ArticleImmune network2019
Zika Virus Impairs Host NLRP3-mediated Inflammasome Activation in an NS3-dependent Manner.
Article in Immune network, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- NLRC5 restricts Japanese encephalitis virus replication and neuroinflammation by interacting with the viral NS3 protein in an IFN-γ-dependent manner.Journal of neuroinflammation · 2026Article
- The Flavivirus NS3 Protein: Its Multifaceted Roles and Therapeutic Potential.Journal of medical virology · 2026Review
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- Macrophage makeover extreme viral edition: mechanisms of immune subversion and therapeutic perspectives.The Journal of general virology · 2026Review
- Zika virus and host innate immunity: mechanisms of activation and evasion.Frontiers in immunology · 2026Review
- Aedes aegypti salivary gland extract enhances Zika virus replication through immune modulation.Memorias do Instituto Oswaldo Cruz · 2026Article
- Zika virus inhibits cell death by inhibiting the expression of NLRP3 and A20.Journal of virology · 2025Article
- Activation and evasion of inflammasomes during viral and microbial infection.Cellular and molecular life sciences : CMLS · 2025Review
- Viral reprogramming of glial metabolism as a driver of neuroinflammation.Frontiers in immunology · 2025Review
- Impaired NLRP3 inflammasome signaling diverts pyroptotic to apoptotic caspase activation in macrophages.Frontiers in immunology · 2025Article
- From defense to offense: Modulating toll-like receptors to combat arbovirus infections.Human vaccines & immunotherapeutics · 2024Review
- From viruses to cancer: exploring the role of the hepatitis C virus NS3 protein in carcinogenesis.Infectious agents and cancer · 2024Review
- Role of NLRP3 inflammasome in central nervous system diseases.Cell & bioscience · 2024Review
- Stimulator of Interferon Gene Agonists Induce an Innate Antiviral Response against Influenza Viruses.Viruses · 2024Article
- Zika Virus-A Reemerging Neurotropic Arbovirus Associated with Adverse Pregnancy Outcomes and Neuropathogenesis.Pathogens (Basel, Switzerland) · 2024Review
- Article
- Early transcriptomic changes at the skin interface during Powassan virus transmission byFrontiers in immunology · 2024Article
- Insights into Zika Virus Pathogenesis and Potential Therapeutic Strategies.Biomedicines · 2023Review
- Offspring affected withEmerging microbes & infections · 2023Article
- Autophagy and Inflammation: Regulatory Roles in Viral Infections.Biomolecules · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) is a mosquito-borne flavivirus associated with severe neurological disorders including Guillain-Barré syndrome and microcephaly. The host innate immune responses against ZIKV infection are essential for protection; however, ZIKV has evolved strategies to evade and antagonize antiviral responses via its nonstructural (NS) proteins. Here, we demonstrated that ZIKV infection unexpectedly inhibits NLRP3-dependent inflammasome activation in bone marrow-derived macrophages and mixed glial cells from mouse brain. ZIKV infection led to increased transcript levels of proinflammatory cytokines such as IL-1β and IL-6 via activating NF-κB signaling. However, ZIKV infection failed to trigger the secretion of active caspase-1 and IL-1β from macrophages and glial cells even in the presence of LPS priming or ATP costimulation. Intriguingly, ZIKV infection significantly attenuated NLRP3-dependent, but not absent in melanoma 2-dependent caspase-1 activation and IL-1β secretion from both cells. ZIKV infection further blocked apoptosis-associated speck-like protein containing a caspase recruitment domain oligomerization in LPS/ATP-stimulated macrophages. Interestingly, expression of ZIKV NS3 protein reduced NLRP3-mediated caspase-1 activation and IL-1β secretion in macrophages, whereas NS1 and NS5 proteins showed no effects. Furthermore, NLRP3 was found to be degraded by the overexpression of ZIKV NS3 in 293T cells. Collectively, these results indicate that ZIKV evades host NLRP3 inflammasome-mediated innate immune responses in macrophages and glial cells; this may facilitate ZIKV's ability to enhance the replication and dissemination in these cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.