HIV/TB INTERACTION IN THE LUNG

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This study focuses on the transcriptional regulation of HIV-1 replication in alveolar macrophages. Alveolar macrophages from uninflamed lung inhibit HIV-1 replication by expressing a 16kDa inhibitory form of transcription factor C/EBPB (also called NF-IL6 and LIP) producing latent HIV-I infection in the lung. The inflammatory response to tuberculosis reduces C/EBPB expression, derepressing the HIV-1 long terminal repeat and induces another member of the C/EBP transcription factor family which supports high level HIV-1 replication in the lung. The lab was used for the following: DNA isolation, DNA sequencing (automated), ELISA, oligonucleotide synthesis, PCR, recombinant DNA techniques, RNA isolation, Southern analysis, Western analysis, bronchoalveolar lavage processing, EMSA, and use of laminar flow hoods.