Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), continues to pose a major public health problem and is the leading cause of mortality in people infected with human immunodeficiency virus (HIV). HIV infection greatly increases the risk of developing TB even before CD4+ T-cell counts decrease. Co-infection provides reciprocal advantages to both pathogens and leads to acceleration of both diseases. In HIV-coinfected persons, the diagnosis and treatment of tuberculosis are particularly challenging. Intensifying integration of HIV and tuberculosis control programmes has an impact on reducing diagnostic delays, increasing early case detection, providing prompt treatment onset, and ultimately reducing transmission. In this Review, we describe our current understanding of how these two pathogens interact with each other, new sensitive rapid assays for TB, several new prevention methods, new drugs and regimens. Abbreviations: ART = antiretroviral therapy, CRP = C-reactive protein, CYP3A = cytochrome p450 3A, GM-CSF = granulocytemacrophage colony-stimulating factor, HDT = host-directed therapy, HIV = human immunodeficiency virus, ICF = The case finding, INH = isoniazid, IPT = isoniazid preventive therapy, LAM = lipoarabinomannan, LF-LAM = lateral flow lipoarabinomannan, MDR-TB = multidrug-resistant tuberculosis, MDSCs = myeloid-derived suppressor cells, MTB = Mycobacterium tuberculosis, PLWH = people with HIV, QFT = QuantiFERON Gold In-Tube, RIF = rifampicin, Se NPs = selenium nanoparticles, TB = tuberculosis, TB-IRIS = tuberculosis-associated immune reconstitution inflammatory syndrome, TPT = tuberculosis preventive therapy, TSPOT = T.SPOT-TB, TST = TB skin test, XDR-TB = extensively drug-resistant tuberculosis.
