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First NameVinay
Last NamePathak
Designation/Position/RoleHead, Viral Mutation Section
Institute/OrganisationNational Cancer Institute-Frederick
Office Address/LocationNCI-Frederick, Building 535, Room 334
ExpertiseOur goal is to understand how HIV-1 replicates and how its interactions with the host cell influence its replication. We are active in three major research areas. First, we are defining the structure and function of APOBEC3G and 3F proteins. We are identifying the determinants of interaction between HIV-1 Vif and APOBEC3 proteins through genetic and biochemical analysis. We are elucidating the mechanisms by which the APOBEC3 proteins inhibit HIV-1 DNA synthesis, integration, and viral replication. In addition, we are investigating the mechanisms by which APOBEC3 proteins are incorporated into virions and regulated in vivo. Our long-term goal is to identify small-molecule inhibitors that interfere with the interaction between HIV-1 Vif and APOBEC3 proteins, which could form the basis of a new class of antiretroviral drugs.  
Second, we are elucidating mechanisms by which HIV-1 reverse transcriptase (RT) acquires resistance to RT inhibitors. We have identified eight novel mutations in the C-terminal connection and RNase H domains of RT that substantially enhance NRTI and NNRTI resistance. Current genotypic and phenotypic studies only analyze the N-terminal domains of RT for drug resistance and do not include the C-terminal domains. However, our studies indicate that it is important to include the C-terminal  
connection and RNase H domains in future genotypic and phenotypic analyses of drug resistance. The improved genotypic and phenotypic assays might predict antiviral drug resistance more accurately and would lead directly to the development of new clinical protocols designed to improve drug choice in salvage therapy. Our specific research aims are to further define the role of the C-terminal connection and RNase H domains of RT in antiviral drug resistance in subtype B as well as non-B subtypes of HIV-1.  
Third, we are exploring the in vivo mechanisms of reverse transcription by using a novel quantitative strand-specific amplification (SSA) technology that we recently developed. We are using the SSA method to measure the rates of viral DNA synthesis in activated primary CD4+ T cells and macrophages, the target cells of HIV-1 infection. We are studying the mechanism of discontinuous plus-strand DNA synthesis and the influence of RT inhibitors on the kinetics of reverse transcription, providing insights into their mechanisms of inhibition. The SSA technology provides a novel approach to analyzing DNA replication processes and may facilitate the development of new antiretroviral drugs that target specific steps in HIV-1 reverse transcription. 


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