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Updated: Jun 9, 2025
Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice
Published on: October 17, 2018
RT-qPCR Analysis of Inflammatory & Apoptotic Factors-Related Gene Expression in ZIKV-Infected IFNAR1-/- Mice
Dibakar Chowdhury1, Xiao Han Lin1, Sang Heui Seo2,3
1Laboratory of Influenza Research, College of Veterinary Medicine, Chungnam National University, Daejeon, 34134, Republic of Korea.
Abstract:
ZIKV was a mosquito-borne neglected tropical pathogen until it spread into the Pacific and South America, followed by large human outbreaks related to congenital abnormalities in neonates and neurological disorders in adults. The following study used the C57BL/6 IFNAR1 receptor knockout (IFN AR1-/-) mouse model to understand the role of selected cytokines and apoptotic factors in the pathogenicity of ZIKV strain PRVABC59. Mice infected with 102 particles of Zika viruses died until 9 days post infection. The brain, spleen, and lung were collected from intramuscularly infected mice on day 6 post infection (pi) to quantify the mRNA expression of targeted cytokines and apoptosis-mediated factors by RT-qPCR. Upregulation of IL-6, IL-17α, IFN-α, and IFN-β were found in the brain and lung of infected mice. IFN-γ was also significantly upregulated in the infected brain and spleen. The collective findings from our study indicate that a strong immune response was developed against ZIKV PRVABC59 in the infected mice brain.
Insights
Zika virus (ZIKV) infection in mice triggers a robust immune response, with significant upregulation of key cytokines like IL-6 and interferons (IFN-α, IFN-β, IFN-γ) in the brain, lung, and spleen.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- Zika virus (ZIKV) emerged as a significant global health threat, causing severe congenital abnormalities and neurological disorders.
- Understanding the host immune response to ZIKV is crucial for developing effective countermeasures.
Purpose of the Study:
- To investigate the role of cytokines and apoptotic factors in ZIKV pathogenicity using a mouse model.
- To analyze the immune response in different organs following ZIKV infection.
Main Methods:
- Utilized the C57BL/6 IFNAR1 receptor knockout (IFNAR1-/-) mouse model for ZIKV infection.
- Quantified mRNA expression of cytokines and apoptosis-related factors via RT-qPCR in brain, spleen, and lung tissue.
Main Results:
- Infected mice exhibited mortality within 9 days post-infection.
- Significant upregulation of Interleukin-6 (IL-6), Interleukin-17α (IL-17α), Interferon-alpha (IFN-α), and Interferon-beta (IFN-β) in the brain and lung.
- Elevated Interferon-gamma (IFN-γ) levels observed in the brain and spleen.
Conclusions:
- The study demonstrates a strong innate immune response against ZIKV PRVABC59 in the infected mouse brain.
- Cytokine upregulation suggests a key role in the host's defense mechanism against ZIKV.
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