The team found that the virus infiltrates brain cells about the same no matter which gene is involved. But they found that the subsequent activity level of the virus generally mirrored the disease-causing potential of the gene. They found that in animals with the ApoE-4 gene, the virus is less likely to be in the quiet, latent stage of its life cycle, suggesting it has more of an opportunity to replicate. In animals with the ApoE-2 gene, the virus was less active.
The work suggests that ApoE-4 may alter the balance between the HSV life cycle forms. It's possible that the ApoE gene works as a sort of bodyguard that tries to keep cells safe from herpes, perhaps by facilitating latency. Somehow the ApoE-2 version is extremely effective at keeping the virus at bay, while in this study, the ApoE-4 version wasn't any more effective than not having an ApoE gene at all.
The ApoE gene is well known to Alzheimer's researchers. The gene, which normally plays a role in ferrying cholesterol around the body, is associated with both the cellular tangles and amyloid plaques that are found in the brains of patients with the disease. Researchers have found several ways in which the gene might make a person vulnerable to getting a disease like Alzheimer's. In people with the ApoE-4 gene, brain cells don't seem to recover as well from injury, and the cells don't form new connections as well as cells equipped with either ApoE-2 or ApoE-3. Other scientists have shown that the gene plays a role in clearing toxic amyloid beta from the brain.
"Just how ApoE-4 makes people vulnerable to Alzheimer's disease isn't resolved at all," said Federoff, who is director of the University's Center for Aging and Developmental Biology. "It may be that it works in multiple ways."
The team is exploring different ways that herpes might affect the development of Alzheimer's
Source:University of Rochester Medical Center