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10.1186/1746-6148-8-114

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suck abstract from ncbi


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pmid22809544      BMC+Vet+Res 2012 ; 8 (ä): 114
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  • Orf virus interferes with MHC class I surface expression by targeting vesicular transport and Golgi #MMPMID22809544
  • Rohde J; Emschermann F; Knittler MR; Rziha HJ
  • BMC Vet Res 2012[Jul]; 8 (ä): 114 PMID22809544show ga
  • BACKGROUND: The Orf virus (ORFV), a zoonotic Parapoxvirus, causes pustular skin lesions in small ruminants (goat and sheep). Intriguingly, ORFV can repeatedly infect its host, despite the induction of a specific immunity. These immune modulating and immune evading properties are still unexplained. RESULTS: Here, we describe that ORFV infection of permissive cells impairs the intracellular transport of MHC class I molecules (MHC I) as a result of structural disruption and fragmentation of the Golgi apparatus. Depending on the duration of infection, we observed a pronounced co-localization of MHC I and COP-I vesicular structures as well as a reduction of MHC I surface expression of up to 50%. These subversion processes are associated with early ORFV gene expression and are accompanied by disturbed carbohydrate trimming of post-ER MHC I. The MHC I population remaining on the cell surface shows an extended half-life, an effect that might be partially controlled also by late ORFV genes. CONCLUSIONS: The presented data demonstrate that ORFV down-regulates MHC I surface expression in infected cells by targeting the late vesicular export machinery and the structure and function of the Golgi apparatus, which might aid to escape cellular immune recognition.
  • |Animals[MESH]
  • |Antibodies, Monoclonal[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Ecthyma, Contagious/*virology[MESH]
  • |Flow Cytometry[MESH]
  • |Fluorescent Antibody Technique[MESH]
  • |Gene Expression Regulation/*physiology[MESH]
  • |Genes, MHC Class I/genetics/*physiology[MESH]
  • |Golgi Apparatus/*physiology[MESH]
  • |Orf virus/*physiology[MESH]
  • |Protein Transport[MESH]


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