Targeting the HIV-infected brain to improve ischemic stroke outcome
Luc Bertrand (),
Fannie Méroth,
Marie Tournebize,
Ana Rachel Leda,
Enze Sun and
Michal Toborek ()
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Luc Bertrand: Department of Biochemistry and Molecular Biology
Fannie Méroth: Department of Biochemistry and Molecular Biology
Marie Tournebize: Department of Biochemistry and Molecular Biology
Ana Rachel Leda: Department of Biochemistry and Molecular Biology
Enze Sun: Department of Biochemistry and Molecular Biology
Michal Toborek: Department of Biochemistry and Molecular Biology
Nature Communications, 2019, vol. 10, issue 1, 1-14
Abstract:
Abstract HIV-associated cerebrovascular events remain highly prevalent even in the current era of antiretroviral therapy (ART). We hypothesize that low-level HIV replication and associated inflammation endure despite antiretroviral treatment and affect ischemic stroke severity and outcomes. Using the EcoHIV infection model and the middle cerebral artery occlusion as the ischemic stroke model in mice, we present in vivo analysis of the relationship between HIV and stroke outcome. EcoHIV infection increases infarct size and negatively impacts tissue and functional recovery. Ischemic stroke also results in an increase in EcoHIV presence in the affected regions, suggesting post-stroke reactivation that magnifies pro-inflammatory status. Importantly, ART with a high CNS penetration effectiveness (CPE) is more beneficial than low CPE treatment in limiting tissue injury and accelerating post-stroke recovery. These results provide potential insight for treatment of HIV-infected patients that are at risk of developing cerebrovascular disease, such as ischemic stroke.
Date: 2019
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10046-x
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DOI: 10.1038/s41467-019-10046-x
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