The varicella zoster virus, or VZV, causes chickenpox. Once a person has recovered from chickenpox, the virus becomes dormant but can reactivate in the form of shingles later. A new study finds VZV could also be linked with later development of Alzheimer’s, due to its impact on another dormant virus.
Oxford Professor Ruth Itzhaki has long studied the link between Alzheimer’s and herpes simplex virus type 1, or HSV-1, which is a lifelong condition that is usually dormant after infection in the peripheral nervous system. It can be reactivated due to stress or other circumstances. Itzhaki’s team has found that HSV-1 DNA is prevalent in the brains of a high number of older people and that in those with a certain genetic predisposition to Alzheimer’s, the presence of the virus in the brain ups the risk of developing Alzheimer’s.
Followup studies also found links between the virus’ effects and features of Alzheimer’s, and that antiviral treatment of cells with HSV-1 in the lab helped protect against Alzheimer’s. Additionally, researchers at Tufts University had found that human-induced neural stem cells infected with the virus experienced amyloid plaque-like formations, gliosis, neuroinflammation, and lower functionality.
So where does the varicella zoster virus come in? In a study published in the Journal of Alzheimer’s Disease, Professor Itzhaki teamed up with researchers from Oxford and Tufts University to see if VZV may play a similar role to HSV-1. To do this, the team used lab grown brain cells and a 3D brain model.
They found that cells infected with VZV did not experience beta amyloid or abnormally phosphorylated tau formations. However, gliosis and up-regulation of inflammatory cytokines were observed. While the team says that shows it’s unlikely to directly cause the development of Alzheimer’s, VZV could be linked indirectly by reactivating dormant HSV-1.
The evidence for this was increased when the team discovered that when cells with dormant HSV-1 were infected with VZV, this reactivated HSV-1, which was followed by a sharp increase in levels of beta amyloid and abnormally phosphorylated tau. The team says that indicates VZV could indirectly cause Alzheimer’s-like damage in the brain just by reactivating the other virus.
Professor Itzhaki summarizes the findings by saying, “This striking result appears to confirm that, in humans, infections such as VZV can cause an increase in inflammation in the brain, which can reactivate dormant HSV-1. The damage in the brain by repeated infections over a lifetime would lead eventually to the development of AD/dementia. This would mean vaccines could play a greater role than just protecting against a single disease, because they could also indirectly, by reducing infections, provide some protection against Alzheimer’s.”
The team says that this shows Alzheimer’s could possibly be treated, or even prevented, with antivirals. The findings also show how infections can impact our health in different ways later on.