Bovine parainfluenza type 3 virus induces incomplete autophagy to promote viral replication by activated beclin1 in vitro
Copyright © 2024 Elsevier B.V. All rights reserved..
Bovine Parainfluenza virus Type 3 (BPIV3) is one of the most important pathogens in cattle, capable of causing severe respiratory symptoms. Numerous studies have shown that autophagy plays a diverse role in the infection process of various pathogens. The influence of autophagy machinery on BPIV3 infection has not yet been confirmed. In the present study, we initially demonstrated that the expression of LC3 was significantly increased and exhibited a notable increase in double or single-membrane vesicles under a transmission electron microscope during BPIV3 infection. These observations unequivocally establish the induction of steady-state autophagy in vitro consequent to BPIV3 infection. Furthermore, quantification of autophagic flux substantiates the induction of an incomplete autophagic process during BPIV3 infection. Additionally, through targeted interventions, we demonstrate the regulatory impact of pharmacological agents influencing autophagy and RNA interference targeting an autophagy-associated protein on viral replication. Intriguingly, our data revealed that BPIV3 infection enhanced the phosphorylation of rapamycin kinase (mTOR). This result demonstrated that mTOR does not operate as a counteractive regulator of BPIV3-induced autophagy. Instead, we discern an augmentation in the expression of Beclin1, a key autophagy initiator, which complexes with Vps34, constituting a Class III phosphatidylinositol 3-kinase. This phenomenon serves as a hallmark in the inaugural phase of autophagy initiation during BPIV3 infection. Collectively, these discernments underscore that BPIV3 infection actively stimulates autophagy, thereby enhancing viral replication through the activation of Beclin1, independently of the mTOR signaling pathway. This nuanced comprehension significantly contributes to unraveling the intricate molecular mechanisms governing BPIV3-induced autophagy.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:290 |
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| Enthalten in: |
Veterinary microbiology - 290(2024) vom: 15. Feb., Seite 109972 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Han, Yu [VerfasserIn] |
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| Links: |
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| Themen: |
Autophagy |
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| Anmerkungen: |
Date Completed 21.02.2024 Date Revised 21.02.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.vetmic.2023.109972 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM36674450X |
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| 520 | |a Bovine Parainfluenza virus Type 3 (BPIV3) is one of the most important pathogens in cattle, capable of causing severe respiratory symptoms. Numerous studies have shown that autophagy plays a diverse role in the infection process of various pathogens. The influence of autophagy machinery on BPIV3 infection has not yet been confirmed. In the present study, we initially demonstrated that the expression of LC3 was significantly increased and exhibited a notable increase in double or single-membrane vesicles under a transmission electron microscope during BPIV3 infection. These observations unequivocally establish the induction of steady-state autophagy in vitro consequent to BPIV3 infection. Furthermore, quantification of autophagic flux substantiates the induction of an incomplete autophagic process during BPIV3 infection. Additionally, through targeted interventions, we demonstrate the regulatory impact of pharmacological agents influencing autophagy and RNA interference targeting an autophagy-associated protein on viral replication. Intriguingly, our data revealed that BPIV3 infection enhanced the phosphorylation of rapamycin kinase (mTOR). This result demonstrated that mTOR does not operate as a counteractive regulator of BPIV3-induced autophagy. Instead, we discern an augmentation in the expression of Beclin1, a key autophagy initiator, which complexes with Vps34, constituting a Class III phosphatidylinositol 3-kinase. This phenomenon serves as a hallmark in the inaugural phase of autophagy initiation during BPIV3 infection. Collectively, these discernments underscore that BPIV3 infection actively stimulates autophagy, thereby enhancing viral replication through the activation of Beclin1, independently of the mTOR signaling pathway. This nuanced comprehension significantly contributes to unraveling the intricate molecular mechanisms governing BPIV3-induced autophagy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Autophagy | |
| 650 | 4 | |a Beclin1 | |
| 650 | 4 | |a Bovine parainfluenza virus | |
| 650 | 4 | |a Viral replication | |
| 650 | 7 | |a Beclin-1 |2 NLM | |
| 650 | 7 | |a TOR Serine-Threonine Kinases |2 NLM | |
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| 700 | 1 | |a Wang, Chongyang |e verfasserin |4 aut | |
| 700 | 1 | |a Lu, Kejia |e verfasserin |4 aut | |
| 700 | 1 | |a Dong, Xiaoyu |e verfasserin |4 aut | |
| 700 | 1 | |a Chang, Zhengwu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Riteng |e verfasserin |4 aut | |
| 700 | 1 | |a Hou, Qili |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Xinglong |e verfasserin |4 aut | |
| 700 | 1 | |a Xiao, Sa |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Haijin |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Zengqi |e verfasserin |4 aut | |
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