ArticlePLoS pathogens2014
HIV and HCV activate the inflammasome in monocytes and macrophages via endosomal Toll-like receptors without induction of type 1 interferon.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 2 of them syntheses that pooled it.
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Who cites it
116 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review.Immunology letters · 2019Pooled it
- Systematic review and meta-analysis of hepatitis C virus infection and HIV viral load: new insights into epidemiologic synergy.Journal of the International AIDS Society · 2016Pooled it
- The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review.Dentistry journal · 2025Review
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- Targeting inflammasomes as a therapeutic potential for HIV/AIDS.Cellular and molecular life sciences : CMLS · 2025Review
- The inflammasome next door: characterizing pyroptosis induction in HCV-infected and uninfected bystander cellsFrontiers in cellular and infection microbiology · 2025Article
- NLRP3 Inflammasome Activation in Liver Disorders: From Molecular Pathways to Therapeutic Strategies.Journal of inflammation research · 2025Review
- Review
- Precision Phenotyping of Heart Failure in People with HIV: Early Insights and Challenges.Current heart failure reports · 2024Review
- Convergent evolution and targeting of diverse E2 epitopes by human broadly neutralizing antibodies are associated with HCV clearance.Immunity · 2024Article
- SHIV-C109p5 NHP induces rapid disease progression in elderly macaques with extensive GI viral replication.Journal of virology · 2024Article
- Advances in the mechanism of inflammasomes activation in herpes virus infection.Frontiers in immunology · 2024Review
- Distinct Types of Cell Death and Implications in Liver Diseases: An Overview of Mechanisms and Application.Journal of clinical and translational hepatology · 2023Review
- NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases-A Lesson from Cytokine Storm Syndrome.International journal of molecular sciences · 2023Review
- HIV Infection: Shaping the Complex, Dynamic, and Interconnected Network of the Cytoskeleton.International journal of molecular sciences · 2023Review
- Heat-KilledNutrients · 2023Article
- The impact of cannabinoids on inflammasome signaling in HIV-1 infection.NeuroImmune pharmacology and therapeutics · 2023Review
- Article
- Article
- HIV-1 activates oxidative phosphorylation in infected CD4 T cells in a human tonsil explant model.Frontiers in immunology · 2023Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Innate immune sensing of viral infection results in type I interferon (IFN) production and inflammasome activation. Type I IFNs, primarily IFN-α and IFN-β, are produced by all cell types upon virus infection and promote an antiviral state in surrounding cells by inducing the expression of IFN-stimulated genes. Type I IFN production is mediated by Toll-like receptor (TLR) 3 in HCV infected hepatocytes. Type I IFNs are also produced by plasmacytoid dendritic cells (pDC) after sensing of HIV and HCV through TLR7 in the absence of productive pDC infection. Inflammasomes are multi-protein cytosolic complexes that integrate several pathogen-triggered signaling cascades ultimately leading to caspase-1 activation and generation pro-inflammatory cytokines including interleukin (IL)-18 and IL-1β. Here, we demonstrate that HIV and HCV activate the inflammasome, but not Type I IFN production, in monocytes and macrophages in an infection-independent process that requires clathrin-mediated endocytosis and recognition of the virus by distinct endosomal TLRs. Knockdown of each endosomal TLR in primary monocytes by RNA interference reveals that inflammasome activation in these cells results from HIV sensing by TLR8 and HCV recognition by TLR7. Despite its critical role in type I IFN production by pDCs stimulated with HIV, TLR7 is not required for inflammasome activation by HIV. Similarly, HCV activation of the inflammasome in monocytes does not require TLR3 or its downstream signaling adaptor TICAM-1, while this pathway leads to type I IFN in infected hepatocytes. Monocytes and macrophages do not produce type I IFN upon TLR8 or TLR7 sensing of HIV or HCV, respectively. These findings reveal a novel infection-independent mechanism for chronic viral induction of key anti-viral programs and demonstrate distinct TLR utilization by different cell types for activation of the type I IFN vs. inflammasome pathways of inflammation.
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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.