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Single nucleotide polymorphisms (SNPs) calculated from whole genome sequencing (WGS) are ideally suited to study evolutionary relationships of pathogens and their epidemiology. Mycobacterium caprae infections have been documented frequently in cattle and red deer along the Bavarian and Austrian Alps during the last decade. However, little is still known about the transmission within cattle holdings and possible alterations of the genomes of M. caprae during such events. The aim of this study was to study the molecular epidemiology of bovine tuberculosis (bTB) in selected herds based on isolate-specific genome-wide SNPs and to perform a phylogenetic network analysis. In total, 61 M. caprae isolates were collected originating from eight cattle farms over a period of twelve years between 2004 and 2015. Analysis of their sequence data revealed that the M. caprae isolates of an affected farm differ at all in a few SNPs. In contrast, many more SNPs were found when comparing the M. caprae genomes originating from different herds. The results demonstrated that the spread of bTB in the affected farms occurred by direct transmission between the members of each herd rather than between herds and a M. caprae introduction in farms after contact events e. g. on summer pastures can readily be traced by WGS analysis. Furthermore, we assembled a nearly complete whole genome sequence of M. caprae derived from several cattle isolates originating from bTB cases in the Bavarian Alpine region. [ABSTRACT FROM AUTHOR]

Background: Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP1) up-regulates the human leukocyte antigen (HLA) class I antigen presentation machinery (APM). This appears counterintuitive with immune evasion in EBV-associated tumours like nasopharyngeal carcinoma (NPC).Methods: Latent membrane protein 1-transfected epithelial cell lines were used as a model system to study the impact of LMP1 and c-Myc on HLA class I components. The expression of components of the HLA class I APM, c-Myc and Ki-67 was analysed in LMP1+ and LMP1- NPC by immunohistochemistry.Results: In epithelial cells, LMP1 up-regulated HLA class I APM. This effect could be counteracted by c-Myc, which itself was up-regulated by LMP1 apparently through IL6 induction and Jak3/STAT3 activation. Studies of NPC biopsies revealed down-regulation of HLA class I APM expression. No difference was observed between LMP1+ and LMP1- NPC. However, expression of Ki-67 and c-Myc were up-regulated in LMP1+ tumours.Conclusion: These findings raise the possibility that c-Myc activation in NPC might antagonise the effect of LMP1 on HLA class I expression thus contributing to immune escape of tumour cells. [ABSTRACT FROM AUTHOR]