Reference : Malignant catarrhal fever induced by alcelaphine herpesvirus 1 is associated with pro...
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
Malignant catarrhal fever induced by alcelaphine herpesvirus 1 is associated with proliferation of CD8+ T cells supporting a latent infection.
Dewals, Benjamin G mailto [Université de Liège - ULiège > > Immunologie et vaccinologie >]
Boudry, Christel mailto [Université de Liège - ULiège > > Immunologie et vaccinologie >]
Farnir, Frédéric mailto [Université de Liège - ULiège > Département de productions animales > Biostatistique, économie, sélection animale >]
Drion, Pierre mailto [Université de Liège - ULiège > Services généraux (Faculté de médecine vétérinaire) > Méth. expér. des anim. de labo et éthique en expér. animale >]
Vanderplasschen, Alain mailto [Université de Liège - ULiège > > Immunologie et vaccinologie >]
Public Library of Science
Yes (verified by ORBi)
San Franscisco
[en] Alcelaphine herpesvirus 1 (AlHV-1), carried by wildebeest asymptomatically, causes malignant catarrhal fever (WD-MCF) when cross-species transmitted to a variety of susceptible species of the Artiodactyla order. Experimentally, WD-MCF can be induced in rabbits. The lesions observed are very similar to those described in natural host species. Here, we used the rabbit
model and in vivo 5-Bromo-29-Deoxyuridine (BrdU) incorporation to study WD-MCF pathogenesis. The results obtained can be summarized as follows. (i) AlHV-1 infection induces CD8+ T cell proliferation detectable as early as 15 days postinoculation.
(ii) While the viral load in peripheral blood mononuclear cells remains below the detection level during most of the incubation period, it increases drastically few days before death. At that time, at least 10% of CD8+ cells carry the viral genome; while CD11b+, IgM+ and CD4+ cells do not. (iii) RT-PCR analyses of mononuclear cells isolated from the spleen and the popliteal lymph node of infected rabbits revealed no expression of ORF25 and ORF9, low or no expression of ORF50, and high or no expression of ORF73. Based on these data, we propose a new model for the pathogenesis of WD-MCF. This model relies on proliferation of infected CD8+ cells supporting a predominantly latent infection.
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