With the newfound acceptance of senescent cell accumulation as an important contributing cause of aging, a viewpoint that has really only flourished in the research community over the last five years or so, many fields of research relevant to aging are retrofitting senescent cells into their theories and understanding of the aging process. Today's open access paper is an example of this process. Researchers interested in the role of persistent cytomegalovirus (CMV) infection in the aging, a field that has itself seen a surge of interest over the past decade, link it to cellular senescence and the growth of chronic inflammation that occurs in old age.

CMV is a type of herpesvirus that is very prevalent in the population; near everyone is exposed to it at some point in time. There is good epidemiological evidence associating CMV exposure to worse health in later life. CMV provokes the adaptive immune system into specializing ever more resources to tackling it, a futile effort as it cannot be cleared from the body. It hides, latent, to emerge again. The thymus, where T cells of the adaptive immune system mature, atrophies with age, and the supply of new T cells diminishes. Without reinforcements, this continual specialization to CMV depletes the immune system of cells capable of handling other tasks.

One of those tasks is the destruction of senescent cells, rapidly enough to prevent their inflammatory secretions from disrupting tissue maintenance and organ function. The pace of clearance of senescent cells declines with age, and this is one of the contributing factors leading to an increased number of such errant cells in old tissues. Further, the pressure that CMV puts on the immune system produces other more direct issues, such as forcing a greater replication of immune cells that drives them into senescence faster than would otherwise be the case. Senescent immune cells are just as problematic as senescent cells in tissues.

The Immune Response Against Human Cytomegalovirus Links Cellular to Systemic Senescence