Assistant Professor, Medicine: Infectious Diseases and International Health
- BS, Cell Biology and Genetics, Peking University
- MS, Cell Biology and Genetics, Peking University
- PhD, Microbiology and Immunology, Cornell University
PO Box 800734
345 Crispell Drive, MR-6 1st floor, Room 1710
Charlottesville, VA 22908
Human Immunodeficiency Virus (HIV)
The HIV-1 infection is initiated by the sequential binding of the viral envelope glycoproteins (Envs) to the two cellular receptors, CD4 and a chemokine co-receptor, typically either CCR5 or CXCR4. Receptor binding triggers conformational changes in HIV-1 Envs that result in the fusion of the viral and target cell membranes. The ability of HIV-1 Envs to undergo conformational rearrangement is essential for their function in promoting virus entry, and also contributes to escaping from neutralizing antibodies. As the sole viral component on the virion surface, HIV-1 Envs serve as attractive targets in the development of prophylactic approach, including vaccine. An understanding of the structure and the conformational states of HIV-1 Envs is critical to rational attempts to design inhibitors and vaccines. The research in our laboratory is currently focused on:
- HIV-1 entry into target cells.
- The nature and biological relevance of the conformational states sampled by HIV-1 Envs.
- The interactions of gp120 and gp41 that contribute to exposure of CCR5 chemokine co-receptor binding site on HIV-1 Envs.
- HIV/AIDS subunit vaccine development.
- HIV-1 subtypes in relation to pathogenesis, transmission, and disease progression.
- HIV-1 coreceptor tropism in association to disease progression in Sepsis patients in Uganda.