The HIV DRP comprises a basic research component (Retroviral Replication Laboratory) and a clinical component (Host-Virus Interaction Branch).
Retroviral Replication Laboratory
The Retroviral Replication Laboratory (RRL) focuses on obtaining a detailed understanding of important events in the replication cycle of HIV-1, from the initial interactions between the virion and the host cell through reverse transcription and integration to mechanisms of virus assembly and release. The RRL conducts extensive research on the biochemistry and biology of viral replication, drug resistance, recombination, and the generation of mutations. Studies also include discovery, development, and mechanistic analysis of novel replication inhibitors, as well as the development and use of retroviral vectors. The RRL also studies the antiviral innate immune response against a number of human pathogenic viruses, and investigates viral and host gene expression and posttranscriptional regulation by using papillomaviruses and Kaposi’s sarcoma-associated herpesvirus as model viral systems. Read more...
Host-Virus Interaction Branch
As the clinical/translational arm of the HIV DRP, the Host-Virus Interaction Branch (HVIB) uses translational and clinical studies to elucidate HIV-host interactions and to devise approaches to understand, and eventually eliminate, HIV reservoirs. The HVIB is well known for developing highly sensitive assays to study the evolution and clinical significance of HIV drug resistance in vivo, and the persistence of HIV-infected cells in individuals on antiretroviral therapy (ART). Ongoing studies are focused on the following objectives: characterizing the replicating population size and genetics of HIV in infected individuals before, during, and after ART; defining the genetic mechanisms, kinetics of emergence and decay, and clinical consequences of HIV drug resistance; identifying the tissue and cellular sources of persistent viremia despite suppressive ART; and testing novel therapeutics to reduce persistent viremia and deplete HIV reservoirs. Read more...