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The cGAS-STING pathway in HIV-1 and Mycobacterium tuberculosis coinfection
Xiaoxu Han1,2, Xiuwen Wang1,2, Fangping Han3,4
1Beijing Key Laboratory for HIV/AIDS Research, Clinical and Research Center for Infectious Diseases, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
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.
Insights
Human immunodeficiency virus-1 (HIV-1) and Mycobacterium tuberculosis coinfection accelerate disease progression. The cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway is crucial for innate immunity against these pathogens.
Area of Science:
- Immunology
- Infectious Diseases
- Molecular Biology
Background:
- HIV-1/M. tuberculosis coinfection is a major global health concern, accelerating disease progression and mortality.
- HIV-1 increases M. tuberculosis susceptibility, while M. tuberculosis enhances HIV-1 replication and immune activation.
- Understanding coinfection pathogenesis is vital for developing new treatments to reduce tuberculosis burden.
Purpose of the Study:
- To review the role of the cGAS-STING signaling pathway in HIV-1 and M. tuberculosis infections.
- To discuss the potential involvement of the cGAS-STING pathway in HIV-1/M. tuberculosis coinfection.
- To provide insights into coinfection pathogenesis and novel therapeutic strategies.
Main Methods:
- Literature review of studies on cGAS-STING signaling in HIV-1 and M. tuberculosis infections.
- Analysis of the cGAS-STING pathway's role in innate immunity against these pathogens.
- Exploration of the pathway's potential implications in coinfection scenarios.
Main Results:
- The cGAS-STING pathway is a key DNA-sensing innate immune pathway studied in both HIV-1 and M. tuberculosis infections.
- This pathway plays a critical role in the host immune response against individual infections.
- Its specific role in the context of HIV-1/M. tuberculosis coinfection requires further investigation.
Conclusions:
- The cGAS-STING pathway is a significant component of innate immunity against HIV-1 and M. tuberculosis.
- Further research into the cGAS-STING pathway's function during coinfection may reveal novel therapeutic targets.
- Elucidating this pathway's role can lead to improved strategies for managing HIV-1/M. tuberculosis coinfection.
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