WASHINGTON, June 21 (Xinhua) -- American researchers found that two strains of human herpesvirus were found in the brains of people with Alzheimer's disease at levels up to twice as high as in those without Alzheimer's.
A study published on Thursday in the journal Neuron revealed that human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) might play a role in regulatory genetic networks that are believed to lead to the brain disease.
Although the findings did not prove that the viruses directly cause its onset or progression, they have showed the viral DNA sequences and the activation of biological networks may interact with molecular, genetic and clinical aspects of Alzheimer's, according to the study.
This is also the first evidence that integration of HHV genomes into human brain genomes may be linked with the etiology of Alzheimer's. These viruses can cause encephalitis and other chronic conditions.
Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks.
The research group, including experts from Icahn School of Medicine at Mount Sinai and Arizona State University, performed RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer's to quantify which genes were present in the brain.
They examined the influence of each virus on specific genes and proteins in brain cells, and identified associations between specific viruses and amyloid plaques, neurofibrillary tangles, and clinical dementia severity.
To evaluate the robustness of their findings, the team incorporated a further 800 RNA sequencing samples, observing a persistent increase of HHV-6A and HHV-7 abundance in samples from individuals with Alzheimer's.
The researchers suggested that their findings aligned with other current research in the Alzheimer's field on the role of innate immunity in the disease, particularly recent findings that beta-amyloid protein, which is the culprit behind the plaques that build up in the Alzheimer's-affected brain, might accumulate as part of a defense against infections.
In their study, they found that herpesviruses were involved in networks that regulate amyloid precursor proteins.
Joel Dudley, director of the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai and the paper's senior author, said the study could potentially translate to the identification of virus, or virus-related, biomarkers that could improve patient risk stratification and diagnosis.
It could also imply novel viral targets and biological pathways that could be addressed with new preventative and therapeutic drugs, according to Dudley.
