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l-多巴脱羧酶在黄病毒科病毒感染中的新作用。

Emerging Role of l-Dopa Decarboxylase in Flaviviridae Virus Infections.

机构信息

Laboratory of Molecular Virology, Hellenic Pasteur Institute (HPI), 11521 Athens, Greece.

Light Microscopy Unit, Hellenic Pasteur Institute, 11521 Athens, Greece.

出版信息

Cells. 2019 Aug 5;8(8):837. doi: 10.3390/cells8080837.

DOI:10.3390/cells8080837
PMID:31387309
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6721762/
Abstract

l-dopa decarboxylase (DDC) that catalyzes the biosynthesis of bioactive amines, such as dopamine and serotonin, is expressed in the nervous system and peripheral tissues, including the liver, where its physiological role remains unknown. Recently, we reported a physical and functional interaction of DDC with the major signaling regulator phosphoinosite-3-kinase (PI3K). Here, we provide compelling evidence for the involvement of DDC in viral infections. Studying dengue (DENV) and hepatitis C (HCV) virus infection in hepatocytes and HCV replication in liver samples of infected patients, we observed a negative association between DDC and viral replication. Specifically, replication of both viruses reduced the levels of DDC mRNA and the ~120 kDa SDS-resistant DDC immunoreactive functional complex, concomitant with a PI3K-dependent accumulation of the ~50 kDa DDC monomer. Moreover, viral infection inhibited PI3K-DDC association, while DDC did not colocalize with viral replication sites. DDC overexpression suppressed DENV and HCV RNA replication, while DDC enzymatic inhibition enhanced viral replication and infectivity and affected DENV-induced cell death. Consistently, we observed an inverse correlation between DDC mRNA and HCV RNA levels in liver biopsies from chronically infected patients. These data reveal a novel relationship between DDC and replication cycle and the role of PI3K in this process.

摘要

l-多巴脱羧酶（DDC）催化生物活性胺如多巴胺和血清素的生物合成，表达于神经系统和外周组织，包括肝脏，其生理作用尚不清楚。最近，我们报道了 DDC 与主要信号调节剂磷酸肌醇-3-激酶（PI3K）之间的物理和功能相互作用。在这里，我们提供了令人信服的证据表明 DDC 参与病毒感染。在肝细胞中研究登革热（DENV）和丙型肝炎（HCV）病毒感染以及感染患者的肝组织中 HCV 复制，我们观察到 DDC 与病毒复制之间呈负相关。具体而言，两种病毒的复制均降低了 DDC mRNA 的水平和120 kDa SDS 抗性 DDC 免疫反应性功能复合物，同时伴随着 PI3K 依赖性的50 kDa DDC 单体积累。此外，病毒感染抑制了 PI3K-DDC 结合，而 DDC 并未与病毒复制部位共定位。DDC 过表达抑制 DENV 和 HCV RNA 复制，而 DDC 酶抑制增强了病毒复制和感染力，并影响 DENV 诱导的细胞死亡。一致地，我们观察到慢性感染患者肝活检中 DDC mRNA 和 HCV RNA 水平之间存在负相关。这些数据揭示了 DDC 与复制周期之间的新关系以及 PI3K 在该过程中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/a307363a2dd6/cells-08-00837-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/14ef3b38ac8b/cells-08-00837-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/98c4c367ebf2/cells-08-00837-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/6d764c83b9a7/cells-08-00837-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/08d8ddf7e8db/cells-08-00837-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/067914ef148e/cells-08-00837-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/fe661ac6842e/cells-08-00837-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/4f0f818d48b3/cells-08-00837-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/a307363a2dd6/cells-08-00837-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/14ef3b38ac8b/cells-08-00837-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/98c4c367ebf2/cells-08-00837-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/73537fd47114/cells-08-00837-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/6d764c83b9a7/cells-08-00837-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/08d8ddf7e8db/cells-08-00837-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/067914ef148e/cells-08-00837-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/fe661ac6842e/cells-08-00837-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/4f0f818d48b3/cells-08-00837-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a6/6721762/a307363a2dd6/cells-08-00837-g009.jpg

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