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Background: Dobrava-Belgrade virus (DOBV) is a European hantavirus causing hemorrhagic fever with renal syndrome (HFRS) in humans with fatality rates of up to 12%. DOBV-associated clinical cases typically occur also in the northern part of Germany where the virus is carried by the striped field mouse (Apodemus agrarius). However, the causative agent responsible for human illness has not been previously isolated., Methodology/principal Findings: Here we report on characterization of a novel cell culture isolate from Germany obtained from a lung tissue of "spillover" infected yellow necked mouse (A. flavicollis) trapped near the city of Greifswald. Phylogenetic analyses demonstrated close clustering of the new strain, designated Greifswald/Aa (GRW/Aa) with the nucleotide sequence obtained from a northern German HFRS patient. The virus was effectively blocked by specific antibodies directed against β3 integrins and Decay Accelerating Factor (DAF) indicating that the virus uses same receptors as the highly pathogenic Hantaan virus (HTNV). In addition, activation of selected innate immunity markers as interferon β and λ and antiviral protein MxA after viral infection of A549 cells was investigated and showed that the virus modulates the first-line antiviral response in a similar way as HTNV., Conclusions/significance: In summary, our study reveals novel data on DOBV receptor usage and innate immunity induction in relationship to virus pathogenicity and underlines the potency of German DOBV strains to act as human pathogen.

2'-5'-oligoadenylate synthetase, an interferon-induced enzyme and a sensitive indicator of the presence of interferon, was measured in peripheral blood mononuclear cells in children with inflammatory disorders of known and unknown origin in order to assess the value of such a test in patient management. Differences in median 2'-5'-oligoadenylate synthetase values in groups of children with viral or bacterial diseases or healthy children were observed. Considerable overlap of the 2'-5'-oligoadenylate synthetase range in the three groups was observed. All children with acute viral infections had increased levels early in their disease and a low value clearly argued against an acute viral infection. However, as more than one-third of children with bacterial diseases displayed elevated 2'-5'-oligoadenylate synthetase concentrations, distinction between a viral and bacterial cause of disease by measuring this enzyme was difficult. Estimation of 2'-5'-oligoadenylate synthetase concentrations in patients with inflammatory diseases of unknown origin, including juvenile rheumatoid arthritis, systemic lupus erythematosus, idiopathic uveitis and glomerulonephritis did not contribute to establishing a diagnosis or measuring disease activity.