Further studies attempt to combine omentum-wrapping with several other strategies, such as optimizing the microstructure of the L-CCH scaffold, incorporating neurotrophic agents, and seeding supportive cells. Rodent borne hantaviruses are the etiological agent of two zoonotic diseases: hemorrhagic fever with renal syndrome in Eurasia, and hantavirus cardiopulmonary syndrome in the Americas. The bank vole borne PUUV causes HFRS in Europe. Currently no specific treatment or US FDA-approved vaccines are available against HFRS/HCPS. While it has been shown that hantaviruses can deregulate human endothelial cell functions, activate unusual immune responses in patients, and interfere with several signaling pathways in human cells the exact Masitinib msds mechanism of symptoms associated with HFRS/HCPS still remains unknown. Interestingly, while hantaviruses cause a transient infection and disease in humans, infections of the natural rodent hosts seem to be chronic and asymptomatic. It is possible that PUUV and other hantaviruses have developed features that facilitate viral persistence, replication and spread, without harming the natural host. However, due to the lack of specific reagents, it has not been possible to analyze if PUUV interferes with bank vole cell functions, and consequently it is not known if PUUV affects infected cells in a species-specific manner. Activation of innate immune responses is crucial in order to eradicate virus infections. The induction of, as well as response to, type I IFNs during virus infection are important parts of the innate immunity. When pattern recognition receptors detect viruses in infected cells, they activate pathways leading to the induction and production of IFN-a/b. These IFNs then act on infected as well as non-infected bystander cells by inducing IFN-stimulated genes like Mx proteins, which possess antiviral features, thereby inhibiting viral replication and further spread. Consequently, most pathogenic viruses have evolved countermeasures which can inhibit induction of IFNs, and/or can inhibit IFN-induced activation of antiviral responses in infected cells. Understanding how zoonotic virus infections in natural hosts differ from human infections might give important clues to the mechanisms behind pathogenesis in humans. In order to study this there is a need for in vitro-models based on natural hosts cells. Here, we present a model for virus infection experiments in cells derived from bank voles and protocols for studies of bank vole innate immune activation. We here report that VEFs, isolated from bank vole embryos, are susceptible to infection with PUUV, and also to other bank vole borne viruses like TBEV, CPXV and LV, thereby providing the first in vitro-model for experimental studies of viruses having bank voles as a natural reservoir. Importantly, in addition to infection of VEFs with cell line adapted PUUV, successful infection was also established with wild-type PUUV. The bank vole IFN-b and Mx2 genes were partially sequenced, and Q-PCR protocols for quantification of gene expression were developed. Using these newly developed Q-PCR protocols, levels of IFN-b and Mx2 mRNA were analyzed in response to infection with CPXV, LV, PUUV-Kazan-E6 or TBEV.