clearly suggests that PRRSV may have intrinsic properties to inhibit or reduce the induction of interferon- and .