Live attenuated vaccines against mumps virus (MuV) have been traditionally produced by passaging the virus in the embryonated chicken eggs or primary chicken embryo fibroblasts (CEFs). Virus propagation on these cell substrates enables successful virus attenuation and retains it sufficiently antigenic to induce lasting protective immunity in humans. The aim of this study was to identify critical factors for MuV replication in primary CEFs grown on a small-scale level in order to explore possibilities for improvements in the virus replication and yield. The effect of differently prepared cells, culturing conditions, and infection conditions on virus yield was estimated by employing statistical design of experiments (DoE) methodology. Our results show that the preparation of primary CEFs and the way of their infection substantially impact virus yield and are critical for efficient MuV replication. These process parameters should be considered in further process optimization. We also demonstrate the applicability of DoE in optimization of virus replication as a crucial step in obtaining high virus yields.
Human type I interferons (IFNs) comprise one IFN-b, -x, -j, and -e and 12 different IFN-a subtypes, which play an important role in early host antiviral response. Despite their high structural homology and signaling through the same receptor, IFN-a subtypes exhibit different antiviral, antiproliferative, and immunomodulatory activities. Differences in the production of IFN-a subtypes therefore determine the quality of an antiviral response. In this study, we investigated the pattern of IFN-a subtypes induced in infection with different mumps virus (MuV) strains and examined the MuV sensitivity to the action of IFN-a subtypes. We found that all IFN-a subtypes are being expressed in response to MuV infection with a highly similar IFN-a subtype pattern between the virus strains. We assessed an antiviral activity of several IFN-a subtypes: IFN-a1, IFN-a2, IFN-a4, IFN-a6, IFN-a8, IFN-a14, IFN-a17, and IFN-a21. Although they were all effective in suppressing MuV replication, the intensity and pattern of their action varied between MuV strains. Our results indicate that the overall IFN antiviral activity as well as the activity of specific IFN-a subtypes against MuV depend on a virus strain.
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