FENG GAO, M.D.
Associate Research Professor, Department of Medicine

Contact Information
112 Research Park III
919-668-6433 phone
919-668-6435 fax
Fgao@duke.edu

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Education

	MD	Harbin Medical College, Heilongjing, China, 1984
	MS	Biological characterization of human hepatitis A strains, Chinese Academy of Preventive Medicin, Beijing, China, 1987

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Experience

	2001 -present	Associate Research Professor, Duke University Medical Center, Durham, NC
	1999 -present	Adjunct Associate Professor, Kunming Institute of Zoology, Chinese Academy of Science, China
	1999 - 2001	Associate Scientist, AIDS Center, University of Alabama at Birmingham
	1998 - 2001	Research Assistant Professor, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL
	1993 - 1998	Research Instructor, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294
	1992 - 1993	Research Associate, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294
	1987 - 1989	Research Associate, Institute of Virology, Chinese Academy of Preventive Medicine, China

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Selected Publications

1. Gao, F., Yue, L., White, A.T., Pappas, P.G., Barchue, J., Hanson, A.P., Greene, B.M., Sharp, P.M., Shaw, G.M. and Hahn, B.H. Human infection by genetically divers SIVSM related HIV-2 in West Africa. Nature 358:495-499, 1992.
2. Gao, F., Robertson, D.L., Morrison, S.G., Hui, H., Craig, S., Fultz, P.N., Decker, J., Girard, M., Shaw, G.M., Hahn, B.H. and Sharp, P.M. The heterosexual HIV-1 epidemic in Thailand is caused by an intersubtype (A/E) recombinant of African origin. J Virol. 70:7013-1029, 1996.
3. Gao, F., Robertson, D.L., Carruthers, C.D., Morrison, S.G, Jian, B., Chen, Y., Barre-Sinoussi, F., Girard, M., Srinivasan, A., Abimiku, A.G., Shaw, G.M., Sharp, P.M., and Hahn, B. A comprehensive panel of near full length clones and reference sequences for non-subtype B isolates of human immunodeficiency virus type 1. J Virol 72:5680-5698, 1998.
4. Gao, F., Bailes, E., Robertson, D.L., Chen, Y., Rodenburg, C.M., Michael, S.F., Cummins, L.B., Arthur, L.O., Peeters, M., Shaw, G.M., Sharp, P.M. and Hahn, B.H. Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes. Nature. 397:436-441, 1999.
5. Korber, B., Muldoon, M., Theiler, J., Gao. F., Gupta, R., Lapedes, A., Hahn, B.H., Wolinsky, S., Bhattacharya, T. Timing the ancestor of the HIV-1 Pandemic strains. Science. 288:1789-1796, 2000
6. Rodenburg, C.M., Li, Y., Trask,S.A., Chen, Y., Decker, J., Robertson, D.L., Kalish, M.I., Shaw, G.M., Allen, S., Hahn, B.H., Gao, F and the UNAIDS and NIAID Networks for HIV Isolation and Characterization. Near full-length clones and reference sequences for subtype C isolates of HIV-1 from three different continents. AIDS Res. Hum. Retro. 17:161-168, 2001
7. Santiago, M., Rodenburg, C., Kamenya, S., Bibollet-Ruche, Gao, F., Bailes, E., Meleth, S., Soong, S., Kilby, J., Moldoveanu, Z., Fahey, B., Muller, M., Ayouba, A., Nerrienet, E., McClure, H., Heeney, J., Pusey, A., Collins, A., Boesch, C., Wrangham, R., Goodall, J., Sharp, P., Shaw, G.M. and Hahn, B.H. Noninvasive detection and molecular identification of simian immunodeficiency virus in wild-living chimpanzees. Science, 295:465, 2002
8. Marras, D., Bruggeman, L.A., Gao, F., Tanji, N., Mansukhani, M., Cara, A., Ross, M.D., Gusella, G.L., Benson, G., D'Agati, V.D., Hahn, B.H., Klotman M.E. & Klotman P.E. Replication and Compartmentalization of HIV-1 in kidney epithelium of patients with HIV associated nephropathy. Nat. Med., 8:522-526, 2002.
9. Gaschen B, Taylor J, Yusim K, Foley B, Gao F, Lang D, Novitsky V, Haynes B, Hahn BH, Bhattacharya T, Korber B. Diversity considerations in HIV-1 vaccine selection. Science. 296:2354-60, 2002
10. Gao F, Bhattacharya T, Gaschen, B, Taylor J, Moore JP, Novitsky V, Yusim K, Lang D, Foley B, Beddows S, Alam M, Haynes B, Hahn BH, and Korber B. Consensus and Ancestral State HIV Vaccines. Science. 299:1517-1518. 2003

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Short Research Interest Descriptor

Retrovirus evolution and AIDS vaccine development.

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Research Interest

Antiretroviral drug combination has been effective in dramatically reducing HIV-related mortality and morbidity. However, nearly half of HIV-infected patients still fail the treatment. Although genetic analyses of viral genomes from these patients show multiple-drug resistance mutations in the pol gene, the molecular mechanisms for the emergence of drug-resistance are not yet known. Therefore, it is important to delineate the mechanisms for multiple-drug resistance in order to more efficiently control HIV infection. We are interested in studying the role of viral recombination in generation of multiple-drug resistance during therapy. We will genetically characterize the treatment baseline viral population and determine their predictive values for treatment failure by sequencing multiple clones from each patient before treatment. To determine the role of recombination in generation of multiple-drug resistance, we will compare the drug-resistant viral population with the baseline viral population and identify recombinant genomes and recombinant index increase of the viral population from patients who fail the treatment. We will also obtain viral populations before and after each treatment failure in the consecutive treatment regimes and analyze the dynamic changes of viral populations to determine mechanisms of repeated drug-resistance and fitness of drug-resistance viruses. Understanding the viral population changes, drug-resistance mechanisms and viral fitness during HAART will allow for the development of more effective antiretroviral agents, better treatment regimens and accurate prediction of treatment efficacy. Knowledge obtained from this study can be broadly applied toward understanding mechanisms of viral escape from immune surveillance and other selective forces.

HIV infection/AIDS has become a major threat to public health globally. The discovery and administration of anti-HIV drugs have decreased HIV-related morbidity and mortality in industrial counties. However, people in underdeveloped countries, where the most of HIV infected people have been reported, cannot benefit from antiviral drugs due to the unaffordable price. Moreover, drug resistance and toxicity in the treated patients significantly reduce the effectiveness of drug treatment. Therefore, the most effective way to control the devastating disease is to develop a safe, practical, and effective vaccine that can either prevent new infection or slow down disease progression. We are currently developing novel vaccine approaches using the molecular clones that we have generated for all major subtypes of HIV-1 group M viruses and artificial consensus genes that have a significantly decreased genetic distance between the vaccine immunogens and field viruses. The latter approach will give us an opportunity to develop universal immunogens that will overcome the extraordinary genetic variation of HIV-1. We are also currently using viral vector systems (semliki forest virus, murine leukemia virus, vaccina virus and adenovirus) to develop AIDS vaccines that will induce stronger immune responses.

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