Human Immune Response to Tuberculosis and the Effects of HIV

Tuberculosis is responsible for more deaths worldwide than any other infectious disease. Caused by the bacteria Mycobacterium tuberculosis (Mtb), the disease is especially deadly for people living with HIV. Despite the prevalence of tuberculosis, however, no vaccine exists, and knowledge of the pathways by which the human immune system controls the progression of tuberculosis remains incomplete.

David Russell, Microbiology and Immunology, in collaboration with Henry Charles Mwandumba (Liverpool School of Tropical Medicine), is identifying pathways involved in the human immune response to Mtb that are active or impaired in HIV-infected and HIV-uninfected individuals. A key component of the human immune response to Mtb is a type of white blood cell called a macrophage. This research will yield a functional phenotype of various macrophage lineages present in human lung airways, including alveolar macrophages from HIV-positive donors in which transcriptionally active HIV-1 genomes are present.

Through this project, researchers hope to characterize the impairment of lung immunity in people living with HIV-1 that renders them hypersusceptible to both tuberculosis and other lower respiratory tract infections. Furthermore, the goal of this research—the functional and phenotypic typing of Mtb-infected human lung macrophages—could generate testable models for immune-mediated control of Mtb growth that will inform future tuberculosis vaccine development programs.

NIH Award Number: 1R01AI155319-01

Cornell Researchers

Funding Received

$3.3 Million spanning 5 years