Electronic Poster | Session 1
002 – Assessment of a potential relationship between Herpes simplex virus type-1 latent infection of the central nervous system and host susceptibility to experimental autoimmune encephalomyelitis.
Luisa Fernanda Duarte (1) – Máximo Diaz (2, 3) – Cecilia Opazo (2, 3) – Bárbara Gutiérrez (2, 3) – María José Altamirano (1) – Omar Vallejos (1) – Susan M. Bueno (1) – Alexis M. Kalergis (1, 4) – Claudia A. Riedel (2, 3) – Pablo A. González (1)
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile (1) – Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile (2) – Laboratorio de Endocrino-Inmunología, Departamento de Ciencias Biológicas, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile (3) – Departamento de Endocrinología, Escuela de Medicina, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile (4)
Multiple sclerosis is an autoimmune inflammatory disease characterized by the infiltration of autoreactive immune cells into the central nervous system (CNS). Although the etiology of this disease is still unknown, latent viral infections have been defined as possible environmental triggers, which may play a role in the pathogenesis and disease. Herpes simplex virus type 1 (HSV-1) is a pathogen widely distributed in the population, with nearly two-thirds of the world population infected with this virus. Importantly, HSV-1 can reach the brain throughout life and infect neurons in this tissue in a latent form without inducing clinical symptoms. Accumulating evidence suggests that asymptomatic HSV-1 infection of the CNS may lead to neurodegenerative disorders. However, despite epidemiologic and clinical findings suggesting a relationship between HSV-1 and multiple sclerosis, the potential contribution of latent HSV-1 in the CNS and mechanism have not been elucidated. At present, we are evaluating whether exposure of the CNS to a sub-lethal infection with HSV-1 modulates the severity of experimental autoimmune encephalomyelitis (EAE) in a mouse model, a widely used experimental model that shares hallmarks with multiple sclerosis in humans. This study should help better understand possible relationships between HSV-1 latent infection of the CNS and multiple sclerosis onset and severity, and could contribute to the identification of new molecular targets or therapies to prevent or treat multiple sclerosis and its relapses.