期刊
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2022.948980
关键词
immune profiles; ZIKV; variable pathogenicity; transcriptome; multi-organization
资金
- National key research and development program [2021YFC2301300]
- CAMS Innovation Fund for Medical Sciences [2021-I2M-1-061]
- National Natural Science Foundation of China [92169106, 31900472]
- special research fund for central universities, Peking Union Medical College [2021-PT180-001]
- Suzhou science and technology development plan [szs2020311]
The study investigates the immune response to Zika virus infection and its impact on neural tissue damage. The results suggest that Zika viruses with high pathogenicity can induce sustained activation of the immune system, leading to nerve tissue damage.
The Zika virus is responsible for neurological diseases such as microcephaly, Guillain-Barre syndrome, neuropathy, and myelitis in human adults and children. Previous studies have shown that the Zika virus can infect nerve progenitor cells and interfere with neural development. However, it is unclear how the immune system responds to infection with Zika viruses with variable pathogenicity. Here, we used two Zika strains with relatively different pathogenicity, the Asian ancestral strain CAM/2010 and the America pandemic strain GZ01/2016, to infect the brains of mice. We found that both strains elicited a strong immune response. Notably, the strain with relatively high pathogenicity, GZ01/2016, caused more intense immune regulation, with stronger CD8+ T cell and macrophage activation at 14 days post infection (dpi), as well as a greater immune gene disturbance. Notably, several TNF family genes were upregulated at 14 dpi, including Tnfrsf9, Tnfsf13, Tnfrsf8, Cd40, and Tnfsf10. It was notable that GZ01/2016 could maintain the survival of nerve cells at 7dpi but caused neurological disorders at 14dpi. These results indicate that Zika viruses with high pathogenicity may induce sustained activation of the immune system leading to nerve tissue damage.
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