The accurate determination of antiviral IFN activity is a cumbersome issue. In the ''classical'' bioassay, serial dilutions of both a test sample with unknown IFN activity and a type I IFN standard are incubated with an appropriate cell line prior to infection with a cytolytic virus such as vesicular stomatitis virus (VSV), encephalomyocarditis virus, or Sendai virus [14, 15] . The reciprocal value of the highest type I IFN dilution mediating protection of 50% of the cells from virus-induced cytopathic effects (CPE) is defined as one unit of type I IFN per volume. This classical IFN bioassay is time-consuming because the CPE normally needs 24 hours or more to develop. A faster readout can be achieved with recombinant viruses expressing reporter proteins such as green fluorescent protein (GFP) or firefly luciferase [16, 17, 18, 19] . However, any work with live virus requires appropriate biosafety containment. For example, a recently published IFN bioassay can only be performed in biosafety level 3 (BSL-3) facilities, because the test makes use of a recombinant Rift Valley Fever virus [19] . Viral replicon-based bioassays that take advantage of disabled propagation-incompetent viruses may provide an attractive alternative to live virusbased bioassays. A human hepatoma cell line harbouring a selectable hepatitis C virus replicon has been successfully employed for the measurement of type I IFN from patients with chronic hepatitis C virus infection [20] . However, as type I IFNs act in a species-dependent manner, this system may not be applicable to animal IFNs. Transgenic cell lines expressing a reporter gene under control of an IFN-responsive promoter may also be used to determine IFN activity under biosafe conditions [21, 22] . However, it is difficult to simply relate transcriptional reporter gene activation to antiviral activity.