Microbiology and Molecular Genetics Michigan State University
2215 Biomedical Physical Sciences East Lansing, MI 48824-4320
Undergrads:
517-884-5284
P: 517-884-5292
F: 517-353-8957
B.A. , 1988, Biochemistry, Jilin University, China
Ph.D. , 1998, Medical Sciences, Hokkaido University, Japan
Postdoctoral Fellow , 1998-1999, Vanderbilt University
Post-doctoral Scientist , 1999-2004, University of California, San Francisco
Assistant Researcher , 2004-2005, University of California, San Francisco
Address:
Department of Microbiology and Molecular Genetics
4174 Biomedical Physical Sciences
Michigan State University
East Lansing, MI 48824
Welcome to Zheng Laboratory. This lab is established in 2005, operating under supports from a MSU startup package and a NIAID RO1 grant. We are studying the molecular virology of human immunodeficiency virus type 1 (HIV-1), a retrovirus causes acquired immunodeficiency syndrome (AIDS). According to the Joint United Nations Programme on HIV/AIDS (UNAIDS), an estimated 38.6 million people worldwide were living with HIV in 2005, 4.1 million became newly infected with HIV, and 2.8 million lost their lives to AIDS. Our long-term interest is to develop a successful therapeutic strategy for HIV treatment by studying the function of host restriction factors, which have the capability to inhibit retroviral replication.
On human chromosome 22, a cluster of genes encodes a family of seven APOBEC3 (A3) antiretroviral proteins: A3A, A3B, A3C, A3DE, A3F, A3G, and A3H. They are cytidine deaminases with one or two enzymatic domains. A3G is the first identified potently blocks HIV replication. Later, A3F, A3B, and A3DE were also discovered for their anti-HIV activities. During viral replication, these A3 proteins are packaged into HIV virions and introduce C-to-U hypermutations in the viral genome during reverse-transcription. This event disables virus for replication. Nevertheless, the replication of HIV is not affected because this virus produces a viral infectivity factor, Vif, which inhibits these proteins by triggering their degradation. Thus, there is a fierce battlefield between HIV infection and the host defense system, and the winner is the virus. Our goal is to restore the power of this innate immunity so HIV infection can be blocked. Currently, our research efforts are focusing on these three aspects: 1) To discover new types of restriction factors for HIV; 2) To understand the precise mechanism of how A3 proteins block retroviral replication; 3) To interfere HIV-1 Vif function. These studies will illuminate the little known architecture of our innate antiretroviral immunity and lead to new avenues for boosting this immunity for HIV-1 infection.
Search PubMed at the National Library of Medicine:
