Research Fellow: Dr. Guanhan Li

Post-doctoral Fellow, Department of Neurology

Dr. Guanhan Li received his medical degree from Zhejiang Medical University in 1987, an M.S. degree from Shanghai Medical University, and a PhD from The Chinese Academy of Preventive Medicine. He first trained as a post-doctoral fellow at the University of Massachusetts Medical School and then joined the Nath lab in 2005 to continue his post-doctoral fellowship training.

Dr. Li's major research interest is to understand the mechanisms by which HIV establishes a reservoir in the brain. Accumulating evidences demonstrate that HIV-1 can infect astrocytes. Compared with CD4+ T lymphocytes and macrophages, the efficiency of HIV-1 infection in astrocytes is lower. However, astrocyte is the most frequent cell type of brain, which outnumbers neurons by 10-50:1, so it not only serves as a reservoir for HIV-1 infection, but also may play an important role in the pathogenesis of HIV dementia.

To investigate the mechanisms that contribute to restriction of HIV-1 infection and replication in astrocytes, Dr. Li hypothesizes that cellular factors restrict HIV-1 replication. Understanding the mechanisms by which astrocytes restrict HIV replication may provide important clues on how to control HIV replication in other cell types such as lymphocytes and macrophages. Some cellular factors (e.g., TRIM5, TRIM19/PML, APOBEC3G, etc.) have been widely investigated as factors to counteract infection of retroviruses, whereas their role in astrocytes is not yet known.

In collaboration with Drs. Mumper and Woodward at the University of Kentucky, Dr. Li is also working on an NIH funded project to help develop a vaccine using the HIV Tat protein. While Tat is a critical molecule that is required for HIV replication, it has poor immunogenicity and hence escapes the immune system. Dr. Mumper has developed novel nanoparticle based techniques for immunization of proteins antigens. Dr. Li has developed some assays to test the effects of these Tat-immunized antisera to block the effects on various Tat functions including HIV replication.