Tu165 - Asymptomatic Brain Infection with Herpes Simplex Virus Induces the Expression of Senescence-related Biomarkers in the Central Nervous System

Luisa Duarte – Pontificia Universidad Católica de Chile; Verónica Villalobos – Millennium Institute on Immunology and Immunotherapy, Universidad de Chile; Mónica Farías – Millennium Instiute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile; María Rángel – Millennium Instititute on Immunology and Immunotherapy, Universidad Andrés Bello; Enrique González – Millennium Institute on Immunology and Immunotherapy, Universidad Andrés Bello; Claudia Riedel – Millennium Institute on Immunology and Immunotherapy, Universidad Andres Bello; Susan Bueno – Millennium Institute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile; Alexis Kalergis – 1Millennium Institute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile; Mónica Cáceres – 1Millennium Institute on Immunology and Immunotherapy, Universidad de Chile

Abstract Text: Previously, we have described that asymptomatic brain infection with herpes simplex virus type 1 (HSV-1) induces an earlier onset, and more severe form of experimental autoimmune encephalomyelitis (EAE) in mice, which is an autoimmune disease related to the central nervous system (CNS) that has biological similarities with multiple sclerosis (MS) in humans. Noteworthy, asymptomatic brain infection with HSV-1 in humans is common, and likely leads to persistent inflammation in this tissue. However, the effects of this type of infection in the brain and CNS are not fully understood. Here, we explored the expression of cellular senescence biomarkers in the CNS after asymptomatic brain infection with HSV-1, with or without later EAE induction. Importantly, we observe a significant increase in senescence markers in brain and spinal cord after infection and/or EAE, which varies depending on the treatment. Overall, these findings suggest that asymptomatic brain infection with HSV-1 induces senescence in the CNS, which in time could contribute to increased onset or severity of neurodegenerative diseases. Additional studies related to these findings could provide a better understanding of the long-term effects of persistent CNS infection with neurotropic pathogens as HSV-1 and minimize their effects over these tissues.