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Loyola University Chicago Study
Suggests a Way to Stop HIV in its Tracks
MAYWOOD, Ill., November 30, 2017 – When HIV-1 infects an immune cell, the virus travels to the nucleus so quickly there’s not enough time to set off the cell’s alarm system.
Now, a Loyola University Chicago study has discovered the protein that helps the virus travel so fast. Researchers found that without this protein, the virus became stranded in the cytoplasm, where it was detected by the viral defense system. (The cytoplasm is the portion of the cell outside the nucleus.)
“By preventing its normal movement, we essentially turned HIV-1 into a sitting duck for cellular sensors,” said Edward M. Campbell, PhD, corresponding author of the study, published in the Proceedings of the National Academy of Sciences. Campbell is an associate professor in the Department of Microbiology and Immunology of Loyola University Chicago Stritch School of Medicine.
HIV-1 infects and kills immune system cells, including T cells and macrophages that were used in the study. This cripples the immune system, making the patient vulnerable to common bacteria, viruses and other pathogens that are usually harmless in people with healthy immune systems.
After HIV-1 enters a cell, it has to work its way through the cytoplasm to the nucleus. Once inside the nucleus, HIV-1 takes control of the cell and makes additional HIV-1 copies. But getting through the cytoplasm is not easy. Cytoplasm consists of fluid that is thick with proteins and structures such as mitochondria. “Something the size of a virus cannot just diffuse through the cytoplasm,” Campbell said. “It would be like trying to float to the bathroom in a very crowded bar. You need to have a plan.”
HIV-1 is able to get to the nucleus quickly via tubular tracks called microtubules. The virus attaches itself to a molecular motor called dynein, which moves down the microtubule like a train car on tracks.
Campbell and colleagues discovered the “ticket” HIV-1 needs to get on the train — a protein called bicaudal D2. HIV-1 binds to bicaudal D2, which then recruits the dynein molecular motor to transport the HIV-1 towards the nucleus.
The finding raises the possibility of developing a drug that would prevent HIV-1 from binding to bicaudal D2, thus stranding the virus in the cytoplasm. This would not only prevent infection, but also give the cell time to turn on antiviral genes that would protect it and neighboring cells from infection.
The study is titled “Bicaudal D2 facilitates the cytoplasmic trafficking and nuclear import of HIV-1 genomes during infection.”
In addition to Campbell, other co-authors are Adarsh Dharan, PhD, (first author), Omar Abdel-Rahim, Sevnur Komurlu Keceli, PhD, and Sabrina Imam of Loyola and Silvana Opp, PhD, and Felipe Diaz-Griffero, PhD, of Albert Einstein College of Medicine.
About Loyola University Chicago
Founded in 1870, Loyola University Chicago is one of the nation’s largest Jesuit, Catholic universities, with nearly 16,500 students. More than 11,000 undergraduates call Loyola home. The University has four campuses: three in the greater Chicago area and one in Rome, Italy, as well as course locations in Beijing, China; Saigon-Ho Chi Minh City, Vietnam; Vernon Hills, Illinois (Cuneo Mansion and Gardens); and a Retreat and Ecology Campus in Woodstock, Illinois. The University features 11 schools and colleges, including the Quinlan School of Business, Marcella Niehoff School of Nursing, Stritch School of Medicine, College of Arts and Sciences, School of Communication, School of Continuing and Professional Studies, School of Education, School of Law, School of Social Work, Graduate School, and Arrupe College of Loyola University Chicago. Ranked a top 100 national university by U.S. News & World Report, Loyola is also among a select group of universities recognized for community service and engagement by prestigious national organizations like the Carnegie Foundation and the Corporation for National and Community Service. To learn more about Loyola, visit LUC.edu, “like” us at Facebook.com/LoyolaChicago, or follow us on Twitter via @LoyolaChicago or @LoyolaNewsroom.
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