Send to

Choose Destination
Cell Rep. 2017 Feb 7;18(6):1473-1483. doi: 10.1016/j.celrep.2017.01.027.

Astrocytes Resist HIV-1 Fusion but Engulf Infected Macrophage Material.

Author information

The Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
Division of Structural Biology, University of Oxford, The Henry Wellcome Building for Genomic Medicine, Headington, Oxford OX3 7BN, UK; Wellcome Trust Centre for Human Genetics, Cellular Imaging Core, University of Oxford, Oxford OX3 7BN, UK.
Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
The Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. Electronic address:


HIV-1 disseminates to diverse tissues and establishes long-lived viral reservoirs. These reservoirs include the CNS, in which macrophage-lineage cells, and as suggested by many studies, astrocytes, may be infected. Here, we have investigated astrocyte infection by HIV-1. We confirm that astrocytes trap and internalize HIV-1 particles for subsequent release but find no evidence that these particles infect the cell. Astrocyte infection was not observed by cell-free or cell-to-cell routes using diverse approaches, including luciferase and GFP reporter viruses, fixed and live-cell fusion assays, multispectral flow cytometry, and super-resolution imaging. By contrast, we observed intimate interactions between HIV-1-infected macrophages and astrocytes leading to signals that might be mistaken for astrocyte infection using less stringent approaches. These results have implications for HIV-1 infection of the CNS, viral reservoir formation, and antiretroviral therapy.


HIV-1; astrocyte; brain; fusion; macrophage; phagocytosis

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center