Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit

Corona, Abigail K.; Saulsbery, Holly M.; Velazquez, Angel F. Corona; Jackson, William T.

doi:10.1016/j.celrep.2018.03.003

Cited by 115 publications

(127 citation statements)

References 40 publications

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“…Surprisingly, we found that PV mediates instability of the ULK1/2 complex, as the protein levels of all ULK complex members decrease during infection (81). Whether PV induces bona fide autophagy has yet to be determined; PV and other picornaviruses cleave SQSTM1 during infection, confounding our ability to measure autophagic flux (81)(82)(83). PV also does not significantly alter the levels and phosphorylation states of MTOR and AMPK, suggesting that PV-mediated autophagic induction is independent of the MTOR-ULK1/2 signaling axis (81) (Fig.…”

Section: Ulk1/2-independent Autophagy Induction Ulk1/2-independent Aumentioning

confidence: 91%

So Many Roads: the Multifaceted Regulation of Autophagy Induction

Velazquez

Jackson

2018

Molecular and Cellular Biology

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102

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Autophagy is an evolutionary conserved, degradative process from single-cell eukaryotes, such as , to higher mammals, such as humans. The regulation of autophagy has been elucidated through the combined study of yeast,, mice, , and humans. MTOR, the major negative regulator of autophagy, and activating nutrient kinases, such as 5'-AMP-activated protein kinase (AMPK), interact with the autophagy regulatory complex: ULK1/2, RB1CC1, ATG13, and ATG101. The ULK1/2 complex induces autophagy by phosphorylating downstream autophagy complexes, such as the BECN1 PIK3 signaling complex that leads to the creation of LC3 autophagosomes. We highlight in this review various reports of autophagy induction that are independent of these regulators. We discuss reports of MTOR-independent, AMPK-independent, ULK1/2-independent, and BECN1-PIK3C3-independent autophagy. We illustrate that autophagy induction and the components required vary by the nature of the induction signal and type of cell and do not always require canonical members of the autophagy signaling pathway. We illustrate that rather than thinking of autophagy as a linear pathway, it is better to think of autophagy induction as an interconnecting web of key regulators, many of which can induce autophagy through different requirements depending on the type and length of induction signals.

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Section: Ulk1/2-independent Autophagy Induction Ulk1/2-independent Aumentioning

confidence: 91%

So Many Roads: the Multifaceted Regulation of Autophagy Induction

Velazquez

Jackson

2018

Molecular and Cellular Biology

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102

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“…The cleaved SNAP29, which reportedly regulated formation of autolysosome, facilitated EV-D68 in early infection but was later cleaved. In addition, SNAP47 whose role is unknown in autophagy pathway, was suggested to play a role in regulating EV-D68 induced autophagy and viral release [104]. These findings suggest that EV-D68 benefits from early stage of autophagy and blocks autophagic flux through cleavage of important factors which regulate autolysosome formation, thereby remodeling autophagic trafficking to facilitate viral release.…”

Section: Other Enterovirusesmentioning

confidence: 91%

“…Enterovirus D68 (EV-D68) also benefits from induced autophagy in host cells, as inhibition of autophagy by depletion of E1-like enzyme ATG7 or treatment with bafilomycin A1 undermined viral yield, while induction of autophagy by starvation promoted EV-D68 propagation [104]. Similar to the aforementioned CVB3 infection [89,94], accumulation of GFP-LC3 puncta and cleavage of SNAP29 and SQSTM1 by EV-D68 3C protease were detected in EV-D68 infected Hela cells [104]. The cleaved SNAP29, which reportedly regulated formation of autolysosome, facilitated EV-D68 in early infection but was later cleaved.…”

Section: Other Enterovirusesmentioning

confidence: 99%

The interplay of autophagy and enterovirus

Huang

Yue

2020

Seminars in Cell & Developmental Biology

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A B S T R A C T Autophagy, an evolutional conserved lysosomal degradation process, has been implicated to play an important role in cellular defense against a variety of microbial infection. Interestingly, numerous studies found that some pathogens, especially positive-single-strand RNA viruses, actually hijacked autophagy machinery to promote virus infection within host cells, facilitating different stages of viral life cycle, from replication, assembly to egress. Enterovirus, a genus of positive-strand RNA virus, can cause various human diseases and is one of main public health threat globally, yet no effective clinical intervention is available for enterovirus infection. Here we summarized recent literature on how enteroviruses regulate and utilize autophagy process to facilitate their propagation in the host cells. The studies on the interplay between enterovirus and autophagy not only shed light on the molecular mechanisms underlying how enterovirus hijacks cellular components and pathway for its own benefits, but also provide therapeutic option against enterovirus infection.

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“…Autophagy can be modulated to favor viral replication ( Figure 1) [23]. First, viruses can hijack host autophagy pathway to deliver their particles to the replication sites.…”

Section: Propagation Processesmentioning

confidence: 99%

Orchestrated efforts on host network hijacking: Processes governing virus replication

et al. 2020

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With the high pervasiveness of viral diseases, the battle against viruses has never ceased. Here we discuss five cellular processes, namely "autophagy", "programmed cell death", "immune response", "cell cycle alteration", and "lipid metabolic reprogramming", that considerably guide viral replication after host infection in an orchestrated manner. On viral infection, "autophagy" and "programmed cell death" are two dynamically synchronized cell survival programs; "immune response" is a cell defense program typically suppressed by viruses; "cell cycle alteration" and "lipid metabolic reprogramming" are two altered cell housekeeping programs tunable in both directions. We emphasize on their functionalities in modulating viral replication, strategies viruses have evolved to tune these processes for their benefit, and how these processes orchestrate and govern cell fate upon viral infection. Understanding how viruses hijack host networks has both academic and industrial values in providing insights toward therapeutic strategy design for viral disease control, offering useful information in applications that aim to use viral vectors to improve human health such as gene therapy, and providing guidelines to maximize viral particle yield for improved vaccine production at a reduced cost. ARTICLE HISTORY

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Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit

Cited by 115 publications

References 40 publications

So Many Roads: the Multifaceted Regulation of Autophagy Induction

So Many Roads: the Multifaceted Regulation of Autophagy Induction

The interplay of autophagy and enterovirus

Orchestrated efforts on host network hijacking: Processes governing virus replication

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