Authors: Martha Powell, Future Science Group
Research from Yale University (CT, USA) has shed light on the mechanisms behind the neurological complications of Zika virus, suggesting that it’s the host immune response, rather than the virus itself, which cause these symptoms.
The study, published recently in Nature Microbiology, used mouse models to uncover the mechanisms behind Zika infection. The mice had the type I interferon receptor knocked out, a model that exhibits high viral burden in the nervous system, and were used to examine the spread of infection.
The researchers discovered that when the virus crosses the blood–brain barrier and infects astrocytes, this triggers an influx CD8 T cells to the brain. They observed that, while the T cells clearly limit the infection of nerve cells, they may also initiate Zika-associated paralysis.
Akiko Iwasaki from Yale University, who led the study, commented: “The immune cells that are generated by infection start attacking our own neurons. The damage is not occurring through the virus infection, but rather the immune response to the virus.”
The study uncovers a mechanism of Zika neuropathogenesis in this susceptible animal model, suggesting a blood–brain barrier breakdown and T-cell mediated pathology as possible underpinnings of neurological conditions in Zika infection. The findings could lead to new methods to treat patients with Zika-related conditions, including Guillain-Barré syndrome.
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Sources: Jurado KA, Yockey LJ, Wong PW, Lee S, Huttner AJ, Iwasaki A. Antiviral CD8 T cells induce Zika-virus-associated paralysis in mice. Nat. Microbiol. doi:10.1038/s41564-017-0060-z (2017) (Epub ahead of print); www.eurekalert.org/emb_releases/2017-11/yu-znd111617.php