| Literature DB >> 32386801 |
Maria Elena Marcocci1, Giorgia Napoletani1, Virginia Protto1, Olga Kolesova1, Roberto Piacentini2, Domenica Donatella Li Puma2, Patrick Lomonte3, Claudio Grassi2, Anna Teresa Palamara4, Giovanna De Chiara5.
Abstract
Herpes simplex virus-1 (HSV-1) establishes latency preferentially in sensory neurons of peripheral ganglia. A variety of stresses can induce recurrent reactivations of the virus, which spreads and then actively replicates to the site of primary infection (usually the lips or eyes). Viral particles produced following reactivation can also reach the brain, causing a rare but severe form of diffuse acute infection, namely herpes simplex encephalitis. Most of the time, this infection is clinically asymptomatic. However, it was recently correlated with the production and accumulation of neuropathological biomarkers of Alzheimer's disease. In this review we discuss the different cellular and molecular mechanisms underlying the acute and long-term damage caused by HSV-1 infection in the brain.Entities:
Keywords: Alzheimer’s disease; HSV-1; encephalitis; herpes simplex virus-1; neurodegeneration latency/reactivation
Mesh:
Year: 2020 PMID: 32386801 DOI: 10.1016/j.tim.2020.03.003
Source DB: PubMed Journal: Trends Microbiol ISSN: 0966-842X Impact factor: 17.079