GALVESTON, Texas –A recent study by The University of Texas Medical Branch at Galveston identified a protein that allows the West Nile virus to invade our bodies and replicate itself, causing infection and disease. The study is available in The Journal of Clinical Investigation.
The UTMB scientists learned that the protein, Peli1, that normally helps fight infections, actually is a key link in the West Nile virus’ ability to attack the immune system.
“We identified a protein that increases the risk of West Nile virus infection and brain inflammation, gaining a better understanding of how this occurs,” said UTMB’s Tian Wang, a professor in the department of microbiology and immunology. “Our findings will ultimately help to develop treatments for West Nile infection and subsequent inflammation.”
The mosquito-borne West Nile virus has caused disease outbreaks in Asia, Europe and Australia and has been a leading cause of viral encephalitis – an inflammation of the brain – in the U.S. for more than a decade. Up to 50 percent of people who had the disease are reported to have long-term neurological damage. Currently, there is no specific treatment or available vaccine for West Nile viral infections.
Peli1 plays a key role in regulating the body’s immune response to viruses, especially within the brain cells. Peli1 produces inflammation in certain types of brain cells and promotes the release of immune cells into the central nervous system.
The research team found that the protein is essential for the West Nile virus to infect and ultimately multiply within host cells. Mice that were engineered to lack the Peli1 protein were more resistant to West Nile virus infection. Similarly, an analysis of the brain tissue of people who died from West Nile virus disease showed high levels of Peli1 compared with brain tissue of people who did not have the infection.
“Next, we plan to determine the role of Peli1 in other viral infections that preferentially attack the nervous system,” said Wang.
Other authors include Huanle Luo,Evandro Winkelmann,Shuang Zhu,Wenjuan Ru,Elizabeth Mays,Jesus Silvas,Junling Gao,Bi-Hung Peng,Nathen Bopp, Courtney Cromer, Chao Shan,Guorui Xie,Guangyu Li,Robert Tesh,Vsevolod Popov,Pei-Yong Shi, Ping Wu, Shao-Jun Tang, Wenbo Zhang andPatricia Aguilar; Lauren Vollmer and Robyn Klein,from Washington University School of Medicine as well as Shao-Cong Sun from The University of Texas MD Anderson Cancer Center.