interferon and immune responses

This study shows that IFN-lambda reduces HSV skin disease severity by limiting neutrophil-driven inflammation, independent of viral load.

This study shows that PKR activation can both restrict and enhance LCMV replication, revealing a complex role for PKR in mammarenavirus infection.

This study investigates PARP13's role in transcriptome regulation during basal and antiviral states, finding it shifts target localization but not binding preferences and supports ISGylation-related gene expression.

This paper identifies ISG15/USP18/STAT2 as a molecular hub that regulates autocrine IFN-I signaling to control Dengue and Zika virus replication.

This study designs and synthesizes fluorinated cGAMP analogs that are stable against poxin cleavage and show high STING activation, with structural insights into their binding modes.

The paper investigates whether micronuclei activate the cGAS-STING pathway and finds that MN do not robustly trigger this pathway.

The paper investigates the role of Dicer's helicase domain in antiviral immunity, finding that a truncated mutant acts RNAi-independently via PKR and NF-kB pathways.

The paper models SARS-CoV-2 infection spread using a cellular automaton, showing that heterogeneity in infections arises from sensitivity near a critical threshold and that few IFN-primed cells can limit viral proliferation.

The paper examines the evolutionary arms race between 5'ppp-RNA virus and the MDA5 receptor in RIG-I-lost teleost fish, showing how MDA5 compensates for RIG-I loss and how the virus counteracts this through m6A methylation.

This study uses CRISPR activation to identify anti-viral ISGs by testing their ability to prevent viral replication and cytopathic effects.

The paper investigates how C. elegans Dicer collaborates with DRH-1 and RDE-4 to cleave dsRNA, revealing their roles in antiviral defense mechanisms.

This study shows that the cGAS-STING pathway drives microglial chemotaxis and inflammation in response to DNA damage, linking genome instability to neuroinflammation.

The paper identifies critical antiviral residues in IFN subtypes and designs improved IFN molecules with enhanced antiviral activity against HIV and HBV.

This study identifies a mechanism by which tick-borne flaviviruses inhibit interferon signaling by targeting TYK2 catalytic activity through their NS5 protein.

The paper models the antagonism between viral infection and innate immunity at the single-cell level using an agent-based stochastic approach, revealing three levels of viral interference with the immune response.

VExD curates human gene expression data from viral infections to identify expression changes and support experimental validation.

The paper shows STAT1 is essential for establishing IFNγ-induced transcriptional memory but not for maintaining it, with GBP genes being poised for rapid activation upon secondary exposure.

This study shows DUX4 and mouse Dux interact with STAT1 and inhibit IFN-gamma-induced ISG expression by reducing STAT1 and Pol-II recruitment.

This study identifies how IFITM3 inhibits influenza virus entry by stabilizing hemifusion through lipid sorting in endosomal membranes.

This study shows that the cGAS-STING pathway restricts noroviruses by detecting leaked genomic and mitochondrial DNA, leading to IFN responses.

The paper identifies epigenetic features that regulate cell type-specific interferon beta responses in mouse cells by analyzing chromatin and gene expression changes.

The paper identifies HELZ2 as an ISG protein that inhibits LINE-1 retrotransposition and reduces IFN- induction by interacting with L1 RNA and ORF1p.

This study shows that constitutively active STING in mice leads to neuroinflammation and dopaminergic neuron degeneration, suggesting therapeutic targeting of this pathway.

This study investigates TE activation in SARS-CoV-2 infection, finding it induces a weaker IFN response compared to other viruses, with TE expression and viral load explaining immune response diversity.

The paper identifies a Neandertal introgressed haplotype in the OAS1 gene associated with increased risk of severe COVID-19 and shows it impairs SARS-CoV-2 clearance through genetic regulation of OAS1 expression.

This study identifies IFN pathway lupus risk alleles associated with COVID-19 mortality and develops predictive models combining genetics and biomarkers.

The paper develops a high-content assay to identify viral genes that suppress innate immunity and validates known and novel immune suppressors from various viral families.

The paper investigates monocyte subset heterogeneity and its impact on influenza virus susceptibility across populations, revealing differences in transcriptional responses and infection resistance between African and European ancestry individuals.

The paper develops a spatial multicellular model of RNA virus replication and interferon responses, showing how interferon concentrations and diffusion rates affect plaque growth dynamics.

The paper identifies OLFML3 as a rhinovirus-inducible IFN antagonist using surfaceome CRISPR screening, showing its role in suppressing innate immunity.