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Tissue tropism and neuroinvasion of West Nile virus do not differ for two mouse strains with different survival rates.西尼罗河病毒在两种存活率不同的小鼠品系中的组织嗜性和神经侵袭情况并无差异。
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2
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3
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West Nile Virus spread and differential chemokine response in the central nervous system of mice: Role in pathogenic mechanisms of encephalitis.西尼罗河病毒在小鼠中枢神经系统中的传播和差异趋化因子反应:在脑炎发病机制中的作用。
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本文引用的文献

1
West nile virus activity--United States, January 1-November 7, 2006.西尼罗河病毒活动情况——美国,2006年1月1日至11月7日
MMWR Morb Mortal Wkly Rep. 2006 Nov 10;55(44):1204-5.
2
Murine model for dengue virus-induced lethal disease with increased vascular permeability.登革病毒诱导的致死性疾病伴血管通透性增加的小鼠模型。
J Virol. 2006 Oct;80(20):10208-17. doi: 10.1128/JVI.00062-06.
3
Long-term clinical and neuropsychological outcomes of West Nile virus infection.西尼罗河病毒感染的长期临床和神经心理学结果。
Clin Infect Dis. 2006 Sep 15;43(6):723-30. doi: 10.1086/506939. Epub 2006 Aug 10.
4
PKR and RNase L contribute to protection against lethal West Nile Virus infection by controlling early viral spread in the periphery and replication in neurons.蛋白激酶R(PKR)和核糖核酸酶L(RNase L)通过控制西尼罗河病毒在周围组织中的早期传播以及在神经元中的复制,有助于抵御该病毒的致死性感染。
J Virol. 2006 Jul;80(14):7009-19. doi: 10.1128/JVI.00489-06.
5
Temporal analyses of the neuropathogenesis of a West Nile virus infection in mice.小鼠西尼罗河病毒感染神经发病机制的时间分析。
J Neurovirol. 2006 Apr;12(2):129-39. doi: 10.1080/13550280600758341.
6
Gamma interferon plays a crucial early antiviral role in protection against West Nile virus infection.γ干扰素在抵御西尼罗河病毒感染的早期抗病毒过程中发挥着关键作用。
J Virol. 2006 Jun;80(11):5338-48. doi: 10.1128/JVI.00274-06.
7
Potentiation of West Nile encephalitis by mosquito feeding.通过蚊虫叮咬增强西尼罗河脑炎
Viral Immunol. 2006 Spring;19(1):74-82. doi: 10.1089/vim.2006.19.74.
8
Alpha/beta interferon protects against lethal West Nile virus infection by restricting cellular tropism and enhancing neuronal survival.α/β干扰素通过限制细胞嗜性和增强神经元存活来预防西尼罗河病毒致死性感染。
J Virol. 2005 Nov;79(21):13350-61. doi: 10.1128/JVI.79.21.13350-13361.2005.
9
Envelope protein glycosylation status influences mouse neuroinvasion phenotype of genetic lineage 1 West Nile virus strains.包膜蛋白糖基化状态影响基因谱系1西尼罗河病毒株的小鼠神经侵袭表型。
J Virol. 2005 Jul;79(13):8339-47. doi: 10.1128/JVI.79.13.8339-8347.2005.
10
Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis.Toll样受体3介导西尼罗河病毒进入大脑,引发致死性脑炎。
Nat Med. 2004 Dec;10(12):1366-73. doi: 10.1038/nm1140. Epub 2004 Nov 21.

西尼罗河病毒在两种存活率不同的小鼠品系中的组织嗜性和神经侵袭情况并无差异。

Tissue tropism and neuroinvasion of West Nile virus do not differ for two mouse strains with different survival rates.

作者信息

Brown Ashley N, Kent Kim A, Bennett Corey J, Bernard Kristen A

机构信息

Wadsworth Center, New York State Department of Health, P.O. Box 509, Albany, NY 12201-0509, USA.

出版信息

Virology. 2007 Nov 25;368(2):422-30. doi: 10.1016/j.virol.2007.06.033. Epub 2007 Aug 6.

DOI:10.1016/j.virol.2007.06.033
PMID:17675128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2814419/
Abstract

West Nile virus (WNV) is a mosquito-borne flavivirus that infects the central nervous system of humans and other animals. In this study, we found that C3H/HeN (C3H) mice exhibited a higher morbidity and mortality than C57BL/6 (B6) mice. We compared tissue tropism, viral replication and kinetics for C3H and B6 mice during acute viral infection. WNV was detected in multiple tissues, including novel sites such as the skin, duodenum and pancreas, but the tropism was identical for the two strains. Additionally, viral load and kinetics of spread did not differ substantially between strains. Neuroinvasion occurred in both strains by day 3 post-inoculation with early detection in the olfactory bulbs and spinal cord, suggesting that WNV neuroinvades at specific sites. Furthermore, neuroinvasion and viral load in the CNS did not predict disease outcome. Our data suggest that the disparities in morbidity and mortality between C3H and B6 mice are not due to differences in tropism, viral load or kinetics during acute WNV infection.

摘要

西尼罗河病毒(WNV)是一种由蚊子传播的黄病毒,可感染人类和其他动物的中枢神经系统。在本研究中,我们发现C3H/HeN(C3H)小鼠比C57BL/6(B6)小鼠表现出更高的发病率和死亡率。我们比较了急性病毒感染期间C3H和B6小鼠的组织嗜性、病毒复制和动力学。在包括皮肤、十二指肠和胰腺等新部位在内的多个组织中检测到了WNV,但两种品系的嗜性相同。此外,品系之间的病毒载量和传播动力学没有显著差异。接种后第3天,两种品系均发生神经侵袭,在嗅球和脊髓中早期检测到,这表明WNV在特定部位发生神经侵袭。此外,CNS中的神经侵袭和病毒载量并不能预测疾病结果。我们的数据表明,C3H和B6小鼠在发病率和死亡率上的差异并非由于急性WNV感染期间嗜性、病毒载量或动力学的差异。