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- Title
Zika Virus and Host Interactions: From the Bench to the Bedside and Beyond.
- Authors
Limonta, Daniel; Hobman, Tom C.
- Abstract
Keywords: zika; host; interferon; cell death; placenta; NS5; peroxisome; mosquito; guinea pig; tight junction EN zika host interferon cell death placenta NS5 peroxisome mosquito guinea pig tight junction 2463 1 11/30/20 20201101 NES 201101 Before the emergence of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), the causative agent of the current COVID-19 (coronavirus disease 2019) pandemic [[1]], another RNA virus, Zika virus (ZIKV) belonging to the flavivirus family, re-emerged and was declared a Public Health Emergency of International Concern by the WHO in February 2016 because of clusters of microcephaly cases and other neurological disorders in Brazil [[2]]. In this Special Issue, Martinez-Rojas et al. [[5]] showed how extracellular vesicles (EVs) released from ZIKV-infected mosquito cells (C6/36) may affect not only bystander mosquito cells, but also human cell types, that are important ZIKV targets. Roby et al. [[12]] showed that NS5 of ZIKV as well as those from other flaviviruses, such as West Nile virus and Japanese encephalitis virus, antagonize host cell Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling downstream of interferons / . The authors demonstrated that ZIKV infection depletes peroxisomes in human fetal brain cells, while the peroxisome biogenesis factor PEX11B restricts ZIKV replication likely by increasing peroxisome numbers and enhancing downstream antiviral interferon signaling.
- Subjects
ZIKA virus; ZIKA Virus Epidemic, 2015-2016; ZIKA virus infections; TROPHOBLAST; BCL-2 proteins; COVID-19; JAPANESE encephalitis viruses
- Publication
Cells (2073-4409), 2020, Vol 9, Issue 11, p2463
- ISSN
2073-4409
- Publication type
Editorial
- DOI
10.3390/cells9112463