Abstract
Canine distemper virus (CDV) exhibits a profound lymphotropism that causes immunosuppression and increased susceptibility of affected dogs to opportunistic infections. Similar to human measles virus, CDV is supposed to inhibit terminal differentiation of dendritic cells (DCs), responsible for disturbed repopulation of lymphoid tissues and diminished antigen presenting function in dogs. In order to testify the hypothesis that CDV-infection leads to an impairment of professional antigen presenting cells, canine DCs have been generated from peripheral blood monocytes in vitro and infected with CDV. Virus infection was confirmed and quantified by transmission electron microscopy, CDV-specific immunofluorescence, and virus titration. Flow cytometric analyses revealed a significant down-regulation of the major histocompatibility complex class II and co-stimulatory molecules CD80 and CD86 in CDV-infected DCs, indicative of disturbed antigen presenting capacity. Molecular analyses revealed an increased expression of the immune inhibitory cytokine interleukin-10 in DCs following infection. Results of the present study demonstrate that CDV causes phenotypical changes and altered cytokine expression of DCs, which represent potential mechanisms to evade host immune responses and might contribute to immune dysfunction and virus persistence in canine distemper.
Highlights
Canine distemper is a worldwide occurring infectious disease of dogs, caused by a morbillivirus, closely related to measles virus (MV) [1,2]
The percentage of gated cells was determined to characterize the phenotype of cells and the geometrical mean fluorescent intensity (GMFI) for the quantification of surface marker expression of monocytes and Monocyte-derived dendritic cells (moDCs), respectively
An increased percentage of cells expressing the co-stimulatory molecule CD86 at day seven compared to day one in culture was noticed (p = 0.031), while no statistical differences were found for CD1a, CD11c, CD14, CD80 and major histocompatibility complex (MHC) class II
Summary
Canine distemper is a worldwide occurring infectious disease of dogs, caused by a morbillivirus, closely related to measles virus (MV) [1,2]. Similar to human measles clinical findings in canine distemper virus (CDV)-infected dogs include fever, rash, respiratory signs, and lymphopenia. A disturbed function of antigen presenting cells, including DCs, is supposed to contribute to immunosuppression in measles patients [16,17,18,19]. During the chronic disease stage of canine distemper, cells with a DC-like morphology seem to serve as the primary host cells for the virus, which might promote viral persistence in lymphoid organs [21]. An inhibited terminal differentiation of DCs is currently discussed to be responsible for diminished antigen presenting function and disturbed repopulation of lymphoid tissues in CDV-infected dogs, as suggested for MV-infection [14,21,22,23]. Whether CDV has the ability to infect canine DCs and direct viral effects upon these professional antigen presenting cells have not yet been confirmed
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