Virus-Induced Cytoplasmic Aggregates and Inclusions Are Critical Cellular Regulatory and Antiviral Factors

Olasunkanmi, Oluwatayo Israel; Chen, Sijia; Mageto, James; Zhong, Zhaohua

doi:10.3390/v12040399

Cited by 21 publications

(28 citation statements)

References 108 publications

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“…Recent work on coxsackievirus A16 revealed that SGs induced early during infection were later cleared by autophagy as a means to suppress antiviral immune signaling [380]. Some viruses hijack the autophagic degradation pathway or use autophagosome-derived compartments to support their replication [381,382]. Infectious bursal disease virus is an example of a virus that subverts the autolysosome for virus assembly and maturation in an acidic environment [383].…”

Section: Granulophagymentioning

confidence: 99%

Dance with the Devil: Stress Granules and Signaling in Antiviral Responses

Eiermann

Haneke

Sun

et al. 2020

Viruses

117

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Cells have evolved highly specialized sentinels that detect viral infection and elicit an antiviral response. Among these, the stress-sensing protein kinase R, which is activated by double-stranded RNA, mediates suppression of the host translation machinery as a strategy to limit viral replication. Non-translating mRNAs rapidly condensate by phase separation into cytosolic stress granules, together with numerous RNA-binding proteins and components of signal transduction pathways. Growing evidence suggests that the integrated stress response, and stress granules in particular, contribute to antiviral defense. This review summarizes the current understanding of how stress and innate immune signaling act in concert to mount an effective response against virus infection, with a particular focus on the potential role of stress granules in the coordination of antiviral signaling cascades.

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Section: Granulophagymentioning

confidence: 99%

Dance with the Devil: Stress Granules and Signaling in Antiviral Responses

Eiermann

Haneke

Sun

et al. 2020

Viruses

117

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“…I propose that APOLs, PI4KB and PHB participate in the formation of autophagosomes induced by type I interferon‐mediated inflammation [145] (Fig. 5).…”

Section: Discussionmentioning

confidence: 99%

“…Hypothetical involvement of APOLs in the formation of autophagosomes induced by type I interferon. Aggresomes are virus‐induced aggregates that become enclosed in autophagic structures to limit infection and favour cell recovery [145], but such structures may be used by some viruses for their replication [131,147]. APOLs could control the initiation of isolation membranes by Golgi‐derived vesicles, owing to their effect on PI(4)P synthesis by PI4KB [8], which is key to autophagy initiation [56,166].…”

Section: Apols and Viral Infectionmentioning

confidence: 99%

“…Therefore, I propose that APOLs, PI4KB and PHB participate in the formation of autophagosomes induced by infection, particularly by viruses. More specifically, these proteins would generate and elongate phagophores enclosing virus-induced aggresomes for their degradation in autophagosomes [145] (Fig. 5).…”

Section: Apols and Viral Infectionmentioning

confidence: 99%

“…5). While APOLs control the activity of [145], but such structures may be used by some viruses for their replication [131,147]. APOLs could control the initiation of isolation membranes by Golgi-derived vesicles, owing to their effect on PI(4)P synthesis by PI4KB [8], which is key to autophagy initiation [56,166].…”

Section: Apols and Viral Infectionmentioning

confidence: 99%

See 2 more Smart Citations

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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Widespread amyloid aggregates formation by Zika virus proteins and peptides

Giri,

Bhardwaj,

Kapuganti

et al. 2023

Protein Science

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Viral pathogenesis typically involves numerous molecular mechanisms. Protein aggregation is a relatively unknown characteristic of viruses, despite the fact that viral proteins have been shown to form terminally misfolded forms. Zika virus (ZIKV) is a neurotropic one with the potential to cause neurodegeneration. Its protein amyloid aggregation may link the neurodegenerative component to the pathogenicity associated with the viral infection. Therefore, we investigated protein aggregation in the ZIKV proteome as a putative pathogenic route and one of the alternate pathways. We discovered that it contains numerous anticipated aggregation‐prone regions in this investigation. To validate our prediction, we used a combination of supporting experimental techniques routinely used for morphological characterization and study of amyloid aggregates. Several ZIKV proteins and peptides, including the full‐length envelope protein, its domain III (EDIII) and fusion peptide, Pr N‐terminal peptide, NS1 β‐roll peptide, membrane‐embedded signal peptide 2K, and cytosolic region of NS4B protein, were shown to be highly aggregating in our study. Because our findings show that viral proteins can form amyloids in vitro, we need to do a thorough functional study of these anticipated APRs to understand better the role of amyloids in the pathophysiology of ZIKV infection.

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Virus-Induced Cytoplasmic Aggregates and Inclusions Are Critical Cellular Regulatory and Antiviral Factors

Cited by 21 publications

References 108 publications

Dance with the Devil: Stress Granules and Signaling in Antiviral Responses

Dance with the Devil: Stress Granules and Signaling in Antiviral Responses

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

Widespread amyloid aggregates formation by Zika virus proteins and peptides

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