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小鼠K乳头多瘤病毒对裸鼠的慢性感染。

Chronic infection of nude mice by murine K papovavirus.

作者信息

Greenlee J E

出版信息

J Gen Virol. 1986 Jun;67 ( Pt 6):1109-14. doi: 10.1099/0022-1317-67-6-1109.

DOI:10.1099/0022-1317-67-6-1109
PMID:3711864
Abstract

Nude (nu/nu) mice were inoculated intracranially with 10(6.5) newborn mouse 50% lethal doses of K virus and were studied over a period of 28 weeks using serological methods, virus assay and immunohistological staining for viral antigens. K virus infection of nude mice, although clinically asymptomatic, was slowly progressive despite prompt IgM and IgG antibody response. The highest titres of K virus infectivity were reached in spleens, kidneys and intestines. Vascular endothelial cells represented the major site of viral replication, as has been shown to be the case in immunologically normal mice, with extensive involvement of intestinal capillaries. In addition, however, unlike immunologically normal mice, nude mice inoculated with K virus developed multifocal infection of renal tubular epithelial cells. Nude mice did not develop histologically detectable evidence of central nervous system involvement by K virus, and K virus infection did not result in neoplasia. Infected vascular endothelial cells and renal tubular epithelial cells in animals studied at 16 and 27 weeks after inoculation were grouped in scattered clusters, suggesting local spread of infection. The present study indicates that nude mice with preserved B cell function but impaired T cell-mediated immunity are able to limit systemic dissemination of K virus but are unable to prevent local progression of infection by cell-to-cell spread. K virus is capable of altering its cellular tropism during chronic infection.

摘要

将10(6.5)个新生小鼠50%致死剂量的K病毒颅内接种到无胸腺(nu/nu)小鼠体内,并使用血清学方法、病毒检测和病毒抗原免疫组织化学染色对其进行了28周的研究。无胸腺小鼠感染K病毒后,尽管临床上无症状,但尽管迅速出现IgM和IgG抗体反应,感染仍呈缓慢进展。脾脏、肾脏和肠道中的K病毒感染性滴度最高。血管内皮细胞是病毒复制的主要部位,这与免疫正常小鼠的情况相同,肠道毛细血管广泛受累。然而,除此之外,与免疫正常小鼠不同的是,接种K病毒的无胸腺小鼠出现了肾小管上皮细胞的多灶性感染。无胸腺小鼠未出现组织学上可检测到的K病毒累及中枢神经系统的证据,且K病毒感染未导致肿瘤形成。在接种后16周和27周研究的动物中,受感染的血管内皮细胞和肾小管上皮细胞呈散在簇状分布,提示感染的局部扩散。本研究表明,B细胞功能保留但T细胞介导的免疫受损的无胸腺小鼠能够限制K病毒的全身扩散,但无法阻止通过细胞间传播的感染局部进展。K病毒在慢性感染期间能够改变其细胞嗜性。

相似文献

1
Chronic infection of nude mice by murine K papovavirus.小鼠K乳头多瘤病毒对裸鼠的慢性感染。
J Gen Virol. 1986 Jun;67 ( Pt 6):1109-14. doi: 10.1099/0022-1317-67-6-1109.
2
The major site of murine K papovavirus persistence and reactivation is the renal tubular epithelium.鼠K多瘤病毒持续存在和重新激活的主要部位是肾小管上皮。
Microb Pathog. 1991 Oct;11(4):237-47. doi: 10.1016/0882-4010(91)90028-9.
3
Pathogenesis of K virus infection in mice.小鼠中K病毒感染的发病机制。
Prog Clin Biol Res. 1983;105:325-42.
4
Persistent infection and transformation of mouse glial cultures by K virus, a murine papovavirus.小鼠乳多空病毒K病毒对小鼠神经胶质细胞培养物的持续感染和转化
J Gen Virol. 1984 Jul;65 ( Pt 7):1253-8. doi: 10.1099/0022-1317-65-7-1253.
5
Effect of host age on experimental K virus infection in mice.宿主年龄对小鼠实验性K病毒感染的影响。
Infect Immun. 1981 Jul;33(1):297-303. doi: 10.1128/iai.33.1.297-303.1981.
6
Pathogenesis of K papovavirus infection in athymic nude mice.无胸腺裸鼠中K乳头瘤病毒感染的发病机制。
Infect Immun. 1983 Jul;41(1):434-6. doi: 10.1128/iai.41.1.434-436.1983.
7
Interaction of K papovavirus with hamster cells: transformation of glial cells in vitro but failure of the virus to produce central nervous system tumors in vivo.K乳多空病毒与仓鼠细胞的相互作用:体外转化神经胶质细胞,但该病毒在体内无法产生中枢神经系统肿瘤。
Arch Virol. 1985;83(3-4):207-15. doi: 10.1007/BF01309917.
8
Pathogenesis of K virus infection in newborn mice.新生小鼠K病毒感染的发病机制。
Infect Immun. 1979 Nov;26(2):705-13. doi: 10.1128/iai.26.2.705-713.1979.
9
Distribution of K-papovavirus in infected newborn mice.K乳多空病毒在受感染新生小鼠中的分布。
J Comp Pathol. 1994 Oct;111(3):259-68. doi: 10.1016/s0021-9975(05)80004-0.
10
Reactivation of persistent papovavirus K infection in immunosuppressed mice.免疫抑制小鼠中持续性乳头多瘤空泡病毒K感染的重新激活。
J Virol. 1984 Aug;51(2):425-9. doi: 10.1128/JVI.51.2.425-429.1984.

引用本文的文献

1
Morphological and immunohistochemical studies of the central nervous system involvement in papovavirus K infection in mice.小鼠乳头多瘤空泡病毒K感染中枢神经系统的形态学和免疫组织化学研究。
Acta Neuropathol. 1988;77(2):175-81. doi: 10.1007/BF00687428.