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一种来自蜱虫的过氧化物酶影响沙粒病毒在仓鼠细胞系中的复制。

A Peroxiredoxin From the Tick Affects Langat Virus Replication in a Hamster Cell Line.

机构信息

Laboratory of Parasitology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.

Laboratory of Infectious Diseases, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, Japan.

出版信息

Front Cell Infect Microbiol. 2020 Jan 28;10:7. doi: 10.3389/fcimb.2020.00007. eCollection 2020.

Abstract

Ticks are hematophagous arthropods, and their blood feeding on vertebrate hosts is essential for their development. The vertebrate blood contains high levels of free iron that can react with oxygen in ticks, resulting in the production of hydrogen peroxide (HO), one of the reactive oxygen species. Peroxiredoxins (Prxs), HO-scavenging enzymes, take on an important role in the ticks' oxidative stress coping mechanism. Ticks also transmit several disease-causing pathogens, including tick-borne encephalitis virus (TBEV), in animals and humans. Therefore, the control of ticks and tick-borne pathogens is a key issue that needs to be addressed. Infection with an arthropod-borne flavivirus is known to induce oxidative stress in insect cells. We hypothesize that vector-derived Prxs could have an effect on the infection and/or replication of flaviviruses in the hosts, since ticks Prxs are possibly transmitted from ticks to their hosts. In this study, we established stable strains of baby hamster kidney (BHK) cells expressing two types of HO-scavenging Prxs from the hard tick (BHK-HlPrx and BHK-HlPrx2 cells). Although the infection of TBEV surrogate Langat virus (LGTV) did not induce HO production in normal BHK cells, the mortality rate and the virus titer of LGTV infected BHK-HlPrx cells increased. In addition, HlPrx proteins in BHK cells can facilitate LGTV replication in cells, while HlPrx2 proteins in BHK cells cannot. The results also demonstrated that this facilitation of LGTV replication by the 1-Cys Prx in the BHK cells is not by scavenging HO but by an unknown mechanism. In order to understand this mechanism, more studies using tick-derived cells and ticks are necessary.

摘要

蜱是吸血节肢动物,它们以脊椎动物宿主的血液为食,这对它们的发育至关重要。脊椎动物血液中含有高水平的游离铁,这种铁可以与蜱体内的氧气反应,产生过氧化氢(HO),HO 是活性氧物种之一。过氧化物酶(Prxs)是清除 HO 的酶,在蜱的氧化应激应对机制中发挥着重要作用。蜱还在动物和人类中传播几种致病病原体,包括蜱传脑炎病毒(TBEV)。因此,控制蜱和蜱传病原体是一个需要解决的关键问题。已知节肢动物传播的黄病毒感染会导致昆虫细胞产生氧化应激。我们假设,源自媒介的 Prxs 可能会对宿主中黄病毒的感染和/或复制产生影响,因为蜱 Prxs 可能从蜱传播到它们的宿主。在这项研究中,我们建立了稳定表达硬蜱两种 HO 清除 Prxs 的 BHK 细胞系(BHK-HlPrx 和 BHK-HlPrx2 细胞)。尽管 TBEV 替代 Langat 病毒(LGTV)的感染不会诱导正常 BHK 细胞产生 HO,但 BHK-HlPrx 细胞中 LGTV 的感染死亡率和病毒滴度增加。此外,BHK 细胞中的 HlPrx 蛋白可以促进 LGTV 在细胞中的复制,而 BHK 细胞中的 HlPrx2 蛋白则不能。结果还表明,BHK 细胞中的 1-Cys Prx 对 LGTV 复制的促进作用不是通过清除 HO 实现的,而是通过未知机制实现的。为了了解这种机制,需要使用源自蜱的细胞和蜱进行更多的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0511/6997474/32c738de40c3/fcimb-10-00007-g0001.jpg

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