Journal
TRENDS IN MICROBIOLOGY
Volume 28, Issue 8, Pages 619-632Publisher
CELL PRESS
DOI: 10.1016/j.tim.2020.03.015
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Funding
- National Institutes of Health (NIH) [R01AI134240, R01AI135726, R01AI123047, R01AI111914, R01AI111943, UH3AI122320, U19AI1112111, P51OD0111133]
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HIV co-infection is the most critical risk factor for the reactivation of latent tuberculosis (TB) infection (LTBI). While CD4(+) T cell depletion has been considered the major cause of HIV-induced reactivation of LTBI, recent work in macaques co-infected with Mycobacterium tuberculosis (Mtb)/simian immunodeficiency virus (SIV) suggests that cytopathic effects of SIV resulting in chronic immune activation and dysregulation of T cell homeostasis correlate with reactivation of LTBI. This review builds on compelling data that the reactivation of LTBI during HIV co-infection is likely to be driven by the events of HIV replication and therefore highlights the need to have optimum translational interventions directed at reactivation due to co-infection.
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