Herpes Virus Might Contribute to Alzheimer's Disease Risk

Emma Hitt, PhD

April 11, 2011

April 11, 2011 — The interaction of herpes simplex virus type 1 (HSV-1) with amyloid precursor protein (APP) may alter the normal transport and distribution of APP in cells, potentially contributing to the risk for Alzheimer's disease in HSV-1–seropositive individuals, a new study suggests.

Shi-Bin Cheng, MD, PhD, with the Department of Pathology and Laboratory Medicine, Alpert Medical School of Brown University, Providence, Rhode Island, and colleagues reported their findings in PLoS ONE on March 31, 2011.

HSV-1 seropositivity has previously been linked to Alzheimer's disease, the researchers write. "While a role for HSV-1 in Alzheimer's disease remains controversial, the notion is especially intriguing since HSV-1 infection offers a potentially treatable target," they note. The current study describes a way in which HSV-1 may contribute to Alzheimer's disease risk.

The researchers used HSV-1 tagged with green fluorescent protein to observe new virus particles leaving infected cells and entering cellular membranes containing APP. This interaction changed the cellular architecture and distribution of APP within the cell, highlighting an effect of HSV-1 on APP.

Most of the tagged viral particles colocalized (72.8% ± 6.7%) and traveled (81.1% ± 28.9%) with APP in infected cells. The association of HSV-1 with APP increased the velocity of viral particles, facilitating viral transport.

This interplay of HSV-1 and APP also altered the localization of APP in the cell from mostly within the trans-Golgi network to throughout the entire cytoplasm within 7 hours after infection.

"The interactions of HSV-1 with APP shown here suggest a molecular mechanism for the observed epidemiological correlation," Dr. Cheng and colleagues write. "Long-term chronic active HSV-1 infection would affect APP distribution, expression, and processing and thereby have significantly more impact than previously considered," they add.

The study was not commercially funded. The study authors have disclosed no relevant financial relationships.

PLoS ONE. Published online March 31, 2011.


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