ArticlemBio2021
Toll-Like Receptor (TLR) Signaling Enables Cyclic GMP-AMP Synthase (cGAS) Sensing of HIV-1 Infection in Macrophages.
Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Hydroxylation of the HIV-1 antisense protein promotes immune evasion of HIV-1 via modulation of TBK1.Nature communications · 2026Article
- Exploring the pathogenesis of MAFLD from an immunological perspective: from the perspective of the cGAS/STING/NF-κB signaling pathway.Frontiers in immunology · 2025Review
- A cGAS-mediated type I interferon response in human CD4+ T cells depends on productive infection and is conserved over HIV types and strains.Journal of virology · 2024Article
- Inhibition of cGAS attenuates neonatal hypoxic-ischemic encephalopathy via regulating microglia polarization and pyroptosis.Translational pediatrics · 2024Article
- Article
- Understanding nucleic acid sensing and its therapeutic applications.Experimental & molecular medicine · 2023Review
- Significance of the cGAS-STING Pathway in Health and Disease.International journal of molecular sciences · 2023Review
- Toll-like Receptor Response to Human Immunodeficiency Virus Type 1 or Co-Infection with Hepatitis B or C Virus: An Overview.International journal of molecular sciences · 2023Review
- Association between Intestinal Microecological Changes and Atherothrombosis.Microorganisms · 2023Review
- Inflammasomes as mediators of inflammation in HIV-1 infection.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Human immunodeficiency virus-1 core: The Trojan horse in virus-host interaction.Frontiers in microbiology · 2022Review
- What role of the cGAS-STING pathway plays in chronic pain?Frontiers in molecular neuroscience · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
HIV-1 replicates in cells that express a wide array of innate immune sensors and may do so simultaneously with other pathogens. How a coexisting innate immune stimulus influences the outcome of HIV-1 sensing, however, remains poorly understood. Here, we demonstrate that the activation of a second signaling pathway enables a cyclic GMP-AMP synthase (cGAS)-dependent type I interferon (IFN-I) response to HIV-1 infection. We used RNA sequencing to determine that HIV-1 alone induced few or no signs of an IFN-I response in THP-1 cells. In contrast, when supplemented with suboptimal levels of bacterial lipopolysaccharide (LPS), HIV-1 infection triggered the production of elevated levels of IFN-I and significant upregulation of interferon-stimulated genes. LPS-mediated enhancement of IFN-I production upon HIV-1 infection, which was observed in primary macrophages, was lost by blocking reverse transcription and with a hyperstable capsid, pointing to viral DNA being an essential immunostimulatory molecule. LPS also synergistically enhanced IFN-I production by cyclic GMP-AMP (cGAMP), a second messenger of cGAS. These observations suggest that the DNA sensor cGAS is responsible for a type I IFN response to HIV-1 in concert with LPS receptor Toll-like receptor 4 (TLR4). Small amounts of a TLR2 agonist also cooperate with HIV-1 to induce type I IFN production. These results demonstrate how subtle immunomodulatory activity renders HIV-1 capable of eliciting an IFN-I response through positive cross talk between cGAS and TLR sensing pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.