Immune Aging and Chronic Infections

“Back then, I wasn’t ill so often”: With advancing age not only the skin loses its elasticity – many organs lose their functions. So does the immune system: Defense cells do not react promptly anymore, and immunological memory is not established. As a result, we are poorly protected by vaccines and more susceptible to infections. While the mechanisms of immune aging remain unknown, it is speculated that chronic viral infections play a crucial role in this age-related loss of immune functions. Read more about how pathogens may have an impact on the real age of our immune system.

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Our Research

Investigation of an infection with the cytomegalovirus (CMV).

With advancing age many organs lose their functions. So does the immune system: The aging-related loss of immune function, called immune senescence, manifests itself by poor response to vaccines and increased susceptibility to infections. The scientists from the junior research group “Immune senescence and chronic infections” want to understand the mechanisms behind this phenomenon. 

Understanding the mechanisms that delay immune senescence may give us preventive and therapeutic tools to improve significantly the quality of life of seniors, an increasingly important task in an aging society. Chronic infections seem to play a crucial role during immune senescence. The research group thus analyses infections with Cytomeglovirus and the loss of immune functions. Cytomegalovirus (CMV) is a herpes virus that is latently maintained in the vast majority of the human population worldwide. Epidemiological studies in otherwise healthy elderly showed that CMV carriers had poor survival prognosis, compared to uninfected individuals. CMV infection was also associated with the exhaustion of T-lymphocytes, and thus it was speculated that latent CMV infection may accelerate immune aging, yet experimental proof remained pending.

The research group "Immune senescence and Chronic Infections" is developing a novel model of life-long mouse CMV infection, to match the clinical observations and confirm that latent CMV infection induces several T-cell phenotype changes consistent with rapid immune aging.

The researchers propose to address two major aims in this unique model:

  1. (1) define the cellular and molecular mechanisms underlying the loss of immune protection after CMV infection, and
  2. (2) assess the broader biological relevance of immune exhaustion by CMV and other persistent viruses, by testing if they decrease immune protection against bacterial infections and tumors.

Given the ubiquitous presence of CMV, and the aging demographic trend in developed countries, the results of this project are likely to have high medical and social impact.

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