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鼠源 CD163 的异位表达使其在发现 63 年后可在细胞培养中分离到乳酸脱氢酶升高病毒。

Ectopic expression of murine CD163 enables cell-culture isolation of lactate dehydrogenase-elevating virus 63 years after its discovery.

机构信息

Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison School of Medicine and Public Health , Madison, Wisconsin, USA.

Department of Biology, Georgia State University , Atlanta, Georgia, USA.

出版信息

J Virol. 2023 Oct 31;97(10):e0093023. doi: 10.1128/jvi.00930-23. Epub 2023 Oct 4.


DOI:10.1128/jvi.00930-23
PMID:37792000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10617578/
Abstract

Mouse models of viral infection play an especially large role in virology. In 1960, a mouse virus, lactate dehydrogenase-elevating virus (LDV), was discovered and found to have the peculiar ability to evade clearance by the immune system, enabling it to persistently infect an individual mouse for its entire lifespan without causing overt disease. However, researchers were unable to grow LDV in culture, ultimately resulting in the demise of this system as a model of failed immunity. We solve this problem by identifying the cell-surface molecule CD163 as the critical missing component in cell-culture systems, enabling the growth of LDV in immortalized cell lines for the first time. This advance creates abundant opportunities for further characterizing LDV in order to study both failed immunity and the family of viruses to which LDV belongs, (aka, arteriviruses).

摘要

病毒感染的小鼠模型在病毒学中起着特别重要的作用。1960 年,发现了一种小鼠病毒,即乳酸脱氢酶升高病毒(LDV),并发现它具有逃避免疫系统清除的特殊能力,使其能够在不引起明显疾病的情况下持续感染个体小鼠的整个生命周期。然而,研究人员无法在培养物中生长 LDV,最终导致该系统作为免疫失败的模型而消亡。我们通过鉴定细胞表面分子 CD163 作为细胞培养系统中关键缺失的成分来解决这个问题,从而首次使 LDV 在永生化细胞系中生长。这一进展为进一步研究 LDV 提供了丰富的机会,以研究免疫失败以及 LDV 所属的病毒家族,即动脉病毒。

相似文献

[1]
Ectopic expression of murine CD163 enables cell-culture isolation of lactate dehydrogenase-elevating virus 63 years after its discovery.

J Virol. 2023-10-31

[2]
Biogenesis of non-structural protein 1 (nsp1) and nsp1-mediated type I interferon modulation in arteriviruses.

Virology. 2014-6

[3]
Pigs Lacking the Scavenger Receptor Cysteine-Rich Domain 5 of CD163 Are Resistant to Porcine Reproductive and Respiratory Syndrome Virus 1 Infection.

J Virol. 2018-7-31

[4]
Simian hemorrhagic fever virus cell entry is dependent on CD163 and uses a clathrin-mediated endocytosis-like pathway.

J Virol. 2014-10-29

[5]
Replacement of Porcine CD163 Scavenger Receptor Cysteine-Rich Domain 5 with a CD163-Like Homolog Confers Resistance of Pigs to Genotype 1 but Not Genotype 2 Porcine Reproductive and Respiratory Syndrome Virus.

J Virol. 2017-1-3

[6]
Susceptible cell lines for the production of porcine reproductive and respiratory syndrome virus by stable transfection of sialoadhesin and CD163.

BMC Biotechnol. 2010-6-29

[7]
Generation of murine macrophage-derived cell lines expressing porcine CD163 that support porcine reproductive and respiratory syndrome virus infection.

BMC Biotechnol. 2017-11-9

[8]
Autoantibodies against golgi apparatus induced by arteriviruses.

Cell Mol Biol (Noisy-le-grand). 2002-5

[9]
Modulation of CD163 expression by metalloprotease ADAM17 regulates porcine reproductive and respiratory syndrome virus entry.

J Virol. 2014-9

[10]
Immune response to lactate dehydrogenase-elevating virus: isolation of infectious virus-immunoglobulin G complexes and quantitation of specific antiviral immunoglobulin G response in wild-type and nude mice.

Infect Immun. 1982-9

引用本文的文献

[1]
CD81 is a receptor for equine arteritis virus (family: ).

mBio. 2025-7-9

[2]
Ineffectual immunity in a resurrected mouse model of persistent viremia.

J Virol. 2025-6-17

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