Lack of Fas/FasL Does Not Protect from Latent Herpes Simplex 1 Infection but Decreases Virus-Induced Neurodegeneration.

ABSTRACT: Many studies have shown an association between herpes simplex virus type 1 (HSV-1) infection and the development of neurodegeneration processes later in life, such as Alzheimer's disease. The Fas/FasL death pathway plays an important role in the complex regulation of the local inflammatory response and mounting of the specific antiviral response in HSV-1 infection. Here, we applied a mouse model of latent HSV-1 neuroinfection to Fas- and FasL-deficient mice (lpr and gld) to explore whether the lack of functional Fas/FasL pathway protects from inflammation-related neurodegeneration. The latently infected Fas- and FasL-deficient mice (lpr and gld) were not protected from virus replication despite the accumulation of virus-specific cytotoxic T cells. However, the lack of Fas/FasL pathway decr

SUBMITTER: Patrycy M 

PROVIDER: S-EPMC12730924 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature