Monitoring Mitochondrial Function in Aedes albopictus C6/36 Cell Line during Dengue Virus Infection.

Monitoring Mitochondrial Function in Aedes albopictus C6/36 Cell Line during Dengue Virus Infection.
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DOI:
10.3390/insects12100934
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发表时间:
2021-10-14
期刊:
影响因子:
3
通讯作者:
Pando-Robles V
Pando-Robles V
中科院分区:
农林科学2区
文献类型:
--
作者:
Santana-Román ME;Maycotte P;Uribe-Carvajal S;Uribe-Alvarez C;Alvarado-Medina N;Khan M;Siddiqui A;Pando-Robles V

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登革热是一个重要且日益严重的公共卫生问题。到目前为止,还没有具体的治疗或有效的预防措施。因此,媒介控制仍然是预防登革病毒(DENV)感染人类的主要途径。最近的发现强调,病毒调节线粒体的功能和动态,以促进病毒的增殖。在这项研究中,我们报道了DENV感染对C6/36蚊虫细胞线粒体生理的调节。我们的结果表明,DENV改变了氧化还原代谢和线粒体膜电位,而对细胞的ATP库或活性没有任何明显的影响。此外,我们观察到呼吸控制率的保存和丝裂原蛋白向线粒体的移位。这些结果表明,线粒体融合可能是维持感染DENV的C6/36蚊子细胞线粒体功能所必需的。埃及伊蚊和白纹伊蚊是全球热带和亚热带地区登革热病毒(DENV)传播的罪魁祸首,据估计,那里有30亿人面临接触DENV的风险。登革热病毒感染者的症状从亚临床或轻微到出血热不等。被感染的蚊子不会表现出可检测到的疾病迹象,尽管这种病毒会终身持续感染。病毒与宿主线粒体之间的相互作用是病毒复制和致病的关键。脊椎动物细胞中的DENV感染调节线粒体的功能和动态,以促进病毒的增殖。在这里,我们描述了DENV还调节感染的C6/36蚊子细胞(来源于白纹伊蚊)的线粒体功能和形态。我们的结果表明,DENV感染增加了ROS(活性氧)的产生,调节了线粒体的跨膜电位,并诱导了线粒体呼吸的变化。此外,我们提供了DENV导致C6/36蚊子细胞系中有丝分裂素转位到线粒体的第一个证据。另一种蛋白DRP-1(动力素相关蛋白1)在DENV感染的细胞中不定位于线粒体。因此,这一观察结果排除了上述线粒体功能改变与线粒体分裂有关的可能性。总而言之,这份报告提供了一些关于DENV感染蚊子细胞中病毒-线粒体串扰的关键见解。
Dengue is an important and growing public health problem. To date, no specific therapeutic or effective prophylactic measures exist. Therefore, vector control remains the primary approach to prevent dengue virus (DENV) infection in humans. Recent findings highlight that viruses regulate mitochondrial function and dynamics to facilitate viral proliferation. In this study, we report that DENV infection modulates mitochondrial physiology in C6/36 mosquito cells. Our results revealed that DENV alters redox metabolism and mitochondrial membrane potential without any significant change in cellular ATP pool or viability. In addition, we observed preservation of the respiratory control ratio and translocation of mitofusins to mitochondria. These results suggest that mitochondrial fusion could be required for the maintenance of mitochondrial function in C6/36 mosquito cells infected with DENV. Aedes aegypti and Aedes albopictus mosquitoes are responsible for dengue virus (DENV) transmission in tropical and subtropical areas worldwide, where an estimated 3 billion people live at risk of DENV exposure. DENV-infected individuals show symptoms ranging from sub-clinical or mild to hemorrhagic fever. Infected mosquitoes do not show detectable signs of disease, even though the virus maintains a lifelong persistent infection. The interactions between viruses and host mitochondria are crucial for virus replication and pathogenicity. DENV infection in vertebrate cells modulates mitochondrial function and dynamics to facilitate viral proliferation. Here, we describe that DENV also regulates mitochondrial function and morphology in infected C6/36 mosquito cells (derived from Aedes albopictus). Our results showed that DENV infection increased ROS (reactive oxygen species) production, modulated mitochondrial transmembrane potential and induced changes in mitochondrial respiration. Furthermore, we offer the first evidence that DENV causes translocation of mitofusins to mitochondria in the C6/36 mosquito cell line. Another protein Drp-1 (Dynamin-related protein 1) did not localize to mitochondria in DENV-infected cells. This observation therefore ruled out the possibility that the abovementioned alterations in mitochondrial function are associated with mitochondrial fission. In summary, this report provides some key insights into the virus–mitochondria crosstalk in DENV infected mosquito cells.
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发表时间: 2018-03
期刊: PLoS pathogens
影响因子: 6.7
作者:
Chotiwan N;Andre BG;Sanchez-Vargas I;Islam MN;Grabowski JM;Hopf-Jannasch A;Gough E;Nakayasu E;Blair CD;Belisle JT;Hill CA;Kuhn RJ;Perera R
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