ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Suppressor of cytokine signaling 3 inhibits antiviral IFN-beta signaling to enhance HIV-1 replication in macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 96 citations in OpenAlex.
- Gene Expression of Suppressor of Cytokine Signaling 3 (SOCS3), Interferons Alpha and Beta (IFN-α and β) in Common Warts.Indian dermatology online journal · 2026Article
- A chicken lncRNA is identified as a critical regulator that increases influenza virus replication by impairing innate antiviral responses.Veterinary research · 2025Article
- Article
- Persistent type I interferon signaling within the brain of people with HIV on ART with cognitive impairment.PLoS pathogens · 2025Article
- Designing Nanomedicines for Breast Cancer Therapy.Biomolecules · 2023Article
- Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Promotes HIV-1 Replication through Modulating microRNAs in Macrophages.Journal of virology · 2023Article
- ZIKV Strains Elicit Different Inflammatory and Anti-Viral Responses in Microglia Cells.Viruses · 2023Article
- Negative regulation of type I interferon signaling by integrin-linked kinase permits dengue virus replication.PLoS pathogens · 2023Article
- A Rationale and Approach to the Development of Specific Treatments for HIV Associated Neurocognitive Impairment.Microorganisms · 2022Review
- Mechanisms contributing to adverse outcomes of COVID-19 in obesity.Molecular and cellular biochemistry · 2022Review
- TDRD3 is an antiviral restriction factor that promotes IFN signaling with G3BP1.PLoS pathogens · 2022Article
- SOCS proteins and their roles in the development of glioblastoma.Oncology letters · 2022Review
- TLR7 Activation of Macrophages by Imiquimod Inhibits HIV Infection through Modulation of Viral Entry Cellular Factors.Biology · 2021Article
- HIV-Infected Macrophages Are Infected and Killed by the Interferon-Sensitive Rhabdovirus MG1.Journal of virology · 2021Article
- Article
- T Cell-Intrinsic CDK6 Is Dispensable for Anti-Viral and Anti-Tumor ResponsesFrontiers in immunology · 2021Article
- Yellow Fever Virus Down-Regulates mRNA Expression of SOCS1 in the Initial Phase of Infection in Human Cell Lines.Viruses · 2020Article
- Single cell RNA sequencing identifies an early monocyte gene signature in acute respiratory distress syndrome.JCI insight · 2020Article
- Leukemia Inhibitory Factor Inhibits Plasmacytoid Dendritic Cell Function and Development.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes.Viruses · 2020Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
HIV-1 replication within macrophages of the CNS often results in cognitive and motor impairment, which is known as HIV-associated dementia (HAD) in its most severe form. IFN-beta suppresses viral replication within these cells during early CNS infection, but the effect is transient. HIV-1 eventually overcomes this protective innate immune response to resume replication through an unknown mechanism, initiating the progression toward HAD. In this article, we show that Suppressor of Cytokine Signaling (SOCS)3, a molecular inhibitor of IFN signaling, may allow HIV-1 to evade innate immunity within the CNS. We found that SOCS3 is elevated in an in vivo SIV/macaque model of HAD and that the pattern of expression correlates with recurrence of viral replication and onset of CNS disease. In vitro, the HIV-1 regulatory protein transactivator of transcription induces SOCS3 in human and murine macrophages in a NF-kappaB-dependent manner. SOCS3 expression attenuates the response of macrophages to IFN-beta at proximal levels of pathway activation and downstream antiviral gene expression and consequently overcomes the inhibitory effect of IFN-beta on HIV-1 replication. These studies indicate that SOCS3 expression, induced by stimuli present in the HIV-1-infected brain, such as transactivator of transcription, inhibits antiviral IFN-beta signaling to enhance HIV-1 replication in macrophages. This consequence of SOCS3 expression in vitro, supported by a correlation with increased viral load and onset of CNS disease in vivo, suggests that SOCS3 may allow HIV-1 to evade the protective innate immune response within the CNS, allowing the recurrence of viral replication and, ultimately, promoting progression toward HAD.
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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.