Researchers discovered mutations of the OPTN gene resulted in increased herpesvirus 1 growth in the brains of mice, leading to the death of local neurons. This resulted in accelerated neurodegeneration. OPTN deficiency was also associated with impairments in immune response. While these findings are specific to the HSV-1 virus, researchers believe the findings may apply to up to eight herpesvirus infections.
A new study reveals why some people with the herpes simplex 1 virus experience painful lesions, while others have no symptoms and yet still spread the infection. Researchers say the difference could be a result of how variations in the way certain strains of HSV-1 activate gene expression in neurons.
Herpes virus simplex type 1 infection can spread to the fetal brain during pregnancy, resulting in an increased risk of neurodevelopmental disabilities and neurological deficits.
Study identifies a specific type of immune cell that induces inflammation in herpes simplex virus (HSV) encephalitis.
A 3D human tissue culture model demonstrated a possible causal relationship between Alzheimer's disease and herpes simplex virus 1 (HSV-1) infection. 40 Alzheimer's associated genes were over-expressed in the HSV-1 infected brain tissue, including genes associated with the production of amyloid-beta.
Herpes simplex virus type 1 (HSV-1) and respiratory syncytial virus (RSV) interact with biological fluids, creating a coat of proteins around the viral surface. This results in the viruses becoming more infectious and can contribute to the formation of amyloid plaques. In animal models, researchers found these viruses can bind to amyloid proteins, which aggregate into plaques that contribute to Alzheimer's disease. HSV-1 is able to accelerate the transformation of soluble amyloid proteins into amyloid plaques.
Herpes and other viruses that attack the nervous system may thrive by disrupting cell function in order to hijack a...