Essential domains of phosphatidylinositol‐4 kinase III β required for enterovirus replication

Arita, Minetaro

doi:10.1111/1348-0421.12718

Cited by 7 publications

(9 citation statements)

References 30 publications

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“…Moreover, I44 and H54 are important for stabilizing the ACBD3-PI4KB complex and are critical for EV-A71 replication (Xiao et al, 2017). Surprisingly, a recent study on trans-rescue of EV-A71 pseudovirus replication with PI4KB deletion mutants suggested that ACBD3-binding site of PI4KB is not essential for EV-A71 replication (Arita, 2019). The role of ACBD3-PI4KB interaction involved in EV-A71 infection need to be further investigated.…”

Section: Acbd3 In Enterovirus Infection Enterovirus A71 (Ev-a71)mentioning

confidence: 99%

“…They demonstrated that ACBD3 promoted PV replication by more than 10-fold (Lyoo et al, 2019). A recent study on trans-rescue of PV1 pseudovirus replication with PI4KB deletion mutants showed that ACBD3-binding site of PI4KB is not essential for PV1 pseudovirus replication (Arita, 2019). Whether the interaction of ACBD3-PI4KB is involved in bona fide PV1 infection need more studies to clarify.…”

Section: Poliovirus (Pv)mentioning

confidence: 99%

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Emerging Role for Acyl-CoA Binding Domain Containing 3 at Membrane Contact Sites During Viral Infection

Shi

Zhang

2020

Front. Microbiol.

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Acyl-coenzyme A binding domain containing 3 (ACBD3) is a multifunctional protein residing in the Golgi apparatus and is involved in several signaling pathways. The current knowledge on ACBD3 has been extended to virology. ACBD3 has recently emerged as a key factor subverted by viruses, including kobuvirus, enterovirus, and hepatitis C virus. The ACBD3-PI4KB complex is critical for the role of ACBD3 in viral replication. In most cases, ACBD3 plays a positive role in viral infection. ACBD3 associates with viral 3A proteins from a variety of Picornaviridae family members at membrane contact sites (MCSs), which are used by diverse viruses to ensure lipid transfer to replication organelles (ROs). In this review, we discuss the mechanisms underlying the involvement of ACBD3 in viral infection at MCSs. Our review will highlight the current research and reveal potential avenues for future research.

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Section: Acbd3 In Enterovirus Infection Enterovirus A71 (Ev-a71)mentioning

confidence: 99%

Section: Poliovirus (Pv)mentioning

confidence: 99%

Emerging Role for Acyl-CoA Binding Domain Containing 3 at Membrane Contact Sites During Viral Infection

Shi

Zhang

2020

Front. Microbiol.

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“…While PHB and APOLs seem to be part of an autophagy system linked to infection, PI4KB is likely to be associated with this system given involvement of this enzyme in both autophagy and viral replication [56,118–131]. Accordingly, PI4KB was found to be involved in autophagy linked to infection by group A Streptococcus [144].…”

Section: Apols and Viral Infectionmentioning

confidence: 99%

“…3). PI4KB is also crucially involved in the PI (4)P-dependent remodelling of cellular membranes induced by different viruses in order to build membranous structures such as replication organelles or inclusion bodies, where new virions are assembled [118][119][120][121][122][123][124][125][126][127][128][129][130] (review in Ref. [131]).…”

Section: Apols and Viral Infectionmentioning

confidence: 99%

The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection

Pays

2020

The FEBS Journal

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The discovery that apolipoprotein L1 (APOL1) is the trypanolytic factor of human serum raised interest about the function of APOLs, especially following the unexpected finding that in addition to their protective action against sleeping sickness, APOL1 C-terminal variants also cause kidney disease. Based on the analysis of the structure and trypanolytic activity of APOL1, it was proposed that APOLs could function as ion channels of intracellular membranes and be involved in mechanisms triggering programmed cell death. In this review, the recent finding that APOL1 and APOL3 inversely control the synthesis of phosphatidylinositol-4-phosphate (PI(4)P) by the Golgi PI(4)-kinase IIIB (PI4KB) is commented. APOL3 promotes Ca 2+-dependent activation of PI4KB, but due to their increased interaction with APOL3, APOL1 C-terminal variants can inactivate APOL3, leading to reduction of Golgi PI(4)P synthesis. The impact of APOLs on several pathological processes that depend on Golgi PI(4)P levels is discussed. I propose that through their effect on PI4KB activity, APOLs control not only actomyosin activities related to vesicular trafficking, but also the generation and elongation of autophagosomes induced by inflammation.

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“…However, PI4KB and ACBD3 recruitment by CVB3 and HRV 3A likely independent of GBF1/Arf1 and ACBD3 (Dorobantu et al, 2014(Dorobantu et al, , 2015. And recent research about PI4KB using trans complementation with PI4KB mutants in a PI4KB-knockout cell line shows that interaction of PI4KB with host proteins (ACBD3, RAB11A, and 14-3-3) is not essential for EV replication once PI4KB has been expressed and that PI4KB is functionally independent from host proteins regarding EV replication (Arita, 2019). They are different from the above results, which may be due to the use of siRNA to knock down endogenous GBF1 and ACBD3 levels but not cause a complete knock out.…”

Section: Pimentioning

confidence: 99%

Enterovirus Replication Organelles and Inhibitors of Their Formation

Wang

Cheng

et al. 2020

Front. Microbiol.

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Enteroviral replication reorganizes the cellular membrane. Upon infection, viral proteins and hijacked host factors generate unique structures called replication organelles (ROs) to replicate their viral genomes. ROs promote efficient viral genome replication, coordinate the steps of the viral replication cycle, and protect viral RNA from host immune responses. More recent researches have focused on the ultrastructure structures, formation mechanism, and functions in the virus life cycle of ROs. Dynamic model of enterovirus ROs structure is proposed, and the secretory pathway, the autophagy pathway, and lipid metabolism are found to be associated in the formation of ROs. With deeper understanding of ROs, some compounds have been found to show inhibitory effects on viral replication by targeting key proteins in the process of ROs formation. Here, we review the recent findings concerning the role, morphology, biogenesis, formation mechanism, and inhibitors of enterovirus ROs.

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Essential domains of phosphatidylinositol‐4 kinase III β required for enterovirus replication

Cited by 7 publications

References 30 publications

Emerging Role for Acyl-CoA Binding Domain Containing 3 at Membrane Contact Sites During Viral Infection

Emerging Role for Acyl-CoA Binding Domain Containing 3 at Membrane Contact Sites During Viral Infection

The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection

Enterovirus Replication Organelles and Inhibitors of Their Formation

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