Molecular, cellular, and clinical changes that arise from an infection with a latent virus can result in shortened telomeres and a decrease in longevity. The telomeres (image) are repetitive DNA sequences at each end of each of our chromosomes. Studies show that in every cell division, the telomere is shortened. As a result, the telomere limits the cell to a fixed number of divisions and a limited life span. An essential part of human cells, telomeres affect how our cells age - as people with longer telomeres tend to live longer lives. Surprisingly, people who are infected with a latent virus, that is, an asymptomatic virus, have shorter telomeres. This is an important observation and a great mystery. Is the virus causing the telomere shortening, and how? And if this is the case, what does it mean in terms of the relationship between the latent viruses and longevity? Now, an article titled “The Latent Cytomegalovirus Decreases Telomere Length by Microcompetition” by Dr. Hanan Polansky and Dr. Adrian Javaherian, published online on June 27, 2015 in the open-access journal Open Medicine by De Gruyter Open, provides some answers to these questions. As it turns out, a certain gene, called telomere repeat binding factor 2 (Terf2), belongs to a complex of six telomere-associated proteins, termed shelterin. The protein produced by the Terf2 gene protects the chromosome ends of the DNA from damage, and controls telomere maintenance by the telomerase enzyme. When does a cell produce the Terf2 protein? It does so after receiving a signal that tells a transcription factor called GABP to bind the Terf2 gene. One can think of GABP as a finger that pushes the “ON” button on the Terf2 gene. Now, consider a case where a latent virus called cytomegalovirus (CMV) infects the cell.
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