Part 1: Mutation Story    Progeria

Hi there, my name is Paul, I am a gene in my host’s Tom’s body. However, I am not like any other gene. In fact, I am extremely special and rare. One in four million newborn babies in the world today would have me as their gene. In the beginning, I was just a gene a normal gene, known as lamin A which makes a protein necessary for holding nucleus of a cell together. But I had a defect, this defect made the cell I was in unstable, which leaded to my young host to rapidly age. When my host was first born, the effects weren’t at all that noticeable on the outside of him. As eighteen to twenty-four months passed, my hosts parents slowly started to notice that Tom was beginning to look abnormal. His facial appearance included prominent eyes, a thin nose with a beaked tip, thin lips, small chin, and protruding ears. Moreover, he also had thin hair and aged-looking skin, joint abnormalities, and a loss of fat under the skin. In other words, he was beginning to look like an old man. Immediately, he was taken to the hospital where the doctors found out that he had progeria or Hutchinson–Gilford progeria syndrome. When Tom reached fourteen, his health began to deteriorate drastically so he had to go to the hospital constantly for checkups and treatments.  Now how did his health worsen? I will explain. As a defective gene, I cause my host to experience severe hardening of the arteries which greatly increases the chances of having a heart attack or stroke at a young age. Unfortunately, this means that Tom didn’t get to play sports or eat whatever he wants like all the other kids. That year, Tom suffered many strokes and heart attacks and eventually died in a hospital. Almost all hosts of the defective lamin A gene die at an age of fourteen as there isn’t a cure for it presently. Despite the severity and rarity of me, I am not inheritable. So if even if Tom ever got to have kids, the chances of them hosting me again isn’t at all that great.