#Dengue virus pumps out RNA to evade attack Duke university National University of Singapore right Original Study Posted by Karen Loh-NUS on September 29 2014 A newly discovered pathway lets the dengue virus avoid being destroyed by the body s antiviral response. The findings which appear in PLOS Pathogens provide knowledge that could help researchers treat the disease more effectively. For years the conventional approach to target the dengue virus was through control of the vectorâ the mosquito that carries the disease from one host to another. The elusive mechanics of the virus have hampered the development of effective treatments and vaccines. Typically when a virus enters the body and infects cells it induces the production and release of interferonsâ proteins that raise the body s antiviral defense mechanisms. In examining the dengue virus-2 strain a team at Duke-NUS Graduate Medical school Singapore observed that when the dengue virus enters the cell it produces large quantities of a non-coding highly structured viral ribonucleic acid (RNA). This attaches to proteins in the cell that help in the production of antiviral proteins in response to interferons. The interaction renders the cell unable to launch its defenses to protect against virus replication. In 30 years of dengue-related research this new mechanism was discovered never according to senior author Professor Mariano Garcia-Blanco of the Program in Emerging Infectious diseases. We not only found a new way in which the pathogen (dengue virus) interferes with the host response (human immune system) we also uncovered the first mechanistic insight into how this non-coding RNA works says Garcia-Blanco. He believes that the latest discovery opens the door to exploring therapeutics through this channel. These findings shed greater light on how the human immune response is regulated and for dengue how the virus has managed to evade these defenses. The work also highlights the differences between the four dengue strains and how more research is necessary to understand this highly complex virus. Source: National University of Singaporeyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license n
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