Autophagy during Early Virus–Host Cell Interactions

Viret, Christophe; Rozières, Aurore; Faure, Mathias

doi:10.1016/j.jmb.2018.04.018

Cited by 42 publications

(29 citation statements)

References 117 publications

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“…The identity of the winner often defines whom from the virus or the host will take over the other. This is perfectly illustrated by the works from the groups of Alain and Faure on the autophagy-related events [15] and battle for ribosomes and translation [16] during the early steps of virus infection. Viral entry processes have a significant impact on these subsequent mechanisms.…”

Section: Early Virus-host Cell Interactionsmentioning

confidence: 88%

Early Virus–Host Cell Interactions

Lozach

2018

Journal of Molecular Biology

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Section: Early Virus-host Cell Interactionsmentioning

confidence: 88%

Early Virus–Host Cell Interactions

Lozach

2018

Journal of Molecular Biology

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“…As a gate for viral infection control, autophagosomes are considered as an integral part of the immune system. They can deliver cytosolic pathogen-associated molecular patterns (PAMPs) to endosomal pattern recognition receptors (PRRs) and major histocompatibility complex (MHC) loading compartments for innate and adaptive immune stimulation, respectively, or directly exert foreign particle clearance roles by degrading virions [21]. For example, Lee et al demonstrated that plasmacytoid dendritic cells could recognize certain single-stranded RNA viruses via TLR7 upon transport of cytosolic viral replication intermediates into lysosomes through autophagy [22].…”

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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“…During this process, the autophagy machinery can target components of replicating microbes for degradation but also entire microorganisms such as Group A Streptococcus (GAS) or Salmonella enterica Serovar Typhimurium (S. Typhimurium) [5,6,7]. As viruses are, by definition, intracellular parasites, autophagy is often mobilized to oppose viral invasion/multiplication both in vitro [8,9,10] and in vivo [11,12,13], including during the earliest steps of virus-host cell interactions [14]. Perhaps, the strongest indication that autophagy represents a highly efficient host defense mechanism to oppose invasion by intracellular microbes is the variety of mechanisms microbes use to escape, counteract or subvert the autophagy machinery [8,9,10].…”

Section: Introductionmentioning

confidence: 99%

Regulation of anti-microbial autophagy by factors of the complement system

Viret¹,

Rozières²,

Duclaux-Loras³

et al. 2020

Microb Cell

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The complement system is a major component of innate immunity that participates in the defense of the host against a myriad of pathogenic microorganisms. Activation of complement allows for both local inflammatory response and physical elimination of microbes through phagocytosis or lysis. The system is highly efficient and is therefore finely regulated. In addition to these well-established properties, recent works have revealed that components of the complement system can be involved in a variety of other functions including in autophagy, the conserved mechanism that allows for the targeting and degradation of cytosolic materials by the lysosomal pathway after confining them into specialized organelles called autophagosomes. Besides impacting cell death, development or metabolism, the complement factors-autophagy connection can greatly modulate the cell autonomous, antimicrobial activity of autophagy: xenophagy. Both surface receptorligand interactions and intracellular interactions are involved in the modulation of the autophagic response to intracellular microbes by complement factors. Here, we review works that relate to the recently discovered connections between factors of the complement system and the functioning of autophagy in the context of host-pathogen relationship. Abbreviations:ATG -autophagy-related factor; CD4 T -mature T lymphocytes of the CD4 lineage; C3aR -C3a receptor; C5aR -C5a receptor; EGF-epidermal growth factor; GAS -group A Streptococcus; GOPC -Golgi-associated PDZ and Coiled-Coil Motif containing; GTPases -guanosine triphosphate hydrolase; LC3 (MAP1LC3) -microtubuleassociated protein 1-light chain 3; Mcrmacroglobulin complement-related; mTORC1mammalian target of rapamycin complex 1; MACmembrane attack complex (C5b-9); MASP -MBLassociated serine proteases; MAVS -mitochondrial antiviral signaling; MBL -mannan-binding lectin; MCP -membrane cofactor protein (CD46); MEGF10 -multiple epidermal growth factor-like domain factor 10; MeV -Measles virus; NF-κB -nuclear factor-kappa B; PI(3)P -phosphatidylinositol 3phosphate; RCA -regulators of complement activation; ULK1 -Unc51-like kinase; VPSvacuolar protein sorting.C. Viret et al. (2020) Complement-mediated regulation of xenophagy OPEN ACCESS | www.microbialcell.com 94

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Autophagy during Early Virus–Host Cell Interactions

Cited by 42 publications

References 117 publications

Early Virus–Host Cell Interactions

Early Virus–Host Cell Interactions

Orchestrated efforts on host network hijacking: Processes governing virus replication

Regulation of anti-microbial autophagy by factors of the complement system

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