Herpes simplex type 1 (HSV-1) is a very common human virus that can reside in cells of the nervous system. HSV-1 infection is usually acquired in childhood and begins in the epithelial cells of the oral or nasal mucosa; From there, the virus moves to the neurons of the trigeminal nerve ganglia, where it remains inactive throughout life. Factors such as stress, chronic inflammation or immunosuppression can contribute to the virus gaining access to the brain during aging, a period in which the immune system is more vulnerable and the blood-brain barrier becomes more permeable.
Researchers from the Functional Neuroscience Laboratory of the Pablo de Olavide University of Seville, in collaboration with a group from the Severo Ochoa Molecular Biology Center (CBM, CSIC-UAM), belonging to the Networked Biomedical Research Center for Neurodegenerative Diseases (CIBERNED), have now discovered that the level of herpes simplex virus type 1 infection is related to the concentration of amyloid beta deposits in the brains of asymptomatic older people.
This finding has been published in the journal Alzheimer’s Research & Therapy and suggests that this virus could be a risk factor for the development of Alzheimer’s disease. “Studies in cellular and animal models have shown that recurrent reactivation of HSV-1 increases the brain pathology of Alzheimer’s disease. However, the findings in humans are very scarce and have been obtained in the clinical phases of the disease, when the brain damage is very evident,” explains José Luis Cantero, professor of Physiology at the Pablo de Olavide University and lead author of the study. .
An infection at the origin of Alzheimer’s disease
In this research, it was demonstrated in asymptomatic older people that the level of HSV-1 infection is related to amyloid beta plaques that appear decades before the first symptoms of Alzheimer’s. Furthermore, it was confirmed that this relationship is particularly notable in individuals who carry the APOE4 genetic variant, the most significant genetic risk factor for Alzheimer’s, present in approximately 25% of the population.
These results highlight that the HSV-1 viral load could be a risk factor for the development of beta amyloid plaques, the first neuropathological lesion of Alzheimer’s, “something of which we had no evidence in asymptomatic older people,” says María Jesús. Bullido, professor of Molecular Biology at the Autonomous University of Madrid and co-author of the study.
“It is not that the herpes simplex virus 1 causes Alzheimer’s, it is probably one more factor that contributes to paving the way to the disease”
High levels of HSV-1 could not only increase the amyloid beta load in the brain, but also increase levels of peripheral inflammation, thus facilitating the development of the disease. “It is not that the herpes simplex virus 1 causes Alzheimer’s, it is probably one more factor that contributes to paving the way to the disease,” explains Professor Cantero.
Numerous epidemiological and experimental studies support the infectious hypothesis of Alzheimer’s disease, which suggests that chronic bacterial or viral infections could play a role in the pathogenesis of the disease. This hypothesis may be key to identifying new preventive and therapeutic strategies in this type of dementia that currently has no cure.
