Common Viral Infections Degrade Memory Over Time

ROCHESTER, Minn., Oct. 23 -- Memory loss could be contagious.

A lifetime of infections with rhinoviruses, enteroviruses, or other members of the picornavirus family could lead to cumulative memory loss, according to neuroscientist Charles L. Howe, Ph.D., at the Mayo Clinic here, and colleagues.

"Our findings suggest that picornavirus infections throughout the lifetime of an individual may chip away at the cognitive reserve, increasing the likelihood of detectable cognitive impairment as the individual ages," they wrote in the November issue of Neurobiology of Disease.

The investigators hypothesize that mild memory loss and cognitive impairment could be caused by cumulative insults to the hippocampus and loss of hippocampal neurons from repeated infection with picornaviruses, which comprise the most common viral infectious agents in humans.

They tested the idea not in men, however, but in mice infected intracranially with Theiler's murine encephalomyelitis virus, which causes a murine demyelinating disease analogous to multiple sclerosis in humans. The virus has been shown to specifically infect and kill hippocampal pyramidal neurons, the investigators noted.

The authors chose male mice (ages 10 to 12 weeks) only for their study, to eliminate the possible effects of the estrus cycle on memory performance.

The mice were then subjected to a standard Morris water maze test, in which they were trained to both visually recognize a platform on which they can safely stand (cue training) and to memorize the location of a submerged platform in a pool of opaque water (place training). The animals were then retested to determine how quickly they could locate the platform and get back on firm footing.

The investigators were looking for signs that viral infection could affect the spatial memories of the test animals compared with their sham-infected counterparts.

They found that the brains of virus-infected mice had evidence of encephalitis and hippocampal damage not evident in either uninfected controls or in sham-infected mice.

On water-maze testing, the authors observed that the infected mice committed significantly more errors than their sham-infected counterparts, and could not discriminate the location of the training quadrant during the final probe trial.

In addition, the sham-infected mice tended to be place responders, indicating that their spatial memory was in good working order, whereas the infected mice were cue responders, suggesting that they had a spatial-memory deficit.

"The key observation of these experiments is that the degree of persistent hippocampal injury induced by Theiler's murine encephalomyelitis virus infection is directly and specifically correlated to the loss of spatial memory formation," the authors wrote.

They noted that other infectious agents, such as the herpes viruses and HIV, can inflict damage on the hippocampus through persistent infection, whereas picornaviruses are typically cleared by the immune system.

"Our findings therefore raise an important question: does picornavirus infection of the human CNS result in spatial memory deficits?" they wrote. "Because picornavirus infection is common, and because picornaviruses maintain neurovirulent potential, the possibility of subclinical hippocampal damage in humans is not unlikely."