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 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.
Study finds no link between the abundance of herpes viral DNA or RNA and an increased risk of developing Alzheimer's disease.
The herpes simplex virus 1, the virus responsible for cold sores, may account for 50% of Alzheimer's disease cases. HSV1 causes protein deposits which are characteristic of Alzheimer's disease. Findings also reveal antiviral treatments can help to reduce the risk of developing Alzheimer's in those with HSV1.
A new study reports herpes virus utilizes ancient RNA to proliferate, mimicking the same process tumors have been found to manipulate. The findings could have implications for new treatment options and also may shed light on neurodegenerative diseases.
A new study reports people with schizophrenia have higher levels of antibodies against Epstein-Barr virus, a herpes virus that causes mononucleosis. Researchers propose two explanations for the link to the heightened immune response to the virus: schizophrenia may alter the immune system, making patients more susceptible to EBV, or EBV may increase the risk of developing schizophrenia.
A new study looks at the possible causal link between the herpes virus and Alzheimer's disease. Researchers report antiviral drugs significantly reduce the risk of developing dementia in patients with severe herpes infections.