Viral double whammy: Anyone who has cold sores and has had chickenpox in the past might have an increased risk of Alzheimer’s. Because when the viral pathogens of both diseases – the herpes simplex virus and the varicella zoster virus – come together in the brain, this can trigger the formation of Alzheimer’s-typical protein plaques. The reason for this is probably an inflammatory reaction that reactivates the dormant herpes virus, a research team reports.
Whether cold sores, chickenpox, shingles or Epstein-Barr: The viral causative agents of these diseases all belong to the herpes viruses. A typical feature of these DNA viruses is their ability to be latent: following the initial infection, they remain in the body forever and remain in a kind of dormant state. Only when the immune system is weakened, the herpes viruses active once more.
According to estimates by the WHO, two-thirds of all people carry the causative agent of cold sores, herpes simplex 1 (HSV-1). 95 percent of people are infected with varicella zoster, the cause of chickenpox and shingles.
Alzheimer’s caused by herpes viruses?
It has long been suspected that herpes viruses also play a role in Alzheimer’s dementia. Evidence of this is provided by an increased occurrence of certain herpes viruses in the brain deceased Alzheimer’s patients, but also laboratory experiments with tissue cultures of human brain cells. In these, a team led by Dana Carins from Tufts University in Massachusetts discoveredthat an infection of these cultures with herpes viruses can lead to the increased formation of neurotransmitters and protein deposits typical of Alzheimer’s.
In a further study, Cairns and her colleagues have now examined in more detail what is behind this and when herpes viruses can cause such Alzheimer’s symptoms in the brain. To do this, they grew three-dimensional tissue cultures from neuronal stem cells, which consisted of human neurons and their auxiliary cells, the glial cells. They then infected these cell cultures with herpes simplex and/or varicella zoster.
Alzheimer’s plaques following dual infection
It turned out that if the brain cells were only infected with the shingles virus Varicella zoster, this caused damage to the glial cells and the release of inflammatory messenger substances – but no Alzheimer’s plaques. However, this was different if the brain cells had previously been latently infected with herpes simplex: The double infection reactivated the dormant HSV-1 viruses and triggered a rapid formation of misfolded amyloid beta and tau proteins – the plaques that are typical of Alzheimer’s are.
As a result of this viral chain reaction, the brain cells in the cultures became less active and eventually died. “Our results suggest that varicella infection causes inflammatory signals in the brain, which in turn wake up herpes simplex,” explains Cairns. This supports an indirect role of the chickenpox pathogen in Alzheimer’s dementia. At the same time, this might explain why a latent infestation with herpes simplex alone is apparently not enough to trigger the disease – the virus has to be reactivated.
“It’s a double whammy from two viruses that are very common but mostly harmless when viewed on their own. But when they come together, it can cause problems,” explains Cairns.
Shingles vaccine might protect
The fact that people who have been vaccinated once morest chickenpox and shingles are less likely to develop Alzheimer’s also fits in with the “accomplice” role of the chickenpox virus. They also have fewer cold sores on the lips. Cairns and her team attribute this to the fact that the “wake-up” effect of the inflammation triggered by the varicella virus on the latent herpes infection then fails to appear. The HSV-1 virus remains dormant and can therefore not unfold its damaging effect.
However, whether the shingles vaccination, which is recommended for older people anyway, can actually protect once morest Alzheimer’s or at least reduce the risk needs to be examined more closely. The researchers also concede that the HSV-1 Vren in the brain can also be reactivated by other actors and influencing factors. “It’s possible that other inflammatory events in the brain also lead to a resurgence of the herpes virus,” says Cairns. These include risk factors such as head trauma, obesity or alcohol consumption. (Journal of Alzheimer’s Disease, 2022; two: 10.3233/JAD-220287)
Quelle: Tufts University
