| First Author | De Chiara G | Year | 2019 |
| Journal | PLoS Pathog | Volume | 15 |
| Issue | 3 | Pages | e1007617 |
| PubMed ID | 30870531 | Mgi Jnum | J:284854 |
| Mgi Id | MGI:6391854 | Doi | 10.1371/journal.ppat.1007617 |
| Citation | De Chiara G, et al. (2019) Recurrent herpes simplex virus-1 infection induces hallmarks of neurodegeneration and cognitive deficits in mice. PLoS Pathog 15(3):e1007617 |
| abstractText | Herpes simplex virus type 1 (HSV-1) is a DNA neurotropic virus, usually establishing latent infections in the trigeminal ganglia followed by periodic reactivations. Although numerous findings suggested potential links between HSV-1 and Alzheimer's disease (AD), a causal relation has not been demonstrated yet. Hence, we set up a model of recurrent HSV-1 infection in mice undergoing repeated cycles of viral reactivation. By virological and molecular analyses we found: i) HSV-1 spreading and replication in different brain regions after thermal stress-induced virus reactivations; ii) accumulation of AD hallmarks including amyloid-beta protein, tau hyperphosphorylation, and neuroinflammation markers (astrogliosis, IL-1beta and IL-6). Remarkably, the progressive accumulation of AD molecular biomarkers in neocortex and hippocampus of HSV-1 infected mice, triggered by repeated virus reactivations, correlated with increasing cognitive deficits becoming irreversible after seven cycles of reactivation. Collectively, our findings provide evidence that mild and recurrent HSV-1 infections in the central nervous system produce an AD-like phenotype and suggest that they are a risk factor for AD. |
