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Effect of Mycobacterium Tuberculosis On HIV Replication and The Role of The Immune Response
Effect of Mycobacterium Tuberculosis On HIV Replication and The Role of The Immune Response
Conclusions
• Infection with tuberculosis increases HIV replication as seen in the
increased amount of HIV RNA numbers during tuberculosis infection as
Figure 2. Introduction of MTB and PPD into CD8+ T cell Figure 3. Introduction of MTB and PPD into CD8+ T cell compared to HIV RNA before infection and after successful treatment of
http://www.doctorswithoutborders.org/publications/topten/2008/story.cfm?id=3241
depleted PBMCs from HIV positive, PPD positive induces depleted lymph node mononuclear cells induces HIV Mycobacterium tuberculosis
Methods HIV replication. No effect was seen in the viral load of HIV replication in HIV positive PPD positive cells. The rate of
This study measured the in vivo and in vitro effects of MTB on HIV replication. Plasma in unfractionated PBMCs taken from HIV infected replication is expected to be higher in lymph nodes due to the
was sampled from individuals from a retrospective cohort study as well as a prospective individuals with positive PPD tests. Once CD8+ T cells are role of lymph nodes in immune response and due to the fact •In vitro, using peripheral blood mononuclear cells and lymph node
cohort study from Baltimore, Italy, and New York. The samples were taken from added back into PBMC of HIV Positive, PPD positive that the lymph nodes are a major site of HIV replication. Viral mononuclear cells, HIV is increased in CD8+ T cell depleted lymphocytes of
individuals that were HIV positive before MTB infection as well as from these individuals sample, HIV replication is depleted once again. load decreases once CD8+ T Cells are added back into the HIV infected, PPD positive individuals after stimulation with MTB or PPD
after successful or unsuccessful treatment of MTB. Matched controls were used for culture.
each patient that controlled for CD4+ count and risk factors. The in vitro study used •Increase in HIV replication is most likely due to CD4+ T cell activation to
peripheral blood mononuclear cells (PBMC) which include CD4+, CD8+ lymphocytes,
pathogenic antigens of Mycobacterium tuberculosis
macrophages, and monocytes that were infected with HIV-1. In addition, mechanisms
of MTB on the replication of HIV were evaluated by examining both unfractionated Further experimentation was carried out to evaluate the importance of immune response to MTB in HIV
PBMCs and CD8+ T cell depleted PBMCs in order to focus the study on CD4+ T cells. CD infected individuals. This is measured by PPD positivity. PPD is a derivative of Mycobacterium tuberculosis that •Activation of CD4+ T cells infected with HIV end in cell death and
4+T cells are the site of infection of the HIV virus. when injected in a small amount to the skin of an individual infected with MTB, creates a raised area in the depletion of T cells
skin, demonstrating an immune response to the MTB. This is a primary test of tuberculosis infection.
Results •CD8+ T cells can inhibit viral replication of CD4+ T cells
References
Goletti, Delia, Drew Weissman, Robert W. Jackson, Neil M. Graham, David Vlahov, Robert S. Klein,
Sonal S. Munsiff, Luigi Ortona, Robert Cauda, and Anthony S. Fauci. "Effect Mycobacterium
Tuberculosis on HIV Replication: Role of Immune Replication." The Journal of Immunology 157
(1996): 1271-278. Web.
Kaufmann, Stefan H., and Andrew J. McMicheal. "Nature Medicine." Annulling a Dangerous Liaison:
Vaccination Strategies against AIDS and Tuberculosis 11.4 (2005): 33-44. Web.