interferon and immune responses

This study identifies interferon-stimulated genes (ISGs) in chicken, quail, and duck cells and performs a CRISPR knockout screen to find genes restricting influenza replication, revealing species-specific differences in antiviral immunity.

This study shows adenovirus mutants differentially activate dsRNA sensors, leading to distinct RNP granule assemblies via PKR and OAS3/RNase L pathways.

This study investigates the dual role of IFNγ in coronavirus infection, showing it limits systemic viral spread but increases brain vulnerability, suggesting potential therapeutic modulation.

This study shows type I and II interferons have distinct and overlapping roles in controlling Chlamydia trachomatis infection in the female genital tract, with type I acting earlier and type II later, and both critical for suppression at different stages and locations.

This paper identifies that coronavirus PLpro-TM cleaves Importin α1 to disrupt nuclear transport and suppress antiviral immunity, revealing a conserved immune evasion strategy across coronaviruses.

The paper shows that single-cell heterogeneity in IFN induction potential is heritable and driven by baseline variation in JNK and AP-1 signaling states.

The paper screens TLR signaling inhibitors to identify compounds affecting stress granules and finds PPM18, which inhibits Influenza A Virus without relying on stress granule formation.

The paper shows that MxB's N-terminal domain binds to herpesvirus capsids and is packaged into virions, restricting HSV-1 and PrV infections.

This study compares the innate immune evasion abilities of nucleocapsid proteins from different human coronaviruses, finding significant functional and mechanistic differences.

This study identifies the IFN-STAT1/STAT5B-SOCS1 axis as a mechanism by which respiratory viruses activate autophagy, showing that targeting this pathway can inhibit virus replication without compromising innate immunity.

This study identifies NONO as a critical facilitator of antiviral innate immune response by promoting chromatin accessibility and IFN-I/ISG expression.

The paper develops a model-based analysis of how p53 stress memory influences JAK/STAT1 antiviral signaling, showing it redistributes STAT1 activity and affects viral control outcomes.

This study identifies the RIG-I/MDA5-MAVS-IRF3 axis as the pathway sensing TONV infection and activating the IFN-I response to restrict viral replication.

The paper screens lipid metabolic pathways to identify how they regulate the STING immune response, finding that perturbations in mevalonate, eicosanoid, and fatty acid pathways modulate STING signaling.

This study identifies Tetherin as an immunometabolic checkpoint in adipocytes that restricts type I interferon signaling while preserving glycolytic capacity, improving metabolic homeostasis.

This study shows that TBK1 and IKKε protect target cells from IFNγ-mediated T cell killing by suppressing inflammatory apoptosis and NFκB-driven inflammation.

This study shows that DNA- and RNA-sensing immune pathways differently control genital HSV-2 infection and prevent neuroinvasion.

The paper investigates how TRIM5α restricts orthoflavivirus replication and identifies a mutation in POWV's NS3 gene that allows it to evade TRIM5α inhibition.

This study identifies TRIM52 as a negative regulator of IFN-β production by promoting TBK1 ubiquitination and proteasomal degradation.

This study shows that TLR3 activation in human iPSC-derived microglia-containing cerebral organoids induces antiviral factors against HIV-1.

The paper systematically identifies effector functions of pathogen ORFs across multiple pathways, revealing new roles for known effectors and uncharacterized proteins.

This study shows that C. elegans STA-1, a STAT-like protein, relocalizes from nuclei to cytoplasm during viral infection, acting cell-intrinsically to repress anti-viral defense.

This paper develops a mathematical model of virus-host interactions during RNA virus infection, revealing how immune dynamics and viral strategies determine infection outcomes.

The paper identifies SLC7A1 as the transporter for cGAMP and its analogs in T cells, showing that targeting this transporter can reduce toxicity without affecting arginine transport.

This study identifies USP24 as a novel ISG15 cross-reactive deubiquitinase that de-ISGylates MOV10 to negatively regulate IFN-I production.

This study investigates how the HUSH complex suppresses the type I interferon pathway in human pluripotent cells, revealing its role in preventing self-nucleic acid sensing and maintaining immune evasion.

This study uses in vivo single-cell analysis to show that type I IFN signaling and NK cells limit MHV68 infection in lymph nodes, with IFNAR deficiency increasing infected B cell numbers and NK cell depletion enhancing viral spread.

The paper shows that cell death, not type-1 interferons, limits Chandipura virus propagation at high multiplicity of infection.

The paper shows that type I interferon primes alveolar epithelial cells for regeneration by enhancing their response to reparative signals from tissue-resident macrophages after viral infection.