Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling

Recent studies have indicated that the Zika virus (ZIKV) has a significant impact on the fetal brain, and autophagy is contributing to host immune response and defense against virus infection. Here, we demonstrate that ZIKV infection triggered increased LC3 punctuation in mouse monocyte-macrophage c...

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Main Authors: Yuyi Huang, Yujie Wang, Shuhui Meng, Zhuohang Chen, Haifan Kong, Ting Pan, Gen Lu, Xuefeng Li
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2020/9527147
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author Yuyi Huang
Yujie Wang
Shuhui Meng
Zhuohang Chen
Haifan Kong
Ting Pan
Gen Lu
Xuefeng Li
author_facet Yuyi Huang
Yujie Wang
Shuhui Meng
Zhuohang Chen
Haifan Kong
Ting Pan
Gen Lu
Xuefeng Li
author_sort Yuyi Huang
collection DOAJ
description Recent studies have indicated that the Zika virus (ZIKV) has a significant impact on the fetal brain, and autophagy is contributing to host immune response and defense against virus infection. Here, we demonstrate that ZIKV infection triggered increased LC3 punctuation in mouse monocyte-macrophage cell line (RAW264.7), mouse microglial cell line (BV2), and hindbrain tissues, proving the occurrence of autophagy both in vitro and in vivo. Interestingly, manual intervention of autophagy, like deficiency inhibited by 3-MA, can reduce viral clearance in RAW264.7 cells upon ZIKV infection. Besides, specific siRNA strategy confirmed that autophagy can be activated through Atg7-Atg5 and type I IFN signaling pathway upon ZIKV infection, while knocking down of Atg7 and Atg5 effectively decreased the ZIKV clearance in phagocytes. Furthermore, we analyzed that type I IFN signaling could contribute to autophagic clearance of invaded ZIKV in phagocytes. Taken together, our findings demonstrate that ZIKV-induced autophagy is favorable to activate host immunity, particularly through type I IFN signaling, which participates in host protection and defense against ZIKV infection.
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institution Kabale University
issn 0962-9351
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language English
publishDate 2020-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-9a1cf6c2511941a3a112a9e64734374c2025-02-03T05:44:15ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/95271479527147Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN SignalingYuyi Huang0Yujie Wang1Shuhui Meng2Zhuohang Chen3Haifan Kong4Ting Pan5Gen Lu6Xuefeng Li7The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital; The Second Affiliated Hospital of Guangzhou Medical University, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology; Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaThe Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital; The Second Affiliated Hospital of Guangzhou Medical University, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology; Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaThe Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital; The Second Affiliated Hospital of Guangzhou Medical University, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology; Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaSchool of Public Health (Shenzhen), Sun Yat-sen University, Shenzhen 510006, ChinaNan Shan School, Guangzhou Medical University, Guangzhou 511436, ChinaSchool of Medicine, Sun Yat-sen University, Guangzhou 510080, ChinaGuangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510120, ChinaThe Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital; The Second Affiliated Hospital of Guangzhou Medical University, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology; Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaRecent studies have indicated that the Zika virus (ZIKV) has a significant impact on the fetal brain, and autophagy is contributing to host immune response and defense against virus infection. Here, we demonstrate that ZIKV infection triggered increased LC3 punctuation in mouse monocyte-macrophage cell line (RAW264.7), mouse microglial cell line (BV2), and hindbrain tissues, proving the occurrence of autophagy both in vitro and in vivo. Interestingly, manual intervention of autophagy, like deficiency inhibited by 3-MA, can reduce viral clearance in RAW264.7 cells upon ZIKV infection. Besides, specific siRNA strategy confirmed that autophagy can be activated through Atg7-Atg5 and type I IFN signaling pathway upon ZIKV infection, while knocking down of Atg7 and Atg5 effectively decreased the ZIKV clearance in phagocytes. Furthermore, we analyzed that type I IFN signaling could contribute to autophagic clearance of invaded ZIKV in phagocytes. Taken together, our findings demonstrate that ZIKV-induced autophagy is favorable to activate host immunity, particularly through type I IFN signaling, which participates in host protection and defense against ZIKV infection.http://dx.doi.org/10.1155/2020/9527147
spellingShingle Yuyi Huang
Yujie Wang
Shuhui Meng
Zhuohang Chen
Haifan Kong
Ting Pan
Gen Lu
Xuefeng Li
Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling
Mediators of Inflammation
title Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling
title_full Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling
title_fullStr Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling
title_full_unstemmed Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling
title_short Autophagy Contributes to Host Immunity and Protection against Zika Virus Infection via Type I IFN Signaling
title_sort autophagy contributes to host immunity and protection against zika virus infection via type i ifn signaling
url http://dx.doi.org/10.1155/2020/9527147
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