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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
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ZIKV infection regulates inflammasomes pathway for replication in monocytes
S F Khaiboullina1,2, T Uppal1, R Sarkar1
1Department of Microbiology and Immunology, University of Nevada, Reno School of Medicine, Reno, NV, USA.
Scientific Reports
|November 24, 2017
Summary
Zika virus (ZIKV) infects monocytes, potentially aiding fetal transmission. ZIKV manipulates inflammasome pathways, hindering innate antiviral defenses and suggesting inflammasomes regulate ZIKV transcription.
Area of Science:
- Virology
- Immunology
- Developmental Biology
Background:
- Zika virus (ZIKV) causes microcephaly by crossing the placental barrier.
- The mechanism of ZIKV trans-placental dissemination is not fully understood.
- Monocytes are immune cells capable of crossing tissue barriers.
Purpose of the Study:
- To investigate if monocytes assist ZIKV dissemination to the fetus.
- To determine the interaction between ZIKV, monocytes, and inflammasome pathways.
Main Methods:
- Infection of human monocytes with two ZIKV strains (South American and Nigerian).
- Analysis of viral replication and gene expression changes in infected monocytes.
- Assessment of inflammasome pathway components (NLRP3, ASC, caspase 1, IL-1, IL-18) and interferon-related genes (IFNα, MxA).
Main Results:
- ZIKV infects and replicates in monocytes and macrophages, modulating numerous cellular genes.
- ZIKV targets inflammasome pathways, evidenced by altered transcript levels of NLRP3, ASC, caspase 1, IL-1, and IL-18.
- ZIKV infection suppressed IFNα and MxA, indicating evasion of innate antiviral responses; inflammasome inhibition increased these antiviral markers.
Conclusions:
- Monocytes may play a role in ZIKV's trans-placental spread.
- ZIKV manipulates host inflammasome pathways to evade innate immunity.
- Inflammasomes appear to regulate ZIKV transcription.
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