Journal
TRENDS IN MICROBIOLOGY
Volume 28, Issue 10, Pages 808-820Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.tim.2020.03.003
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Funding
- Italian Ministry of Instruction, University and Research: PRIN [20179JHMZ_006, 2015W729WH_005, 2015W729WH_001, 2017A9MK4R_004]
- French National Research Agency [ANR-18-CE15-0014-01]
- Ateneo 2019 [RP11916B8696E5EC]
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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.
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