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Zika Virus Infection of Cultured Human Fetal Brain Neural Stem Cells for Immunocytochemical Analysis
Published on: February 5, 2018
Simian fetal brain progenitor cells for studying viral neuropathogenesis
Naoko Iwata1, Hiroaki Yoshida, Minoru Tobiume
1Department of Pathology, National Institute of Infectious Disease, Tokyo, Japan.
Journal of Neurovirology
|April 25, 2007
Summary
This study introduces a novel simian brain progenitor cell culture system for investigating simian immunodeficiency virus (SIV) infection. The findings confirm SIV replication in glial and neuronal cells, advancing research into HIV-1 neuropathogenesis.
Area of Science:
- Neuroscience
- Virology
- Cell Biology
Background:
- Human immunodeficiency virus type 1 (HIV-1) pathogenesis in the brain remains poorly understood.
- Simian immunodeficiency virus (SIV) infection in macaques serves as a crucial animal model for HIV-1.
- Studying direct viral effects on neural cells requires a culture system devoid of immune and vascular cells.
Purpose of the Study:
- To characterize simian brain progenitor cells (BPCs) from cynomolgus monkeys.
- To establish and validate a BPC-derived cell culture for SIV infection studies.
- To investigate the direct impact of SIV on neuronal and glial cells.
Main Methods:
- Neurosphere assay for isolating and expanding simian BPCs.
- Immunocytochemistry, flow cytometry, and RT-PCR for characterizing BPCs.
- SIV infection of BPC-derived cultures and analysis of viral replication and cell tropism.
Main Results:
- Simian BPCs possess self-renewal and multilineage differentiation capabilities.
- BPC-derived cultures express SIV entry receptors (CD4, CXCR4, CCR5, etc.) and support productive SIV replication.
- Infected cells were primarily glial (GFAP-positive) and expressed SIV antigens.
Conclusions:
- Simian BPC-derived cultures provide a suitable model for studying SIV infection in neuronal and glial cells.
- This model facilitates direct investigation of SIV's neurotropic effects.
- The findings contribute to understanding HIV-1 neuropathogenesis.
