Abstract
This review describes investigations of specific topics that lie within the general subject of HSV1’s role in AD/dementia, published in the last couple of years. They include studies on the following: relationship of HSV1 to AD using neural stem cells; the apparent protective effects of treatment of HSV1 infection or of VZV infection with antivirals prior to the onset of dementia; the putative involvement of VZV in AD/dementia; the possible role of human herpes virus 6 (HHV6) in AD; the seemingly reduced risk of dementia after vaccination with diverse types of vaccine, and the association shown in some vaccine studies with reduced frequency of HSV1 reactivation; anti-HSV serum antibodies supporting the linkage of HSV1 in brain with AD in APOE-ε4 carriers, and the association between APOE and cognition, and association of APOE and infection with AD/dementia. The conclusions are that there is now overwhelming evidence for HSV1’s role—probably causal—in AD, when it is present in brain of APOE-ε4 carriers, and that further investigations should be made on possible prevention of the disease by vaccination, or by prolonged antiviral treatment of HSV1 infection in APOE-ε4 carriers, before disease onset.
Highlights
Inflammation, and other events can lead to reactivation of the virus, causing a productive infection and consequent damage which, it is suggested, is likely to be greater in people who carry the type 4 allele of the apolipoprotein E gene (APOE-ε4)
The evidence for herpes simplex virus type 1 (HSV1) in brain of APOE-ε4 carriers conferring a strong risk of Alzheimer’s disease (AD) continues to grow, with no experimental counter-evidence published in very recent years—as far as the present author is aware
HSV1 operates over the years to cause the development of the disease are yet to be discovered: a challenge bearing in mind the bewildering array of effects of the virus and the very unfortunate inability at present to detect it even when reactivated in the brain in life
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. In 2017, I emphasised the steady increase in the number of publications supporting directly or indirectly the involvement of herpes simplex virus type 1 (HSV1) in Alzheimer’s disease (AD) [1]. Inflammation, and other events can lead to reactivation of the virus, causing a productive infection and consequent damage which, it is suggested, is likely to be greater in people who carry the type 4 allele of the apolipoprotein E gene (APOE-ε4). The conclusion was that HSV1 in brain, in combination with carriage of an APOE-ε4 allele, confers a high risk of developing. Our finding that in the peripheral nervous system, APOE-ε4 is a major risk factor for cold sores (herpes labialis) provided strong indirect support for this conclusion [2]. The idea that APOE-ε4 carriers are more likely to be infected with HSV1 is demonstrably incorrect: 80+% of most populations are infected with the virus but only some 25–30% are APOE-ε4 carriers
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