Histone deacetylase inhibition by Japanese encephalitis virus in monocyte/macrophages: A novel viral immune evasion strategy

Adhya, Dwaipayan; Dutta, Kallol; Kundu, Kiran; Basu, Anirban

doi:10.1016/j.imbio.2013.04.018

Cited by 19 publications

(13 citation statements)

References 37 publications

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“…In a recent study we had demonstrated that at early time points (6, 12 and 24 h) there is no significant alterations in the expression of MHC-1 or the costimulatory molecules CD80 and CD86 on the surface of JEV-infected macrophages compared to non-infected controls [28]. Hence, it may be assumed that during early infection there is no viral antigen presentation by infected macrophages, and thus there should be no involvement of the adaptive immune system in viral clearance.…”

Section: Discussionmentioning

confidence: 91%

Japanese encephalitis virus infection modulates the expression of suppressors of cytokine signaling (SOCS) in macrophages: Implications for the hosts’ innate immune response

Kundu

Dutta

Nazmi

et al. 2013

Cellular Immunology

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Section: Discussionmentioning

confidence: 91%

Japanese encephalitis virus infection modulates the expression of suppressors of cytokine signaling (SOCS) in macrophages: Implications for the hosts’ innate immune response

Kundu

Dutta

Nazmi

et al. 2013

Cellular Immunology

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“…This viral-induced redistribution may either interfere with the host epigenetic status or favour ASFV replication as reported for other viral infections [ 69 ]. Even though the role of HDAC6 in ASFV cytoplasmic factories formation is still to be proven [ 70 ], our findings on class I HDACs raise the possibility of using HDAC I inhibitors to disrupt ASFV infection, as demonstrated in other viral infections [ 71 , 72 ].…”

Section: Discussionmentioning

confidence: 95%

Alterations of Nuclear Architecture and Epigenetic Signatures during African Swine Fever Virus Infection

Simões

Rino

Pinheiro

et al. 2015

Viruses

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Viral interactions with host nucleus have been thoroughly studied, clarifying molecular mechanisms and providing new antiviral targets. Considering that African swine fever virus (ASFV) intranuclear phase of infection is poorly understood, viral interplay with subnuclear domains and chromatin architecture were addressed. Nuclear speckles, Cajal bodies, and promyelocytic leukaemia nuclear bodies (PML-NBs) were evaluated by immunofluorescence microscopy and Western blot. Further, efficient PML protein knockdown by shRNA lentiviral transduction was used to determine PML-NBs relevance during infection. Nuclear distribution of different histone H3 methylation marks at lysine’s 9, 27 and 36, heterochromatin protein 1 isoforms (HP1α, HPβ and HPγ) and several histone deacetylases (HDACs) were also evaluated to assess chromatin status of the host. Our results reveal morphological disruption of all studied subnuclear domains and severe reduction of viral progeny in PML-knockdown cells. ASFV promotes H3K9me3 and HP1β foci formation from early infection, followed by HP1α and HDAC2 nuclear enrichment, suggesting heterochromatinization of host genome. Finally, closeness between DNA damage response factors, disrupted PML-NBs, and virus-induced heterochromatic regions were identified. In sum, our results demonstrate that ASFV orchestrates spatio-temporal nuclear rearrangements, changing subnuclear domains, relocating Ataxia Telangiectasia Mutated Rad-3 related (ATR)-related factors and promoting heterochromatinization, probably controlling transcription, repressing host gene expression, and favouring viral replication.

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“…Finally, transcription factors such as interferon regulated factor 3 (IRF3)/IRF7 [ 36 , 75 , 86 , 90 – 92 ], activator protein 1 [ 87 ] and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) [ 38 , 39 , 70 , 73 , 75 , 87 ] are found to be implicated during JEV infection. In rat microglia, inhibition of NF-κB abrogates the production of TNF-α and IL-1β by rat microglia [ 88 ].…”

Section: Molecular Components Of Jev Recognitionmentioning

confidence: 99%

“…Importantly, the activity of inflammatory components have also been described to depend on the janus kinase-signal transducer and activator of transcription (JAK-STAT) signalling pathway in JEV infection. This requires the activation of STAT1 [ 24 , 36 , 92 ] and the expression of IFN-dependent and IFN-independent IFN-stimulated genes [ 36 , 37 ].…”

Section: Molecular Components Of Jev Recognitionmentioning

confidence: 99%

Regulation of inflammation in Japanese encephalitis

Lannes

Summerfield

Filgueira

2017

J Neuroinflammation

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Background: Uncontrolled inflammatory response of the central nervous system is a hallmark of severe Japanese encephalitis (JE). Although inflammation is necessary to mount an efficient immune response against virus infections, exacerbated inflammatory response is often detrimental. In this context, cells of the monocytic lineage appear to be important forces driving JE pathogenesis. Main body: Brain-infiltrating monocytes, macrophages and microglia play a major role in central nervous system (CNS) inflammation during JE. Moreover, the role of inflammatory monocytes in viral neuroinvasion during JE and mechanisms of cell entry into the CNS remains unclear. The identification of cellular and molecular actors in JE inflammatory responses may help to understand the mechanisms behind excessive inflammation and to develop therapeutics to treat JE patients. This review addresses the current knowledge about mechanisms of virus neuroinvasion, neuroinflammation and therapeutics critical for JE outcome. Conclusion: Understanding the regulation of inflammation in JE is challenging. Elucidation of the remaining open questions will help to the development of therapeutic approaches avoiding detrimental inflammatory responses in JE.

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Histone deacetylase inhibition by Japanese encephalitis virus in monocyte/macrophages: A novel viral immune evasion strategy

Cited by 19 publications

References 37 publications

Japanese encephalitis virus infection modulates the expression of suppressors of cytokine signaling (SOCS) in macrophages: Implications for the hosts’ innate immune response

Japanese encephalitis virus infection modulates the expression of suppressors of cytokine signaling (SOCS) in macrophages: Implications for the hosts’ innate immune response

Alterations of Nuclear Architecture and Epigenetic Signatures during African Swine Fever Virus Infection

Regulation of inflammation in Japanese encephalitis

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