| Autor: |
Martinez Viedma MDP; J. Craig Venter Institute, 4120 Capricorn Lane, La Jolla, CA 92037, USA. pviedma@jcvi.org., Pickett BE; J. Craig Venter Institute, 9605 Medical Center Drive, Rockville, MD 20850, USA. bpickett@jcvi.org. |
| Jazyk: |
angličtina |
| Zdroj: |
Viruses [Viruses] 2018 Nov 18; Vol. 10 (11). Date of Electronic Publication: 2018 Nov 18. |
| DOI: |
10.3390/v10110649 |
| Abstrakt: |
Zika virus (ZIKV) is a neuropathic virus that causes serious neurological abnormalities such as Guillain-Barre syndrome in adults and congenital Zika syndrome (CZS) in fetuses, which makes it an important concern for global human health. A catalogue of cells that support ZIKV replication, pathogenesis, and/or the persistence of the virus still remains unknown. Here, we studied the behavior of the virus in human placenta (JEG-3) and human microglia (HMC3) cell lines in order to better understand how different host tissues respond during infection. We quantified the host transcriptional response to ZIKV infection in both types of cells at 24 and 72 h post-infection. A panel of 84 genes that are involved in the innate or adaptive immune responses was used to quantify differential expression in both cell lines. HMC3 cells showed a unique set of significant differentially expressed genes (DEGs) compared with JEG-3 cells at both time points. Subsequent analysis of these data using modern pathway analysis methods revealed that the TLR7/8 pathway was strongly inhibited in HMC3 cells, while it was activated in JEG-3 cells during virus infection. The disruption of these pathways was subsequently confirmed with specific small interfering RNA (siRNA) experiments that characterize their role in the viral life cycle, and may partially explain why ZIKV infection in placental tissue contributes to extreme neurological problems in a developing fetus. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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