Mitochondria Redistribution in Enterovirus A71 Infected Cells and Its Effect on Virus Replication
Autor: | Wenliang Zhang, Chunrui Li, Yang Yang, Ning Du, Xiaodong Han, Lei Song, Po Tien, Haolong Cong |
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Rok vydání: | 2019 |
Předmět: |
rho GTP-Binding Proteins
0301 basic medicine Thapsigargin Viral protein 030106 microbiology Immunology GTPase Viral Nonstructural Proteins Biology Mitochondrion Virus Replication medicine.disease_cause Microtubules Mitochondrial Proteins Motor protein Viral Proteins 03 medical and health sciences chemistry.chemical_compound Cytosol Microtubule Virology medicine Humans Host Microbial Interactions Dyneins Enterovirus A Human Mitochondria Cell biology Nocodazole 030104 developmental biology chemistry Viral replication Molecular Medicine Research Article HeLa Cells |
Zdroj: | Virol Sin |
ISSN: | 1995-820X 1674-0769 |
Popis: | Enterovirus A71 (EV-A71) is one of the main causative agents of hand, foot and mouth disease (HFMD) and it also causes severe neurologic complications in infected children. The interactions between some viruses and the host mitochondria are crucial for virus replication and pathogenicity. In this study, it was observed that EV-A71 infection resulted in a perinuclear redistribution of the mitochondria. The mitochondria rearrangement was found to require the microtubule network, the dynein complex and a low cytosolic calcium concentration. Subsequently, the EV-A71 non-structural protein 2BC was identified as the viral protein capable of inducing mitochondria clustering. The protein was found localized on mitochondria and interacted with the mitochondrial Rho GTPase 1 (RHOT1) that is a key protein required for attachment between the mitochondria and the motor proteins, which are responsible for the control of mitochondria movement. Additionally, suppressing mitochondria clustering by treating cells with nocodazole, EHNA, thapsigargin or A23187 consistently inhibited EV-A71 replication, indicating that mitochondria recruitment played a crucial role in the EV-A71 life cycle. This study identified a novel function of the EV-A71 2BC protein and provided a potential model for the regulation of mitochondrial motility in EV-A71 infection. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s12250-019-00120-5) contains supplementary material, which is available to authorized users. |
Databáze: | OpenAIRE |
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