BC Research on HIV 'Marker' Recognized
Lab’s HIV Research Attracts Notice
The recent discovery of a molecule that serves as a marker for HIV activity by the lab of Professor of Biology Ken Williams has been recognized as among the top biological and medical research projects in the world, according to the research library service the Faculty of 1000.
The lab’s research into CD163 shows the molecule, which is shed by monocytes and macrophages during HIV infection, increases in volume in the blood of infected patients. Furthermore, for patients with long-term HIV infection the molecule remains even after anti-retroviral treatment effectively reduces the presence of the disease, the team reported in July edition of the Journal of Infectious Diseases.
“It’s gratifying to see our research recognized by our colleagues at other institutions,” said Research Assistant Professor Tricia Burdo, a member of the Williams lab and lead author of the paper. “What’s exciting is that the inclusion of the lab’s work on CD163 in a highly-respected database can help share this information with other researchers working in this critically important area.”
Burdo said the Faculty of 1000, also known as F1000, reaches an important audience of faculty and researchers in the biological and life sciences.
The research published in July shows that the CD163 molecule is a potential biomarker for the effectiveness of HIV therapies. The marker is viewed as a critical tool to better understand the damage infection can cause to the brain, even after effective therapeutic treatment.
The findings are among the latest from the Williams lab, which has advanced the understanding of the role that seemingly protective monocytes play in the progression of HIV and AIDS in the brain, which is an increasingly critical issue. While mortality rates from AIDS have declined thanks to antiretroviral drugs, AIDS-related dementia remains just as prevalent, particularly as AIDS patients live longer.
White blood cells that play a critical role in the immune system’s response to sickness, monocytes migrate from bone marrow to blood and, in the case of HIV infection, cross the blood-brain barrier, which normally keeps monocyte levels low in the brains of healthy individuals. The lab has studied monocytes and their more aggressive infection-fighting form, macrophages.
Burdo and Williams co-authored the research report with BC colleagues Patrick Autissier and Anitha Krishnan, Massachusetts General Hospital researchers Elkan Halpern and Eric S. Rosenberg, and University of California San Diego researchers Scott Letendre and Ronald J. Ellis.