Grant: Travel Awards - Institute Community Support

Our whole pool of genetic information is held in the hands of our telomeres. Each chromosome is capped by a telomere, for protection during cellular stress, aging, and replication. These telomeres behave strictly as gatekeepers to our chromosomes during replication, ensuring our genetic code stays protected. However the telomere becomes subsequently shorter with each division. The age of an individual can be broadly identified by the length of their telomeres. Thus, shorter telomeres have been associated with higher incidences of age-associated diseases. With antiretroviral treatment for Human Immunodeficiency Virus (HIV) infection, opportunistic infections were quickly replaced with non-AIDS defining illnesses such as cardiovascular disease and cancer. Researchers reluctantly identified them as age-associated diseases due to the early age these diagnoses were presented. Main risk factors associated with premature onset of such maladies were chronic inflammation, antiretroviral toxicity, lifestyle and cytomegalovirus (CMV) infection. Chronic inflammation was identified as the main driving cause of premature age-associated diseases, and the latter, except CMV infection, simply increased progression. Our research revolves around identifying markers of unhealthy aging and identifying the role of CMV infection. CMV infection drives rapid division of immune cells to a detriment, thus altering the immune system by dramatically shortening telomere lengths. It is believed that when a cell reaches a dangerously short telomere length, the cell becomes dysfunctional and could potentially become increasingly inflammatory. Our hypothesis is that circulating immune cells with shorter telomeres increase inflammation leading to premature aging. We propose to understand this relationship using a technique to simultaneously measure inflammatory response and telomere length in various subsets of immune cells.