Interferon-α-modulatory sequences from the genome of porcine circovirus type 2

Porcine circovirus (PCV) type 2 is an emerging pathogen among pigs, which has been associated with several severe disease syndromes. To date little is known of the pathogenesis and epidemiology of PCV, and how the virus affects the immune system of the host. To evaluate one possible mechanism of pat...

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Detalles Bibliográficos
Autor principal: Hasslung, Frida
Formato: Otro
Lenguaje:sueco
Inglés
Publicado: 2003
Materias:
Acceso en línea:https://stud.epsilon.slu.se/11070/
Descripción
Sumario:Porcine circovirus (PCV) type 2 is an emerging pathogen among pigs, which has been associated with several severe disease syndromes. To date little is known of the pathogenesis and epidemiology of PCV, and how the virus affects the immune system of the host. To evaluate one possible mechanism of pathogenesis, the genome of PCV-2 was examined for content of CpG-motifs. Five 20 nucleotide long sequences from the genome were tested for their ability to induce production of IFN-a by porcine peripheral blood mononuclear cells (PBMC). One of the oligodeoxynucleotides (ODNs) proved to inhibit the IFN-a production induced by the other ODNs that were stimulatory. The inhibitory ODN (PCV-2/1) was tested against other known inducers of IFN-a and showed a variable degree of inhibitory action depending on the construct of the inducer. ODNs containing phosphorothioate backbone and poly- G- sequences seemed more resistant to inhibition. Also, the inhibitory activity of ODN PCV-2/1 differed against the viral inducers Aujeszky´s disease virus (ADV) and Sendai virus (SV), and the plasmid pcDNA3. Inhibition was most effective against ADV, moderately effective against pcDNA3, but did not affect the IFN-a production induced by SV. The variation in sensitivity to inhibition among the agents could be due to differences in target cell populations. The presence of immune modulatory sequences in the genome of PCV-2 could possibly explain parts of the pathogenesis of the virus.