Herpes simplex virus type 1 and Alzheimer’s disease: link and potential impact on treatment

ABSTRACT

Introduction: Alzheimer’s disease (AD), the most common form of dementia worldwide, is a multifactorial disease with a still unknown etiology. Herpes simplex virus 1 (HSV-1) has long been suspected to be one of the factors involved in the pathogenesis of the disease.

Areas covered: We review the literature focusing on viral characteristics of HSV-1, the mechanisms this virus uses to infect neural cells, its interaction with the host immune system and genetic background and summarizes results and research that support the hypothesis of an association between AD and HSV-1. The possible usefulness of virus-directed pharmaceutical approaches as potential treatments for AD will be discussed as well.

Expert opinion: We highlight crucial aspects that must be addressed to clarify the possible role of HSV-1 in the pathogenesis of the disease, and to allow the design of new therapeutical approaches for AD.

KEYWORDS:

• Alzheimer’s disease
• human herpes simplex virus type-I
• immunity
• mild cognitive impairment
• pharmaceutical treatments

Article highlights

• A possible role for the reactivation of HSV-1, a virus that commonly infects humans, in the pathogenesis of AD is suggested by a string of observations.

• After the initial infection HSV-1 persists in latent state in trigeminal ganglia and, upon reactivation can reach the brain, as showed by detection of HSV-1 viral genome in brain of elderly people.

• Reactivation of HSV-1 can cause neuronal damage, directly and/or by induction of inflammation.

• Host immunity is critical to control viral reactivation and it is impaired in AD patients.

• If HSV-1 infection is a risk factor for AD, antiviral treatments could be useful in the prevention/treatment of this disease.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with financial interest in or financial conflict with the subject matter or material discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.