Herpes Virus Linked to Alzheimer’s Disease in New Study
BOSTON,MA – June 13,2024 – Researchers have discovered a surprising connection between herpes simplex virus type 1 (HSV-1),the virus responsible for cold sores,and the progress of Alzheimer’s disease. A study published today in Cell Reports details how the virus can interact with tau protein, a hallmark of Alzheimer’s, offering both short-term protection to neurons and, possibly, long-term harm.
For years, scientists have observed the presence of HSV-1 in the brains of Alzheimer’s patients, but the nature of its role remained unclear. The new research, led by a team at Brigham and Women’s Hospital, suggests the virus can trigger a protective response in neurons involving the phosphorylation of tau - a process where phosphate groups are added to the protein.
The team found that in models of the human brain, including “mini-brains” grown from stem cells and rodent neuron cultures, HSV-1 infection increased tau phosphorylation. Notably, antiviral treatment that reduced viral activity also lowered tau phosphorylation, while reactivating the virus caused it to rise again.
Further inquiry revealed a reciprocal relationship: experimentally increasing phosphorylated tau (p-tau) led to decreased levels of ICP27, a viral protein, and considerably improved neuron survival during infection. Cultures without increased p-tau experienced roughly two-thirds neuron death after infection, while those with elevated p-tau saw only a small fraction die.
“These findings help connect two pictures that often seem at odds,” the study explains. Early and controlled phosphorylation of tau may initially help neurons survive HSV-1 infection. However, if this response persists, the modified tau can misfold, clump, and form tangles – a key characteristic of Alzheimer’s disease – disrupting neuron function and leading to degeneration.
researchers emphasize that the study doesn’t portray p-tau as inherently “good.” Instead, context and timing are critical.A protective surge can become detrimental when control is lost and the response becomes chronic.
The research strengthens the understanding that viral infections like HSV-1 can intersect with Alzheimer’s disease, without necessarily being the sole cause. Infection, aging, and genetics likely play complex, interacting roles. The findings also suggest potential therapeutic avenues, including calming viral activity or fine-tuning cellular alarm signals.
The team plans to continue investigating the precise mechanisms by which HSV-1 affects tau protein and contributes to Alzheimer’s disease.
