Abundance of IFN-alpha and IFN-gamma mRNA in blood of resistant and susceptible chickens infected with Marek's disease virus (MDV) or vaccinated with turkey herpesvirus; and MDV inhibition of subsequent induction of IFN gene transcription
2005
Quéré, Pascale, P. | Rivas, Christelle | Ester, K. | Novak, R. | Ragland, W.L. | Bio-Agresseurs, Santé, Environnement [Nouzilly] (UR BASE) ; Institut National de la Recherche Agronomique (INRA) | Division of Molecular Medicine ; Rudjer Boskovic Institute [Zagreb]
International audience
Show more [+] Less [-]English. The effects of the very virulent RB-1B strain of Marek's disease virus (MDV) and turkey herpesvirus (HVT), a vaccinal strain, on abundance of IFN mRNA in the blood were investigated. MDV and HVT infection did not change the circulating level of IFN-γ mRNA 1 and 7 days p.i., but they increased IFN-α mRNA levels slightly in genetically susceptible (to tumour development) B13/B13 chickens. The total number of circulating leukocytes was unchanged and increase in message was accompanied by an increase in circulating CD8α+ and MHC Class II+ cells. On the contrary, both viruses slightly increased IFN-γ transcripts and decreased IFN-α transcripts in genetically resistant B21/B21 chickens. Further, oncogenic MDV was able to block the response to inactivated Newcastle disease virus, a potent inducer of IFN, in both chicken lines. The inhibiting effect on transcription was present for both IFN at days 1 and 7 p.i. in susceptible B13/B13 chickens, but only at day 7thinspp.i. in resistant B21/B21 chickens. By contrast, non-oncogenic HVT did not interfere with induction of either message at one day p.i. and MDV had a more suppressive effect than HVT on IFN gene transcription 7 days p.i. in B21/B21 chickens. Thus, the strong ability of MDV to block induction of IFN gene transcription detected in the blood as soon as one day after infection in susceptible chickens, as opposed to resistant chickens, not only causes immunosuppression but also may be related to the virusrsquos oncogenicity.
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