ArticleJournal of virology2012
Vpu-deficient HIV strains stimulate innate immune signaling responses in target cells.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- SRSF1 acts as an IFN-I-regulated cellular dependency factor decisively affecting HIV-1 post-integration steps.Frontiers in immunology · 2022Article
- Article
- Unravelling the Immunomodulatory Effects of Viral Ion Channels, towards the Treatment of Disease.Viruses · 2021Review
- Ubiquitination modification: critical regulation of IRF family stability and activity.Science China. Life sciences · 2021Review
- People with HIV-1 demonstrate type 1 interferon refractoriness associated with upregulated USP18.Journal of virology · 2021Article
- The Interplay Among HIV, LINE-1, and the Interferon Signaling System.Frontiers in immunology · 2021Review
- Review
- HIV-1 Infection and Type 1 Interferon: Navigating Through Uncertain Waters.AIDS research and human retroviruses · 2019Review
- HIV Vpu Interferes with NF-κB Activity but Not with Interferon Regulatory Factor 3.Journal of virology · 2015Article
- HIV Blocks Interferon Induction in Human Dendritic Cells and Macrophages by Dysregulation of TBK1.Journal of virology · 2015Article
- Innate immunity against HIV-1 infection.Nature immunology · 2015Review
- Early IFN type I response: Learning from microbial evasion strategies.Seminars in immunology · 2015Review
- The enemy within: endogenous retroelements and autoimmune disease.Nature immunology · 2014Review
- Innate antiviral immune signaling, viral evasion and modulation by HIV-1.Journal of molecular biology · 2014Review
- Enhanced human immunodeficiency virus Type 1 expression and neuropathogenesis in knockout mice lacking Type I interferon responses.Journal of neuropathology and experimental neurology · 2014Article
- HIV-1 Vpu does not degrade interferon regulatory factor 3.Journal of virology · 2013Article
- Caught in translation: innate restriction of HIV mRNA translation by a schlafen family protein.Cell research · 2013Article
- Human tetherin exerts strong selection pressure on the HIV-1 group N Vpu protein.PLoS pathogens · 2012Article
- Innate immune sensing of HIV-1 by dendritic cells.Cell host & microbe · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Acute virus infection induces a cell-intrinsic innate immune response comprising our first line of immunity to limit virus replication and spread, but viruses have developed strategies to overcome these defenses. HIV-1 is a major public health problem; however, the virus-host interactions that regulate innate immune defenses against HIV-1 are not fully defined. We have recently identified the viral protein Vpu to be a key determinant responsible for HIV-1 targeting and degradation of interferon regulatory factor 3 (IRF3), a central transcription factor driving host cell innate immunity. IRF3 plays a major role in pathogen recognition receptor (PRR) signaling of innate immunity to drive the expression of type I interferon (IFN) and interferon-stimulated genes (ISGs), including a variety of HIV restriction factors, that serve to limit viral replication directly and/or program adaptive immunity. Here we interrogate the cellular responses to target cell infection with Vpu-deficient HIV-1 strains. Remarkably, in the absence of Vpu, HIV-1 triggers a potent intracellular innate immune response that suppresses infection. Thus, HIV-1 can be recognized by PRRs within the host cell to trigger an innate immune response, and this response is unmasked only in the absence of Vpu. Vpu modulation of IRF3 therefore prevents virus induction of specific innate defense programs that could otherwise limit infection. These observations show that HIV-1 can indeed be recognized as a pathogen in infected cells and provide a novel and effective platform for defining the native innate immune programs of target cells of HIV-1 infection.
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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.