Here researchers provide another data point for the ongoing debate over whether and how persistent viral infection contributes to neurodegeneration. The data is mixed to date, with some studies showing correlation and some not. Some research shows ongoing antiviral drug treatment to correlate to a lower risk of neurodegeneration, while others (such as the work here) do not. Other research suggests that interactions between several different persistent viruses may be required, but this remains a recent discovery and yet to be confirmed. This part of the field is a work in progress: some suggestive data, some contradictory data, a few possible explanations, but no firm conclusion as of yet. Still, the cost-benefit calculation for taking antiviral drugs in later life looks good; they are not that expensive, and a person only has the one brain.
The relationship between herpes simplex virus (HSV) and dementia has not been elucidated fully and results obtained to date are far from unanimous. To better understand the potential effects of HSV on incident Alzheimer's disease (AD) or dementia, suspected interactions with common co-infections, their treatment, and risk-related genes need to be considered in analyses, which has not commonly been reported together. Further, age is the strongest risk factor for dementia, which is difficult to adequately adjust for. The aim of this study was to investigate the roles of HSV, HSV-1 specifically, and cytomegalovirus (CMV) in AD and dementia risk, including examination of potential interactions with APOE ɛ4 carriership and the effects of anti-herpesvirus treatment, in a prospective cohort of same-age individuals.
This study was conducted with 1,002 dementia-free 70-year-olds living in Sweden in 2001-2005 who were followed for 15 years. Serum samples were analyzed to detect anti-HSV and anti-HSV-1 immunoglobulin (Ig) G, anti-CMV IgG, anti-HSV IgM, and anti-HSV and anti-CMV IgG levels. Diagnoses and drug prescriptions were collected from medical records. Cox proportional-hazards regression models were applied.
Cumulative AD and all-cause dementia incidences were 4% and 7%, respectively. Eighty-two percent of participants were anti-HSV IgG carriers, of whom 6% received anti-herpesvirus treatment. Anti-HSV IgG was associated with a more than doubled dementia risk (fully adjusted hazard ratio = 2.26). No significant association was found with AD, but the hazard ratio was of the same magnitude as for dementia. Anti-HSV IgM and anti-CMV IgG prevalence, anti-herpesvirus treatment, and anti-HSV and anti-CMV IgG levels were not associated with AD or dementia, nor were interactions between anti-HSV IgG and APOE ɛ4 or anti-CMV IgG. Similar results were obtained for HSV-1. In conclusion, HSV (but not CMV) infection may be indicative of doubled dementia risk.
Link: https://doi.org/10.3233/JAD-230718
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