The varicella zoster virus (VZV), which causes chickenpox and shingles, may play a role in the development of Alzheimer’s disease (AD), British researchers report today.
There has been growing evidence that herpes simplex virus type 1 (HSV-1), the cold sore virus, is present in the human brain in a high proportion of older people and when it combines with a specific genetic factor it confers a high risk of developing AD.
Professor Ruth Itzhaki, of the Oxford Institute of Population Ageing, worked with the Tufts School of Engineering at the University of Medford, Mass, USA, expanded her 30-year study of viral roles in AD to include another type of herpes virus, varicella zoster virus (VZV).
They looked at if VZV can play a similar role to HSV-1 and using both laboratory-grown brain cells and a 3D brain model, the researchers investigated if VZV infection caused the accumulation of beta amyloid (A?) and abnormally phosphorylated tau (P-tau) and other AD-like features, as is the case with HSV-1.
Writing in the *Journal of Alzheimer’s Disease*, they say while VZV infection of lab-grown brain cells does not lead to the formation of A? and P-tau, VZV infection resulted in both gliosis and up-regulation of inflammatory cytokines.
While this makes it unlikely that VZV could be a direct cause of AD, it suggests it has an indirect effect by reactivating dormant HSV-1.
They also found when cells containing latent HSV-1 were infected with VZV, it caused a reactivation of HSV1 as well as a dramatic increase in levels of A? and P-tau. They say this suggests severe VZV infection in humans could reactivate latent HSV-1 in brain, which could lead to formation of AD-like damage.
Prof Itzhaki, visiting professorial fellow at the Oxford Institute of Population Ageing and emeritus professor at the University of Manchester, said: “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.”
Potential involvement of Varicella Zoster Virus in Alzheimer’s Disease via reactivation of quiescent Herpes Simplex Virus Type 1. *Journal of Alzheimer’s Disease* 2 August 2022
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