Interferon induction by viruses. VII. Mengovirus: "interferon-sensitive" mutant phenotype attributed to interferon-inducing particle activity.
Interferon induction by viruses. VII. Mengovirus: "interferon-sensitive" mutant phenotype attributed to interferon-inducing particle activity.
复制标题
病毒诱导干扰素。
DOI：
10.1089/jir.1981.1.601
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Sekellick,MJ
中科院分区：
文献类型：
--
作者：
Marcus,PI;GuidonJr,PT;Sekellick,MJ
我们假设，“干扰素敏感”表型的一个门戈病毒突变体，是-l，结果从干扰素诱导粒子的病毒粒子的活性，而不是一个内在的敏感性的突变病毒干扰素的行动。突变体是一种良好的IFN诱导剂，每4 × 106个小鼠L（Y）细胞可诱导25，000单位以上的IFN。其野生型亲本是+，诱导的IFN少于5%。我们认为，当细胞内的干扰素被外源性干扰素诱导后反馈到周围的细胞，并可能作用于同一细胞时，突变病毒的表型就表达出来了。我们认为，在这些细胞中干扰素介导的抗病毒状态水平的升高使得突变病毒似乎比其祖先对干扰素更敏感。通过这种内源性诱导的干扰素的额外作用，最终效果是进一步降低感染性病毒的产量，并增强细胞保留-产生归因于突变体-1的表型特征。在野生型（is+）病毒存在下或在用放线菌素D处理的细胞中，通过证明用is+和is-1病毒共感染的细胞或用药物处理的细胞不能产生干扰素，解释了这种is-1表型的消除。作为这一假设的证据，我们证明，当在不能对IFN诱导剂应答的细胞上测试时，“干扰素敏感”突变体及其野生型祖细胞对IFN作用同样敏感。（多重性）-响应通过用这种IFN-γ感染小鼠L（Y）细胞产生的（IFN产率）曲线诱导突变病毒最适合这样的模型，其中所有细胞仅被一种感染性颗粒感染，而被2个或更多个颗粒感染的细胞产生很少或不产生干扰素。对这些曲线的分析提供了突变株的IFN诱导颗粒（IFP）活性的定量，与我们的其他结果一致，我们得出结论，“干扰素敏感”突变体的表型更准确地描述为asifp+。l门戈病毒和这种类型的颗粒和干扰素系统在细胞-病毒持久性和疾病状态中的可能作用。
We hypothesize that the "interferon-sensitive" phenotype of a Mengovirus mutant,is-l, results from aninterferon-inducing particleactivity of the virion rather than an intrinsic sensitivity of the mutant virus to IFN action. Mutantis-lproved to be an excellent inducer of IFN, inducing over 25,000 units per 4 × 106mouse L(Y) cells. Its wildtype parent,is+, induced less than 5% as much IFN. We propose that the phenotype of the mutant virus is expressed when IFN induced byis-lparticles in cells previously exposed to exogenous IFN feeds-back and acts on surrounding cells, and possibly on the self-same cells. We suggest that the resulting elevated levels of an interferon-mediated antiviral state in these cells make itappearthat the mutant virus is more sensitive to IFN than its progenitor. The end effect, through the additional action of this endogenously induced interferon, is to reduce further the yield of infectious virus, and enhance cell-sparing—creating the phenotypic characteristics ascribed to mutantis-l. The abrogation of theis-lphenotype in the presence of wildtype (is+) virus or in cells treated with actinomycin D is accounted for by demonstrating that cells coinfected withis+andis-lvirus or treated with the drug fail to produce interferon. As proof of this hypothesis we demonstrate that both the "interferon-sensitive" mutant and its wildtype progenitor are equally sensitive to IFN action when tested on cells incapable of responding to inducers of IFN.Dose (multiplicity)-response (IFN yield) curves generated by infecting mouse L(Y) cells with this IFN-inducing mutant virus fit best a model in which all cells infected with only one infectious particle produce a quantum yield of IFN, whereas cells infected with 2 or more particles produce little or no interferon. Analyses of these curves provide quantitation of the IFN-inducing particle (IFP) activity of mutantis-lstocks, and in concert with our other results lead us to conclude that the phenotype of the "interferon-sensitive" mutant is more accurately described asifp+.These findings provide a basis for further studies designed to reveal the nature of the IFN-inducer ofis-lMengovirus and the possible role of this type of particle and the interferon system in cell-virus persistence and the disease state.
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影响因子：
3.7
作者：
P. I. Marcus;M. Sekellick
通讯作者：
M. Sekellick
影响因子：
3.7
作者：
P. I. Marcus;M. Sekellick
通讯作者：
M. Sekellick
影响因子：
3.7
作者：
CARVER, DH;MARCUS, PI
通讯作者：
MARCUS, PI
孟戈病毒的干扰素敏感突变体。
影响因子：
3.7
作者：
E. H. Simon;S. Kung;T. Koh;P. Brandman
通讯作者：
P. Brandman
引发：干扰素的非抗病毒功能
影响因子：
5.4
作者：
W. Stewart;L. Gosser;R. Lockart
通讯作者：
R. Lockart