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Review
. 2025 Apr;53(2):495-511.
doi: 10.1007/s15010-024-02429-0. Epub 2024 Nov 7.

The cGAS-STING pathway in HIV-1 and Mycobacterium tuberculosis coinfection

Affiliations
Review

The cGAS-STING pathway in HIV-1 and Mycobacterium tuberculosis coinfection

Xiaoxu Han et al. Infection. 2025 Apr.

Abstract

Mycobacterium tuberculosis (M. tuberculosis) infection is the most common opportunistic infection in human immunodeficiency virus-1 (HIV-1)-infected individuals, and the mutual reinforcement of these two pathogens may accelerate disease progression and lead to rapid mortality. Therefore, HIV-1/M. tuberculosis coinfection is one of the major global public health concerns. HIV-1 infection is the greatest risk factor for M. tuberculosis infection and increases the likelihood of endogenous relapse and exogenous reinfection with M. tuberculosis. Moreover, M. tuberculosis further increases HIV-1 replication and the occurrence of chronic immune activation, accelerating the progression of HIV-1 disease. Exploring the pathogenesis of HIV-1/M. tuberculosis coinfections is essential for the development of novel treatments to reduce the global burden of tuberculosis. Innate immunity, which is the first line of host immune defense, plays a critical role in resisting HIV-1 and M. tuberculosis infections. The role of the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway, which is a major DNA-sensing innate immune signaling pathway, in HIV-1 infection and M. tuberculosis infection has been intensively studied. This paper reviews the role of the cGAS-STING signaling pathway in HIV-1 infection and M. tuberculosis infection and discusses the possible role of this pathway in HIV-1/M. tuberculosis coinfection to provide new insight into the pathogenesis of HIV-1/M. tuberculosis coinfection and the development of novel therapeutic strategies.

Keywords: Mycobacterium tuberculosis; HIV; Innate immune system; cGAS-STING pathway.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

References

    1. UNAIDS, Global HIV. & AIDS statistics — Fact sheet. Accessed 2024.04.01, 2024. https://www.unaids.org/en/resources/fact-sheet
    1. World Health Organization. GLOBAL TUBERCULOSIS REPORT 2023. Licence: CC BY-NC-SA 3.0 IGO.
    1. Dye C, Williams BG. Tuberculosis decline in populations affected by HIV: a retrospective study of 12 countries in the WHO African Region. Bull World Health Organ Jun. 2019;1(6):405–14. https://doi.org/10.2471/blt.18.228577 . - DOI
    1. Dannenberg AM. Jr. Immune mechanisms in the pathogenesis of pulmonary tuberculosis. Rev Infect Dis Mar-Apr. 1989;11(Suppl 2):S369–78. https://doi.org/10.1093/clinids/11.supplement_2.s369 . - DOI
    1. Douek DC, Picker LJ, Koup RA. T cell dynamics in HIV-1 infection. Annu Rev Immunol. 2003;21:265–304. https://doi.org/10.1146/annurev.immunol.21.120601.141053 . - DOI - PubMed

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