Immune Responses to Mycobacterium tuberculosis and the Impact of HIV Infection

Riou, Catherine; Stek, Cari; Bruyn, Elsa Du

doi:10.1007/978-3-030-29108-2_4

Cited by 1 publication

(2 citation statements)

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“…While HIV predominately infects CD4+ T cells, it can also infect macrophages and dendritic cells ( 73 ). Upon infecting alveolar macrophages, HIV impedes receptor-mediated phagocytosis and cell apoptosis which limits the cell’s ability to kill intracellular bacteria ( 74 ). In dendritic cells, HIV can disrupt Mtb antigen processing and presentation which alters the initiation of the adaptive immune response ( 74 ).…”

Section: Mtb- Hiv Interactions In Pre-existing Hiv Infectionmentioning

confidence: 99%

“…Upon infecting alveolar macrophages, HIV impedes receptor-mediated phagocytosis and cell apoptosis which limits the cell’s ability to kill intracellular bacteria ( 74 ). In dendritic cells, HIV can disrupt Mtb antigen processing and presentation which alters the initiation of the adaptive immune response ( 74 ). It has been demonstrated in macrophage cultures that HIV coinfection of macrophages enhances Mtb growth ( 75 ).…”

Section: Mtb- Hiv Interactions In Pre-existing Hiv Infectionmentioning

confidence: 99%

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Systems biology approaches to investigate the role of granulomas in TB-HIV coinfection

Hoerter

Arnett²,

Schlesinger³

et al. 2022

Front. Immunol.

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The risk of active tuberculosis disease is 15-21 times higher in those coinfected with human immunodeficiency virus-1 (HIV) compared to tuberculosis alone, and tuberculosis is the leading cause of death in HIV+ individuals. Mechanisms driving synergy between Mycobacterium tuberculosis (Mtb) and HIV during coinfection include: disruption of cytokine balances, impairment of innate and adaptive immune cell functionality, and Mtb-induced increase in HIV viral loads. Tuberculosis granulomas are the interface of host-pathogen interactions. Thus, granuloma-based research elucidating the role and relative impact of coinfection mechanisms within Mtb granulomas could inform cohesive treatments that target both pathogens simultaneously. We review known interactions between Mtb and HIV, and discuss how the structure, function and development of the granuloma microenvironment create a positive feedback loop favoring pathogen expansion and interaction. We also identify key outstanding questions and highlight how coupling computational modeling with in vitro and in vivo efforts could accelerate Mtb-HIV coinfection discoveries.

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Section: Mtb- Hiv Interactions In Pre-existing Hiv Infectionmentioning

confidence: 99%