Andrésdóttir V, Tang X, Agnarsdóttir G, Andrésson O S, Georgsson G, Skraban R, Torsteinsdóttir S, Rafnar B, Benediktsdóttir E, Matthíasdóttir S, Arnadóttir S, Högnadóttir S, Pálsson P A, Pétursson G
Institute for Experimental Pathology, University of Iceland, Reykjavík, Iceland.
Virus Genes. 1998;16(3):281-93. doi: 10.1023/a:1008030706308.
During the epidemic caused by maedi-visna virus (MVV) of sheep in Iceland, the pulmonary affection, maedi, was the predominant clinical manifestation. In some flocks, however, a central nervous system (CNS) affection, visna, was the main cause of morbidity and mortality. As there is only one breed of sheep in the country, host factors did apparently not play an important role in the different clinical manifestations. To obtain some information on possible viral genetic determinants of neurotropism and neurovirulence we studied both phenotypic and genotypic properties of two maedi-visna virus strains; a strain that was originally isolated from the brain of sheep with encephalitis (visna), and another strain isolated from the lungs of a sheep suffering from pneumonia (maedi). The brain isolate was found to grow faster in sheep choroid plexus cells than the lung isolate, whereas the growth rate in macrophages was similar for the maedi and visna virus strains. Intracerebral inoculation indicated that the visna virus isolate induced more severe brain lesions than the maedi isolate. In addition, a pathogenic molecular clone derived from a visna strain (KV1772kv72/67) was tested for growth in sheep choroid plexus cells and macrophages. The molecularly cloned virus retained the fast growth rate in choroid plexus cells. The nucleotide sequence of the env gene and the U3 of the LTR was determined for the maedi strain and compared to that of the visna strains. There was an 11.7% difference in deduced amino acid sequence in the Env protein and a 6% difference in the LTR. The molecular clone KV1772kv72/67 will be a useful reagent for characterization of viral determinants of cell tropism in vitro and possibly neurovirulence in vivo.
在冰岛绵羊感染梅迪-维斯纳病毒（MVV）引发的疫情期间，肺部感染，即梅迪病，是主要的临床表现。然而，在一些羊群中，中枢神经系统（CNS）感染，即维斯纳病，是发病和死亡的主要原因。由于该国只有一个绵羊品种，宿主因素显然在不同的临床表现中未发挥重要作用。为了获取有关神经嗜性和神经毒力可能的病毒遗传决定因素的一些信息，我们研究了两种梅迪-维斯纳病毒株的表型和基因型特性；一种最初从患有脑炎（维斯纳病）的绵羊大脑中分离出来的毒株，以及另一种从患有肺炎（梅迪病）的绵羊肺部分离出来的毒株。发现脑部分离株在绵羊脉络丛细胞中的生长速度比肺部分离株快，而梅迪和维斯纳病毒株在巨噬细胞中的生长速度相似。脑内接种表明，维斯纳病毒分离株比梅迪分离株诱导更严重的脑部病变。此外，还测试了源自维斯纳毒株（KV1772kv72/67）的致病分子克隆在绵羊脉络丛细胞和巨噬细胞中的生长情况。分子克隆病毒在脉络丛细胞中保持了快速生长速度。测定了梅迪毒株env基因和LTR的U3的核苷酸序列，并与维斯纳毒株的进行了比较。Env蛋白推导氨基酸序列存在11.7%的差异，LTR存在6%的差异。分子克隆KV1772kv72/67将是用于体外鉴定细胞嗜性病毒决定因素以及可能体内神经毒力的有用试剂。
