SAEDNEWS: New research by American scientists has found that the herpes virus, commonly known as cold sore virus (herpesvirus), is a human DNA virus classified under human herpesvirus types 6A (HHV-6A) and 7 (HHV-7).
According to Saednews, Scientists have found in a new study that individuals carrying herpes simplex viruses may be up to twice as likely to develop Alzheimer’s disease, suggesting that viral infections could play a potential role in the progression of brain disorders.
Recent research by American scientists indicates that human herpesviruses—particularly HHV-6A and HHV-7—are present at higher levels in the brains of Alzheimer’s patients compared to those without the disease. These viruses belong to the family of human DNA herpesviruses and have now been detected in significant association with neurodegenerative conditions.
The study revealed a complex network of unexpected interactions between specific viruses and multiple aspects of Alzheimer’s disease. Researchers examined how these viruses may influence particular genes and proteins in brain cells, identifying links with amyloid plaques, neurofibrillary tangles, and the severity of cognitive decline and dementia-related symptoms.
Richard J. Hodes, Director of the U.S. National Institute on Aging, said the findings support a growing hypothesis in neuroscience: “Our main assumption is that viruses play a role in brain-related diseases and disorders. This idea is not new, but this research provides strong evidence supporting it.”
Joel Dudley from the Icahn School of Medicine at Mount Sinai also noted that the work helps define biological networks that could guide new experimental models of Alzheimer’s disease, particularly those involving microbial defense and innate immune function in its pathophysiology.
Researchers found significant overlap between host antiviral responses and genes associated with Alzheimer’s risk. Viral activity appears to influence DNA, RNA, and protein-level processes in the brain, potentially contributing to disease development.
In a large-scale analysis, the research team studied RNA sequencing data from more than 600 post-mortem brain samples, comparing individuals with and without Alzheimer’s disease. Using computational methods, they identified a network of viral accumulation and interactions with Alzheimer’s-related biological markers. They also analyzed 800 additional samples, observing consistent increases in HHV-6A and HHV-7 levels in Alzheimer’s-affected brains.
The findings, published in the journal Neuron, suggest that specific viral strains may directly influence either the risk or progression of Alzheimer’s disease, offering a new framework for understanding how the disease may emerge and evolve at the individual level.
