Scientists have discovered a virus that can remain hidden in the body for years may leave a lasting mark on the brain.
In a new study, researchers found that herpesvirus infection intensified memory problems and other Alzheimer’srelated changes in mice already vulnerable to the disease.
The damage appeared to be driven not simply by the virus itself, but by the immune system’s prolonged attempt to control it.
The findings offer a possible biological explanation for years of research linking common viral infections with an increased risk of dementia.
Herpesviruses are a large family that includes viruses associated with cold sores, childhood infections, and glandular fever. After the initial illness passes, some can remain dormant inside the body and reactivate later, repeatedly drawing the immune system into action.
Scientists from Cardiff University’s School of Medicine, Systems Immunity Research Institute, and Dementia Research Institute investigated whether that persistent immune activity could influence the progression of Alzheimer’s disease.
Their results suggest that T cells, immune cells that identify and attack infected cells, can enter the brain during herpesvirus infection and accelerate cognitive decline.
Dr. Mathew Clement of Cardiff University School of Medicine said: “Infections, including chronic human herpesviruses, which can be associated with cold sores, have long been suspected as increasing the risk of developing Alzheimer’s disease.
However, the mechanisms underlying this association have remained largely unknown.”
The researchers used 3xTg-AD mice, which carry genetic changes that cause them to develop several features associated with Alzheimer’s disease. The animals were infected with murine cytomegalovirus, a-herpesvirus used to study persistent herpesvirus infection.
Some mice received the antiviral medication valganciclovir hydrochloride.
Others were treated with antibodies that targeted CD4 and CD8 T cells, allowing the team to test whether the immune response was contributing to the neurological damage.
The scientists then measured memory and cognitive performance, the loss of cells in the hippocampus, and the accumulation of amyloid and tau proteins (indicative of Alzheimer’s disease). The hippocampus is a brain region central to learning and memory and is among the areas affected early in Alzheimer’s disease.
Following infection, large numbers of immune cells moved into the brain. Most were CD8+ T cells that specifically recognized the virus, showing that they had entered the tissue as part of the body’s attempt to contain the infection.
Similar T cells have previously been found in the brains and spinal fluid of people with Alzheimer’s disease, although their exact role has remained uncertain.
The most important finding came when the immune response was disrupted. Mice treated with antiviral drugs, or those whose white blood cells were removed, performed better on cognitive tests.
The results indicate that a virus-driven immune response can actively speed the progression of Alzheimer’slike disease rather than merely appearing alongside it.
Professor of Viral Pathogenesis and lead codirector of Cardiff University’s Systems Immunity Research Institute, Ian Humphreys said: “It remains unclear how virus-induced T cell presence in the brain leads to disease progression, and understanding this may lead to new insights into Alzheimer’s Disease development.”
