Avian borna virus in psittacine birds : viral distribution, tropism and immune response

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Avian Borna viruses (ABV) are the etiological agents for proventricular dilatation disease (PDD). Distribution patterns of ABV-2 and ABV-4 in experimentally ABV-2 and ABV-4 infected cockatiels were similar to distribution patterns of ABV in naturally PDD affected psittacines. ABV-2 and ABV-4 exhibited broad tissue distribution patterns in all organs in experimentally ABV-2 and ABV-4 infected cockatiels. Inflammatory lesions, ABV antigen, ABV-2 genome and ABV-2 mRNA were mainly detected in the gastrointestinal tract (GIT) and peripheral organs after ABV-2 infection. Inflammatory lesions, ABV antigen, ABV-4 genome and ABV-4 mRNA were predominantly detected in the central nervous system (CNS) and peripheral organs after ABV-4 infection. ABV-2 transcription was effective in the GIT organs after ABV-2 infection. ABV-4 transcription was operative in the CNS after ABV-4 infection. These findings indicate distinct differences in biological behaviour between the used ABV-2 and ABV-4 isolates. By immunohistochemistry, CD3-positive cells were detected in cellular infiltrations in all organs after ABV-2 and ABV-4 infection. Isolation of buffy coat (BC) cells of cockatiels and stimulation with phytohaemagglutinin (PHA-M) were successfully established. Characterization of CD3-positive cells, CD4-positive cells, CD8a-positive cells, monocytes, B cells, and thrombocytes was successful in cockatiel BC by indirect immunofluorescence. Characterization of CD4-positive cells, CD8-positive cells, monocytes, B cells, thrombocytes cells but not CD3-positive cells was possible in cockatiel BC by flow cytometry. ABV antigen and ABV-4 RNA were not found in BC cells of cockatiels from day 0 until day 15 post infection with ABV-4. Moreover, ABV antigen and ABV-4 RNA were not found in stimulated BC cells from day 0 until day 15 after stimulation and ABV-4 infection. These results providing first evidence that cockatiel blood cells could not directly be infected with ABV-4.Further investigations on the role of macrophages or endothelial cells for the dissemination of ABV infection within an infection are therefore required.

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Giessen : VVB Laufersweiler Verlag

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