ArticleAIDS research and human retroviruses2017
HIV-1 Infection Primes Macrophages Through STAT Signaling to Promote Enhanced Inflammation and Viral Replication.
Article in AIDS research and human retroviruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- A tissue-intrinsic mechanism sensitizes HIV-1 particles for TLR-triggered innate immune responses.Nature communications · 2026Article
- Contemporary antiretroviral pharmacology in the male genital tract: implications for HIV treatment and prevention.Antimicrobial agents and chemotherapy · 2026Review
- IL-18 and MIG increase one year after transition to dolutegravir-based dual therapy despite sustained viral suppression.Frontiers in immunology · 2026Article
- Proteomic Characterization of HIV Infection.Advances in experimental medicine and biology · 2026Review
- Integrated bioinformatics analysis identifies hub genes and immune regulatory networks in HIV infection.Frontiers in immunology · 2025Article
- Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells.Science advances · 2023Article
- Article
- Identification of drug candidates targeting monocyte reprogramming in people living with HIV.Frontiers in immunology · 2023Article
- Transcriptome Analysis of Bovine Macrophages (BoMac) Cells after Infection with Bovine Immunodeficiency Virus.Journal of veterinary research · 2022Article
- S100A8-mediated metabolic adaptation controls HIV-1 persistence in macrophages in vivo.Nature communications · 2022Article
- Anti-inflammatory effects of recreational marijuana in virally suppressed youth with HIV-1 are reversed by use of tobacco products in combination with marijuana.Retrovirology · 2022Article
- HIV-1 Accessory Proteins Impart a Modest Interferon Response and Upregulate Cell Cycle-Related Genes in Macrophages.Pathogens (Basel, Switzerland) · 2022Article
- Robust innate immune responses at the placenta during early gestation may limit in utero HIV transmission.PLoS pathogens · 2021Article
- Altered expression of fractalkine in HIV-1-infected astrocytes and consequences for the virus-related neurotoxicity.Journal of neurovirology · 2021Article
- Interactions with Commensal and Pathogenic Bacteria Induce HIV-1 Latency in Macrophages through Altered Transcription Factor Recruitment to the LTR.Journal of virology · 2021Article
- Identification of SARS-CoV-2 3CL Protease Inhibitors by a Quantitative High-Throughput Screening.ACS pharmacology & translational science · 2020Article
- Identification of SARS-CoV-2 3CL Protease Inhibitors by a Quantitative High-throughput Screening.bioRxiv : the preprint server for biology · 2020Article
- Long Noncoding RNA GAS5 Regulates Macrophage Polarization and Diabetic Wound Healing.The Journal of investigative dermatology · 2020Article
- Reversible Human Immunodeficiency Virus Type-1 Latency in Primary Human Monocyte-Derived Macrophages Induced by Sustained M1 Polarization.Scientific reports · 2018Article
- CRISPR/Cas9 knockout of USP18 enhances type I IFN responsiveness and restricts HIV-1 infection in macrophages.Journal of leukocyte biology · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages play important roles in HIV-1 pathogenesis as targets for viral replication and mediators of chronic inflammation. Similar to IFNγ-priming, HIV-1 primes macrophages, resulting in hyperresponsiveness to subsequent toll-like receptor (TLR) stimulation and increased inflammatory cytokine production. However, the specific molecular mechanism of HIV-1 priming and whether cells must be productively infected or if uninfected bystander cells also are primed by HIV-1 remains unclear. To explore these questions, human macrophages were primed by IFNγ or infected with HIV-1 before activation by TLR ligands. Transcriptome profiling by microarray revealed a gene expression profile for IFNγ-primed cells that was further modulated by the addition of lipopolysaccharide (LPS). HIV-1 infection elicited a gene expression profile that correlated strongly with the profile induced by IFNγ (r = .679, p = .003). Similar to IFNγ, HIV-1 enhanced TLR ligand-induced tumor necrosis factor (TNF) protein expression and release. Increased TNF production was limited to productively infected cells. Specific signal transducer and activator of transcription (STAT)1 and STAT3 inhibitors suppressed HIV-1-mediated enhancement of TLR-induced TNF expression as well as HIV-1 replication. These findings indicate that viral replication and inflammation are linked through a common IFNγ-like, STAT-dependent pathway and that HIV-1-induced STAT1 and STAT3 signaling are involved in both inflammation and HIV-1 replication. Systemic innate immune activation is a hallmark of active HIV-1 replication. Our study shows that inflammation may develop as a consequence of HIV-1 triggering STAT-IFN pathways to support viral replication.
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