Conclusions: The prioritization methodology presented here is based on the systematic evaluation of evidence and the involvement of a broad range of external experts. We feel that the results provide internal consistency and are plausible in the public health perspective. Our comprehensive and transparent approach makes the results defensible and shall give guidance for current needs in surveillance and epidemiological research in Germany. The list of ranked pathogens established here will serve as a reference for our mid-term strategic decisions, which will include strengthening the existing or introduction of new surveillance systems for pathogens from the high priority group (e.g., RSV, VZV or Helicobacterpylori) and re-consideration of the research and surveillance needs for those from the lowest priority group. It has already influenced the decision process on the need for the installation of new and continuation of existing national reference centers in Germany and the internal planning for the respective allocation of resources (GK personal communication). We plan to conduct a re-assessment of priorities within a five-year time frame based on the same methodology. The prioritization tool or its components can be applied across different areas of infectious diseases (by re-weighting prioritization criteria by different professional groups for different purposes) and in different geographical areas (by re-scoring pathogens according to their characteristics relevant for particular countries or continents). We hope that the presentation of our methodology could be helpful to other institutions that choose to prioritize their resources based on a transparent and standardized process.  A Vesicular Stomatitis Virus Replicon-Based Bioassay for the Rapid and Sensitive Determination of Multi-Species Type I Interferon Type I interferons (IFN) comprise a family of cytokines that signal through a common cellular receptor to induce a plethora of genes with antiviral and other activities. Recombinant IFNs are used for the treatment of hepatitis C virus infection, multiple sclerosis, and certain malignancies. The capability of type I IFN to suppress virus replication and resultant cytopathic effects is frequently used to measure their bioactivity. However, these assays are time-consuming and require appropriate biosafety containment. In this study, an improved IFN assay is presented which is based on a recombinant vesicular stomatitis virus (VSV) replicon encoding two reporter proteins, firefly luciferase and green fluorescent protein. The vector lacks the essential envelope glycoprotein (G) gene of VSV and is propagated on a G protein-expressing transgenic cell line. Several mammalian and avian cells turned out to be susceptible to infection with the complemented replicon particles. Infected cells readily expressed the reporter proteins at high levels five hours post infection. When human fibroblasts were treated with serial dilutions of human IFN-β prior to infection, reporter expression was accordingly suppressed. This method was more sensitive and faster than a classical IFN bioassay based on VSV cytopathic effects. In addition, the antiviral activity of human IFN-λ (interleukin-29), a type III IFN, was determined on Calu-3 cells. Both IFN-β and IFN-λ were acid-stable, but only IFN-β was resistant to alkaline treatment. The antiviral activities of canine, porcine, and avian type I IFN were analysed with cell lines derived from the corresponding species. This safe bioassay will be useful for the rapid and sensitive quantification of multi-species type I IFN and potentially other antiviral cytokines. IFN-a and IFN-b are structurally related cytokines of the type I interferon family which mediate an early innate immune response to viral infections. There are 13 distinct IFN-a genes present in the human genome, and a single gene encoding for IFN-b. These genes are transcriptionally activated in cells sensing a virus infection through pattern recognition receptors such as the retinoic acid inducible gene I (RIG-I) helicase. Following secretion, IFN-a and IFN-b act similarly by binding to a common, ubiquitously expressed IFN-a/b receptor resulting in the activation of the JAK/STAT signal transduction pathway and transcription of ''IFN-induced genes'' [1, 2] . Several of these genes encode for proteins with strong antiviral activity, i.e. Mx protein, protein kinase R, and 29-59oligo(A) synthetase [3] . Due to their autocrine action, type I IFN may attenuate virus replication in infected cells. Probably more important is the paracrine action of type I IFN, which induces an antiviral state in previously uninfected cells, thereby blocking virus dissemination in the organism. In addition to this ''classical'' antiviral function, type I IFNs are known to affect cell proliferation and differentiation, to modulate the immune response, to inhibit angiogenesis, and to promote apoptosis [4, 5] . Genetically engineered type I IFNs are currently in clinical use for the treatment of multiple sclerosis [6] , chronic hepatitis C virus infection [7] , and certain types of cancer [8, 9] . An issue of increasing importance is the determination of neutralizing antibodies that are induced in some patients following recombinant IFN therapy [10] .