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小鼠单纯疱疹病毒生殖器感染的发病机制。IV. 病毒潜伏的定量研究。

Pathogenesis of genital herpes simplex virus infection in mice. IV. Quantitative aspects of viral latency.

作者信息

Eis A M, Schneweis K E

出版信息

Med Microbiol Immunol. 1986;175(5):281-92. doi: 10.1007/BF02126049.

DOI:10.1007/BF02126049
PMID:3020386
Abstract

Experiments in the mouse model of herpes simplex virus (HSV) infection involving the intact genital mucous membranes as inoculation site yielded the following results. In untreated mice the extent of latency was correlated with the degree of peripheral virus replication. This correlation could not be observed when the course of infection was interrupted by chemotherapy, interferon, or passive immunization. Acyclovir had little effect on peripheral virus multiplication, but markedly reduced latent ganglionic infection. As acute ganglionic infection and virus concentration in the spinal nerves were already reduced, acyclovir is assumed to inhibit either virus penetration into the nerve endings or virus replication in the ganglia. Interferon apparently has an active role in the elimination of virus infected cells from the ganglia, as its effect was restricted to a reduced rate of latency and of lethality. Passive immunization with antiserum led to similar results as ACV-treatment. While lacking a pronounced effect on virus replication in the mucous membranes, specific antibody was found to influence both virus elimination from the ganglia, and conversion from productive to latent ganglionic infection. Immune lymphocytes proved to be the only agent capable of suppressing peripheral infection, thereby inhibiting the neural spread of the virus. These results suggest that the decrease in latency may result from modulations occurring at different stages in the course of infection.

摘要

在以完整的生殖器黏膜作为接种部位的单纯疱疹病毒(HSV)感染小鼠模型中进行的实验产生了以下结果。在未治疗的小鼠中,潜伏程度与外周病毒复制程度相关。当感染过程被化疗、干扰素或被动免疫中断时,这种相关性无法观察到。阿昔洛韦对外周病毒增殖几乎没有影响,但显著降低了潜伏性神经节感染。由于急性神经节感染和脊髓神经中的病毒浓度已经降低,推测阿昔洛韦可抑制病毒侵入神经末梢或神经节中的病毒复制。干扰素显然在从神经节中清除病毒感染细胞方面发挥积极作用,因为其作用仅限于降低潜伏率和致死率。用抗血清进行被动免疫导致了与阿昔洛韦治疗相似的结果。虽然对黏膜中的病毒复制没有显著影响,但发现特异性抗体既影响从神经节中清除病毒,也影响从增殖性神经节感染向潜伏性神经节感染的转变。免疫淋巴细胞被证明是唯一能够抑制外周感染从而抑制病毒向神经扩散的因子。这些结果表明,潜伏性的降低可能是由感染过程中不同阶段发生的调节作用导致的。

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本文引用的文献

1
Protection of mice from fatal herpes simplex virus type 1 infection by adoptive transfer of cloned virus-specific and H-2-restricted cytotoxic T lymphocytes.通过克隆的病毒特异性和H-2限制性细胞毒性T淋巴细胞的过继转移保护小鼠免受致命的1型单纯疱疹病毒感染。
J Gen Virol. 1983 Feb;64 (Pt 2):443-7. doi: 10.1099/0022-1317-64-2-443.
2
Uptake and transport of herpes simplex virus in neurites of rat dorsal root ganglia cells in culture.单纯疱疹病毒在培养的大鼠背根神经节细胞神经突中的摄取与运输。
J Gen Virol. 1984 Jan;65 ( Pt 1):55-64. doi: 10.1099/0022-1317-65-1-55.
3
Restricted replication of herpes simplex virus in spinal ganglia of resistant mice is accompanied by an early infiltration of immunoglobulin G-bearing cells.
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J Virol. 2001 Feb;75(3):1195-204. doi: 10.1128/JVI.75.3.1195-1204.2001.
4
Replication of herpes simplex virus type 1 and 2 in the medulla of the adrenal gland after vaginal infection of mice.小鼠经阴道感染后,单纯疱疹病毒1型和2型在肾上腺髓质中的复制。
Arch Virol. 1996;141(10):1999-2008. doi: 10.1007/BF01718210.
5
Asymptomatic vaginal herpes simplex virus infections in mice: virology and pathohistology.小鼠无症状阴道单纯疱疹病毒感染:病毒学与病理组织学
Arch Virol. 1996;141(2):263-74. doi: 10.1007/BF01718398.
6
The role of the immune system in establishment of herpes simplex virus latency--studies using CD4+ T-cell depleted mice.免疫系统在单纯疱疹病毒潜伏建立中的作用——使用CD4 + T细胞耗竭小鼠的研究
Arch Virol. 1993;133(1-2):179-87. doi: 10.1007/BF01309753.
7
Immunological mechanisms giving rise to latency of herpes simplex virus in the spinal ganglia of the mouse.导致单纯疱疹病毒在小鼠脊髓神经节潜伏的免疫机制。
Med Microbiol Immunol. 1988;177(1):1-8. doi: 10.1007/BF00190305.
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7
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Effects of genetic resistance against Herpes simplex virus in vaginally infected mice.
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Med Microbiol Immunol. 1984;173(4):187-96. doi: 10.1007/BF02122110.