Salvato M, Shimomaye E, Southern P, Oldstone M B
Department of Immunology, Research Institute of Scripps Clinic, La Jolla, California 92037.
Virology. 1988 Jun;164(2):517-22. doi: 10.1016/0042-6822(88)90566-1.
Immunocompetent adult mice mount a vigorous cytotoxic T lymphocyte (CTL) response against the Armstrong (ARM) 53b strain of LCMV after primary inoculation. In contrast, the Clone 13 variant of ARM 53b, originally isolated from the spleen of a persistently infected mouse, suppresses LCMV-specific CTL responses (R. Ahmed et al. (1984) J. Exp Med 60, 521). The induction and generation of CTL maps to the short (S) RNA segment and not the long (L) RNA segment of LCMV (Y. Riviere et al. (1986) J. Immunol. 136, 304). The CTL recognition epitope, expressed in virus-infected target cells, also maps to the S segment of the LCMV ARM genome, and is structurally and functionally intact in Clone 13-infected target cells. Here we report the S RNA sequences of both ARM 53b and its variant Clone 13. Comparison reveals a single amino acid difference. However, sequence divergence at this position also occurs among other strains of LCMV (Pasteur, Traub, WE) which do elicit CTL responses. Hence, (1) the amino acid difference is unrelated to the phenotypic divergence of Clone 13, (2) suppression of the CTL response by Clone 13 is not linked to the CTL recognition epitope, and (3) the structure or function responsible for CTL immunosuppression by Clone 13 most likely maps to the L RNA segment. Further, the availability of the complete S RNA sequence for LCMV ARM and ARM Clone 13 variant allows a detailed comparison with WE (V. Romanowski et al. (1985) Virus Res. 3, 110-114), the only other LCMV S RNA so far sequenced.
免疫活性成年小鼠在初次接种后会对淋巴细胞脉络丛脑膜炎病毒（LCMV）的阿姆斯特朗（ARM）53b毒株产生强烈的细胞毒性T淋巴细胞（CTL）反应。相比之下，最初从持续感染小鼠脾脏中分离出的ARM 53b的克隆13变体可抑制LCMV特异性CTL反应（R. 艾哈迈德等人（1984年），《实验医学杂志》60, 521）。CTL的诱导和产生定位于LCMV的短（S）RNA片段而非长（L）RNA片段（Y. 里维耶等人（1986年），《免疫学杂志》136, 304）。在病毒感染的靶细胞中表达的CTL识别表位也定位于LCMV ARM基因组的S片段，并且在克隆13感染的靶细胞中其结构和功能完整。在此，我们报告了ARM 53b及其变体克隆13的S RNA序列。比较发现有一个氨基酸差异。然而，在其他能引发CTL反应的LCMV毒株（巴斯德、特劳布、WE）之间，这个位置也存在序列差异。因此，（1）氨基酸差异与克隆13的表型差异无关，（2）克隆13对CTL反应的抑制与CTL识别表位无关，（3）克隆13导致CTL免疫抑制的结构或功能很可能定位于L RNA片段。此外，LCMV ARM和ARM克隆13变体完整S RNA序列的可得性使得能够与WE（V. 罗曼诺夫斯基等人（1985年），《病毒研究》3, 110 - 114）进行详细比较，WE是迄今为止唯一已测序的其他LCMV S RNA。
