Congratulations to Luc for his excellent paper being accepted in Nature Communications (IF 12.353)! This work was done with two students from the Université Catholique de Lyon (Fannie Méroth and Marie Tournebize) and two postdoctoral scholars in the laboratory (Ana Leda and Enze Sun).
Bertrand L, Méroth F, Tournebize M, Leda AR, Sun E, Toborek M. Targeting the HIV-infected brain to improve ischemic stroke outcome. Nat Commun. 2019 May 1;10(1):2009. doi: 10.1038/s41467-019-10046-x.
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.
Brain coronal section demonstrating severe tissue damage observed in a HIV-1 infected mouse 4 days after ischemic stroke. The area of injury (absence of green) is surrounded by inflammatory cells (red). MAP2, marker of healthy neurons, is represented in green; Iba1, marker of monocyte/microglial cells, is represented in red; Hoechst, nuclear marker, is represented in blue.