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Janet Butel, Ph.D. was recently recognized for her groundbreaking research at the 2013 BioHouston luncheon honoring Women in Science. Dr. Butel studies how a virus can cause cancer, a crucial line of work considering that the number of viruses associated with cancer continues to increase.
Since her days as a graduate student, Dr. Butel has been fascinated with a virus called SV40, which is known to cause cancer in hamsters. This makes it a great model for studying how related viruses may cause cancer in humans.
SV40’s natural host is monkeys and it is related to a growing number of human-associated viruses in a family called polyomaviruses. Some polyomaviruses are abundant in the human population, although they are only known to cause disease in rare instances, if at all. A recent isolate has been linked to a human cancer, Merkel cell carcinoma. These human viruses are difficult to study, and many of them cannot be grown in a lab. Because the SV40 virus is so similar to several of the human viruses, Dr. Butel’s research may lead to insights about how these human polyomaviruses sometimes cause disease, and eventually how to treat them.
During her graduate research at Baylor College of Medicine, Butel experienced what she describes as one of the high points in her career: “we discovered the oncoprotein for SV40.” The work identified a molecule called “large tumor-antigen” (or large T-antigen) that is made by the virus and is necessary for tumor formation in hamsters.
Dr. Butel’s current research interests are to find out what happens when cells in the host are infected with SV40, what types of cells get infected, where the virus hides from the host immune system, and how it eventually causes disease. On February 6, 2014, Dr. Butel and collaborators published their most recent findings in the journal PLoS Pathogens, describing a mechanism that the SV40 virus may be using to evade the immune system. They showed that a small molecule encoded by the virus called a microRNA helps keep the number of viruses at a low level inside the host. Fewer viruses are more difficult for the immune system to detect. Dr. Butel is very excited about this work because, “It was the first functional study in an intact animal showing that the viral microRNA is expressed and has an effect that we can measure.”
The main function of the microRNA is to target the large T-antigen, the oncoprotein that Dr. Butel discovered in her graduate work. The large T-antigen is essential for promoting viral replication. When the amount of this protein is reduced by the microRNA, fewer viruses are made.
It turns out that by promoting viral replication, the large T-antigen is also creating a potentially cancerous cell. The large T-antigen works by tricking the cell into thinking it is time to replicate itself, thereby providing the conditions so that the virus can replicate. T-antigen also deactivates a protein produced in the host cell called P53. P53 protects the organism by forcing sick or damaged cells to die. However, the virus wants the cell to stay alive long enough to produce new virus particles which can then infect other cells. What if the virus does not kill the cell? With P53 deactivated and the cell in replication mode, this cell is sometimes capable of growing and dividing out of control, and perhaps eventually forming a tumor. (For more on P53 research, see the BioNews Texas exclusive on Dr. Gigi Lozano, another BioHouston honoree.)
Several viruses are known to cause cancer in humans, such as the Merkel cell polyomavirus mentioned earlier. Human Herpesvirus 4, also known as Epstein-Barr virus, is associated with certain cancers of the blood and lymphatic system (leukemia and lymphomas); human papillomavirus, or HPV, is associated with cervical cancer; Hepatitis B and C viruses are associated with liver cancer. Dr. Butel predicts that with new technology making whole genome sequencing easier, we will find more cancer-associated viruses, and most likely some will have unique mechanisms of causing tumors to form. Once many tumor genomes are sequenced, the challenge will be going through the data to find sequences that are not human and determining if they are associated with viruses, known or unknown.
And so, Dr. Butel continues her research in hopes of one day defining the host-pathogen interaction associated with these viruses. She says, “The main goal of the research is to understand how cancer viruses cause cancer,” and she continues, “You need to know the biology, transmission, and pathogenesis of infection to figure out how to interrupt those processes before disease develops.”
Dr. Butel became a fellow of the American Association for the Advancement of Science in 1988 and of the American Academy of Microbiology in 2004. Currently, she is the Distinguished Service Professor and Chair of the Department of Molecular Virology and Microbiology at Baylor College of Medicine in Houston, Texas. In her department a variety of intriguing research projects are being carried out with labs studying cancer-associated viruses and gastroenteritis viruses (the kind that cause intestinal illness). There is a group studying Dengue virus, the most common hemorrhagic (bleeding) disease in the world that is now found in the US. Another group is collaborating with the Houston Zoo to study and develop treatment for the elephant Herpes virus that kills many baby Asian elephants. Other labs in the department are studying the human microbiome, addressing questions such as which microbes normally live in and on the human body, how they benefit or harm the host, and how the microbiome can inform personalized medicine. Several groups are developing and testing vaccines and working towards the development of a flu vaccine that only needs to be taken once, instead of every year.
Dr. Butel is also director of the Center for AIDS Research that fosters collaborative research among those interested in HIV in the Texas Medical Center. Clearly excited by all the projects, Dr. Butel says, “Very seldom do I not want to come to work every morning. It is great to have a job where you want to go to work every day because, even though it may be hard, you like what you are doing!”
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PloS oneno. 10 (2014): e110700-e110700
PLoS pathogensno. 2 (2014): e1003912-e1003912
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