The herpes virus (HSV-1) in connection with the ApoE gene known as ApoE-4 is linked to Alzheimer’s disease.

A  study “links a form of the ApoE gene known as ApoE-4, which after advanced age is the leading known risk factor for getting Alzheimer’s disease, with the form of herpes – herpes simplex 1 or HSV – that infects more than 80 percent of Americans and causes cold sores around the mouth.” (1)

Dr. Bullido wrote that “Alzheimer‘s disease (AD) appears to be the consequence of the interaction between combinations of genes and environmental factors.” (2)

The particular form of ApoE puts people at risk, and “also creates a fertile environment for herpes in the brain, allowing the virus to be more active than other forms of the ApoE gene permit.” (1) Howard Federoff, M.D., Ph.D wrote that “the data suggests that ApoE-4 may support the ability of HSV to be a more virulent pathogen.” (1)

Other researchers have shown “that people with the ApoE-4 version of the gene who are infected with herpes are more likely to get Alzheimer’s disease than people infected with herpes who have a different form of the ApoE gene, or than people who have the ApoE-4 gene but who don’t have herpes.” (1) Additionally (and frighteningly), people who are frequently troubled by cold sores are more likely to have the gene that makes them more vulnerable to Alzheimer’s disease.

“Cold sores that come and go are the outward sign of the two different phases of the virus’s life cycle. Herpes simplex is a chronic infection that lives in a person for a lifetime, periodically flaring up in a ‘lytic’ phase where it causes cell damage, then retreating and seeking safe harbor within the body’s nerves in a ‘latent” phase.’ (1)

Interestingly, many researchers continue to believe that viruses in a latent phase are not dangerous, do not replicate, and do not shed except at very low levels. However, new research is showing that this is not the case.

For instance, one paper noted that both the chronic and latent states of infection contribute to HCMV (Human Cytomegalovirus, which is a herpes virus) persistence and to the high HCMV seroprevalence worldwide. The chronic infection is poorly defined molecularly, but clinically manifests as low-level virus shedding over extended periods of time and often in the absence of symptoms. (3) In addition, “Transcripts and proteins encoded from a region encompassing the major immediate early region are detected in hematopoietic cells following infection in vitro as well as in latently infected individuals.” (4).

These papers showed that latent herpes viruses still replicate, even when they are not active, that is, even when they are not causing an outbreak.

Because of the dangers posed by both active and latent herpes viruses, scientists like Mira Katan, MD said that treatments “…against viruses could decrease the risk for memory problems later in life.”

References:

(1) University of Rochester Medical Center – “Cold sore virus might play role in Alzheimer’s disease.” January 3, 2007.

(2) Bullido MJ1, Martínez-García A, Artiga MJ, Aldudo J, Sastre I, Gil P, Coria F, Muñoz DG, Hachinski V, Frank A, Valdivieso F. “A TAP2 genotype associated with Alzheimer’s disease in APOE4 carriers.” Neurobiol Aging. 2007 Apr;28(4):519-23.

(3) Goodrum F, Caviness K, Zagallo P. Human Cytomegalovirus persistence. Cell Microbiol. 2012 May;14(5):644-55. doi: 10.1111/j.1462-5822.2012.01774.x. Epub 2012 Mar 8.

(4) Felicia Goodrum, Katie Caviness, Patricia Zagallo. Human Cytomegalovirus Persistence. Cell Microbiol. May 2012; 14(5): 644655