Malignant Catarrhal Fever Induced by Alcelaphine herpesvirus 1 Is Associated with Proliferation of CD8+ T Cells Supporting a Latent Infection
Malignant Catarrhal Fever Induced by Alcelaphine herpesvirus 1 Is Associated with Proliferation of CD8+ T Cells Supporting a Latent Infection
复制标题
DOI：
10.1371/journal.pone.0001627
复制
发表时间：
2008-02-20
期刊：
影响因子：
3.7
通讯作者：
Vanderplasschen, Alain
中科院分区：
文献类型：
--
作者：
Dewals, Benjamin;Boudry, Christel;Vanderplasschen, Alain
Alcelaphine疱疹病毒1型（AlHV-1）由角马无症状携带，当跨种传播给偶蹄目的多种易感种时，可引起恶性卡他热（WD-MCF）。实验上，WD-MCF可以在兔中诱导。观察到的病变与自然宿主物种中描述的病变非常相似。本研究采用兔模型和5-溴-2 '-脱氧尿苷（5-Bromo-2'-Deoxyuridine，BrdU）体内掺入法研究WD-MCF的发病机制。所得结果可归纳如下。(i)AlHV-1感染诱导早在接种后15天就可检测到的CD 8（+）T细胞增殖。(ii)虽然外周血单核细胞中的病毒载量在大部分潜伏期内保持低于检测水平，但在死亡前几天急剧增加。届时，至少10%的CD 8（+）细胞携带病毒基因组;而CD 11b（+）、IgM（+）和CD 4（+）细胞则不携带。(iii)从感染兔的脾和腘淋巴结分离的单核细胞的RT-PCR分析显示ORF 25和ORF 9不表达，ORF 50低表达或不表达，ORF 73高表达或不表达。基于这些数据，我们提出了一个新的模型的发病机制的WD-MCF。该模型依赖于受感染的CD 8（+）细胞的增殖，支持主要的潜伏感染。
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-2'-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 post-inoculation. (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.