Molecular basis of reovirus virulence: role of the S1 gene.
Molecular basis of reovirus virulence: role of the S1 gene.
复制标题
呼肠孤病毒毒力的分子基础：S1 基因的作用。
DOI：
10.1073/pnas.74.12.5744
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发表时间：
1977
影响因子：
11.1
通讯作者：
B. Fields
中科院分区：
文献类型：
--
作者：
H. Weiner;D. Drayna;D. Averill;B. Fields
遗传方法已被用于定义呼肠孤病毒1型和3型表现出的不同毒力模式和中枢神经系统细胞趋向性的分子基础。新生小鼠脑内接种呼肠孤病毒3型可引起坏死性脑炎（无室管膜损伤），这是一致致命的。接种呼肠孤病毒1型的动物一般存活，但可能发生附睾细胞损伤（无神经元坏死）和脑积水。利用呼肠孤病毒1型和3型杂交衍生的重组克隆，我们已经能够确定S1基因组片段负责呼肠孤病毒血清型的不同细胞趋向性，并且是神经毒性的主要决定因素。1型S1基因组片段负责室管膜损伤和随后的脑积水；3型S1基因组片段负责神经元坏死和神经毒力。我们假设这些差异是由于sigma1外衣壳多肽（S1基因组片段编码的蛋白质）与室管膜细胞或神经元细胞表面的受体的特定相互作用。
A genetic approach has been used to define the molecular basis for the different patterns of virulence and central nervous system cell tropism exhibited by reovirus types 1 and 3. Intracerebral inoculation of reovirus type 3 into newborn mice causes a necrotizing encephalitis (without ependymal damage) that is uniformly fatal. Animal inoculated with reovirus type 1 generally survive and may develop epedymal cell damage (without neuronal necrosis) and hydrocephalus. Using recombinant clones derived from crosses between reovirus types 1 and 3, we have been able to determine that the S1 genome segment is responsible for the differing cell tropism of reovirus serotypes and is the major determinant of neurovirulence. The type 1 S1 genome segment is responsible for ependymal damage with subsequent hydrocephalus; the type 3 S1 genome segment is responsible for neuronal necrosis and neurovirulence. We postulate that these differences are due to the specific interaction of the sigma1 outer capsid polypeptide (the protein coded for by the S1 genome segment) with receptors on the surface of either ependymal cells or neuronal cells.