The activity of Aurora kinase B is required for dengue virus release

Perez-Olais, Jose-Humberto; Ruíz-Jiménez, Fernando; Calderón-Garcia, Esther J.; Jesús-González, Luis Adrián De; Hernández‐Rivas, Rosaura; Ángel, Rosa M. del

doi:10.1016/j.virusres.2019.197777

Cited by 7 publications

(5 citation statements)

References 34 publications

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“…For instance, the IRE1 kinase inhibitor KIRA6 reduces viral RNA levels in ZIKV infected the human HeLa cell line [90]. DENV infection has been widely reported to be inhibited by inhibitors of different members of the group, as exemplified by treatment with pyruvate kinase PKM2 inhibitor in DENV-infected U937 cells [84], the AurKB inhibitor ZM 447439 in DENV-infected Huh-7 cells [85], and the NAK family inhibitors, sunitinib and erlotinib (AAK1 and GAK subfamilies inhibitors respectively) in DENV-infected Huh-7 cells [18]. PKR is modulated by cyclophilin A, triggering antiviral responses to inhibit HCV infection in Huh 7 cell line [119], and the PKR2 inhibitor HA1077, also known as fasudil restricted HCV replication in mice [105].…”

Section: Other Pksmentioning

confidence: 99%

Potential for Protein Kinase Pharmacological Regulation in Flaviviridae Infections

Blázquez

Saiz

2020

IJMS

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Protein kinases (PKs) are enzymes that catalyze the transfer of the terminal phosphate group from ATP to a protein acceptor, mainly to serine, threonine, and tyrosine residues. PK catalyzed phosphorylation is critical to the regulation of cellular signaling pathways that affect crucial cell processes, such as growth, differentiation, and metabolism. PKs represent attractive targets for drugs against a wide spectrum of diseases, including viral infections. Two different approaches are being applied in the search for antivirals: compounds directed against viral targets (direct-acting antivirals, DAAs), or against cellular components essential for the viral life cycle (host-directed antivirals, HDAs). One of the main drawbacks of DAAs is the rapid emergence of drug-resistant viruses. In contrast, HDAs present a higher barrier to resistance development. This work reviews the use of chemicals that target cellular PKs as HDAs against virus of the Flaviviridae family (Flavivirus and Hepacivirus), thus being potentially valuable therapeutic targets in the control of these pathogens.

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Section: Other Pksmentioning

confidence: 99%

Potential for Protein Kinase Pharmacological Regulation in Flaviviridae Infections

Blázquez

Saiz

2020

IJMS

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“…Aurora kinases activities are important for the replication of a variety of diverse viruses ( 35 – 37 ). These studies demonstrate, for the first time, a potential role for aurora kinases in the HSV-1 lytic life cycle.…”

Section: Discussionmentioning

confidence: 99%

“…During dengue virus replication, aurora B kinase is involved in the viral morphogenesis or release of viral particles. Silencing of aurora B kinase leads to a significant decrease in viral yields ( 36 ). Epstein-Barr virus infection upregulates aurora B kinase expression by enhancing its promoter activity early during infection ( 37 ).…”

Section: Introductionmentioning

confidence: 99%

Inhibitors of One or More Cellular Aurora Kinases Impair the Replication of Herpes Simplex Virus 1 and Other DNA and RNA Viruses with Diverse Genomes and Life Cycles

Pfannenstiel

Pant

et al. 2023

Microbiol Spectr

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“…Recently, multiple viruses from diverse families including Epstein Barr virus (EBV) and Kaposi’s Sarcoma virus (KSHV), hepatitis C virus (HCV) and dengue virus were shown to be affected by or to modulate AURKB activity [ 126 – 129 ]. Of particular note, AURKB is critical for cytoplasmic assembly and plasma membrane budding of dengue virus [ 129 ]. These results are consistent with our observation that an unknown cytoplasmic role of interphase AURKB may regulate membrane function.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 virological synapse formation enhances infection spread by dysregulating Aurora Kinase B

et al. 2023

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HIV-1 spreads efficiently through direct cell-to-cell transmission at virological synapses (VSs) formed by interactions between HIV-1 envelope proteins (Env) on the surface of infected cells and CD4 receptors on uninfected target cells. Env-CD4 interactions bring the infected and uninfected cellular membranes into close proximity and induce transport of viral and cellular factors to the VS for efficient virion assembly and HIV-1 transmission. Using novel, cell-specific stable isotope labeling and quantitative mass spectrometric proteomics, we identified extensive changes in the levels and phosphorylation states of proteins in HIV-1 infected producer cells upon mixing with CD4+ target cells under conditions inducing VS formation. These coculture-induced alterations involved multiple cellular pathways including transcription, TCR signaling and, unexpectedly, cell cycle regulation, and were dominated by Env-dependent responses. We confirmed the proteomic results using inhibitors targeting regulatory kinases and phosphatases in selected pathways identified by our proteomic analysis. Strikingly, inhibiting the key mitotic regulator Aurora kinase B (AURKB) in HIV-1 infected cells significantly increased HIV activity in cell-to-cell fusion and transmission but had little effect on cell-free infection. Consistent with this, we found that AURKB regulates the fusogenic activity of HIV-1 Env. In the Jurkat T cell line and primary T cells, HIV-1 Env:CD4 interaction also dramatically induced cell cycle-independent AURKB relocalization to the centromere, and this signaling required the long (150 aa) cytoplasmic C-terminal domain (CTD) of Env. These results imply that cytoplasmic/plasma membrane AURKB restricts HIV-1 envelope fusion, and that this restriction is overcome by Env CTD-induced AURKB relocalization. Taken together, our data reveal a new signaling pathway regulating HIV-1 cell-to-cell transmission and potential new avenues for therapeutic intervention through targeting the Env CTD and AURKB activity.

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The activity of Aurora kinase B is required for dengue virus release

Cited by 7 publications

References 34 publications

Potential for Protein Kinase Pharmacological Regulation in Flaviviridae Infections

Potential for Protein Kinase Pharmacological Regulation in Flaviviridae Infections

Inhibitors of One or More Cellular Aurora Kinases Impair the Replication of Herpes Simplex Virus 1 and Other DNA and RNA Viruses with Diverse Genomes and Life Cycles

HIV-1 virological synapse formation enhances infection spread by dysregulating Aurora Kinase B

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