Perturbation of differentiated functions during viral infection in vivo. I. Relationship of lymphocytic choriomeningitis virus and host strains to growth hormone deficiency.

Perturbation of differentiated functions during viral infection in vivo. I. Relationship of lymphocytic choriomeningitis virus and host strains to growth hormone deficiency.
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体内病毒感染过程中分化功能的扰动。

DOI:
10.1016/0042-6822(85)90430-1
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发表时间:
1985
期刊:
影响因子:
3.7
通讯作者:
Tishon,A
Tishon,A
中科院分区:
医学3区
文献类型:
--
作者:
Oldstone,MB;Ahmed,R;Buchmeier,MJ;Blount,P;Tishon,A

文献摘要

被引文献

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生长激素缺乏继发的生长和葡萄糖代谢紊乱与持续性淋巴细胞脉络膜脑膜炎病毒(LCMV)感染有关。 C3H/St、BALB/WEHI 和 SWR/J 小鼠出生时感染 LCMV:ARM,其血液和器官中终生携带病毒,但只有 C3H/St 小鼠出现生长激素不足。 BALB/WEHI 和 SWR/J 感染小鼠的垂体中含有正常量的生长激素,并且含有生长激素的细胞中相对较小比例的细胞复制了病毒。在易感的 C3H/St 小鼠中,致病病毒株(LCMV:ARM、E-350 和巴斯德)复制到更高滴度,并感染垂体前叶中绝大多数产生生长激素的细胞。相比之下,LCMV 菌株 Traub 和 WE 在少得多的生长激素产生细胞中复制,并且未能扰乱生长激素合成。在另一篇论文(Y. Riviere、R.Ahmed、P. Southern 和 M. B. A. Oldstone (1985), Virology142, 175–182)中,这些发现用于在 LCMV:ARM(疾病阳性)和 LCMV:WE(疾病无)之间进行重配,并将致病作用映射到 LCMV:ARM 的小 RNA 片段。当通过二维电泳检查时,从感染细胞或对照细胞中分离的生长激素分子中被胰蛋白酶和胰凝乳蛋白酶切割的肽是相同的。此外,将抗体转移到干扰素未能改变这些小鼠的生长激素不足,尽管它纠正了 LCMV 诱导的 BALB 小鼠的肝病,表明干扰素确实在这种疾病中发挥了主导作用。在受感染的动物和培养的 GH-3 细胞中观察到 LCMV:ARM 对含有生长激素的细胞的选择性趋向性高于含有催乳素的细胞。
Disordered growth and glucose metabolism secondary to growth hormone deficiency is associated with persistent lymphocytic choriomeningitis virus (LCMV) infection. C3H/St, BALB/WEHI, and SWR/J mice infected at birth with LCMV:ARM carried virus in their blood and organs throughout life but only C3H/St mice developed growth hormone insufficiency. BALB/WEHI and SWR/J infected mice contained normal amounts of growth hormone in their pituitaries and a relatively small proportion of the cells containing growth hormone replicated the virus. In susceptible C3H/St mice, the disease-causing viral strains (LCMV:ARM, E-350, and Pasteur) replicated to higher titers and infected the vast majority of cells producing growth hormone in the anterior lobe of the pituitary. In contrast, LCMV strains Traub and WE replicated in far fewer growth hormone-producing cells and failed to disorder growth hormone synthesis. In another paper (Y. Riviere, R.Ahmed, P. Southern, and M. B. A. Oldstone (1985),Virology142, 175–182) these findings are used to make reassortants between LCMV:ARM (disease positive) and LCMV:WE (disease nil) and the pathogenic effect is mapped to the small RNA segment of LCMV:ARM. Peptides cleaved by trypsin and chymotrypsin from growth hormone molecules isolated from infected cells or control cells were equivalent when examined by two-dimensional electrophoresis. Further, transfer of antibody to interferon failed to alter the growth hormone insufficiency in these mice, although it corrected LCMV-induced liver disease of BALB mice, suggesting that interferon did riot play a dominant role in this disease. The selective tropism of LCMV:ARM for cells containing growth hormone over cells that contain prolactin was observed in both infected animals and in cultured GH-3 cells.