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Open Access Highly Accessed Open Badges Research article

Orf virus interferes with MHC class I surface expression by targeting vesicular transport and Golgi

Jörg Rohde12, Frederic Emschermann2, Michael R Knittler2 and Hanns-Joachim Rziha12*

Author Affiliations

1 Present address: Department of Immunology, Interfaculty Institute for Cell Biology, University of Tuebingen, Auf der Morgenstelle 15, 72076, Tuebingen, Germany

2 Friedrich-Loeffler-Institute, Federal Research Institute of Animal Health, Institute of Immunology, Greifswald-Insel Riems, Germany

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BMC Veterinary Research 2012, 8:114  doi:10.1186/1746-6148-8-114

Published: 18 July 2012



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.


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.


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.

Orf virus; Parapoxvirus; MHC class I; Subversion; Immunomodulation; Golgi apparatus