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Open AccessArticle

TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy

1
Institute of Biophotonics, National Yang-Ming University, Taipei 11221, Taiwan
2
Brain Research Center, National Yang-Ming University, Taipei 11221, Taiwan
3
Faculty of Medicine, National Yang-Ming University, Taipei 11221, Taiwan
4
Department of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City 22060, Taiwan
5
Department and Institute of Pharmacology, National Yang-Ming University, Taipei 11221, Taiwan
6
Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei 11217, Taiwan
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(19), 4893; https://doi.org/10.3390/ijms20194893
Received: 28 August 2019 / Revised: 29 September 2019 / Accepted: 29 September 2019 / Published: 2 October 2019
(This article belongs to the Special Issue Molecular Research on Emerging Mosquito-Transmitted RNA Viruses)
Dengue virus (DENV) infection triggers the activation of autophagy to facilitate the viral replication cycle from various aspects. Although a number of stimulators are proposed to activate autophagy, none of them appears prior to the uncoating process. Given that T-cell immunoglobulin and mucin domain 1 (TIM-1) receptor is a putative DENV receptor and promotes apoptotic body clearance by autophagy induction, it raises the possibility that TIM-1 may participate in the activation of DENV-induced autophagy. In this study, confocal images first revealed the co-localization of TIM-1 with autophagosomes in DENV-induced autophagy rather than rapamycin-induced autophagy, suggesting the co-transportation of TIM-1 with DENV during infection. The treatment of siRNA to knockdown TIM-1 expression in DENV-infected GFP-microtubule-associated protein light chain 3 (LC3)-Huh7.5 cells revealed that TIM-1 is required not only for DENV cellular internalization but also for autophagy activation. Furthermore, knockdown p85, a subunit of phosphoinositide 3-kinases (PI3Ks), which is co-localized with TIM-1 at rab5-positive endosomes caused the reduction of autophagy, indicating that TIM-1-mediated DENV-induced autophagy requires p85. Taken together, the current study uncovered TIM-1 as a novel factor for triggering autophagy in DENV infection through TIM-1-p85 axis, in addition to serving as a DENV receptor. View Full-Text
Keywords: dengue virus; autophagy; TIM-1; p85; rab5; early endosome dengue virus; autophagy; TIM-1; p85; rab5; early endosome
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Chu, L.-W.; Yang, C.-J.; Peng, K.-J.; Chen, P.-L.; Wang, S.-J.; Ping, Y.-H. TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy. Int. J. Mol. Sci. 2019, 20, 4893.

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