Karen Mossman

Herpes simplex virus ICP0 and ICP34.5 counteract distinct interferon-induced barriers to virus replication.

Activation and inhibition of virus and interferon: the herpesvirus story.

The herpes simplex virus ICP0 RING finger domain inhibits IRF3- and IRF7-mediated activation of interferon-stimulated genes.

Innate cellular response to virus particle entry requires IRF3 but not virus replication.

Analysis of anti-interferon properties of the herpes simplex virus type I ICP0 protein.

Herpesviruses and the innate immune response.

The role of ICP0-Null HSV-1 and interferon signaling defects in the effective treatment of breast adenocarcinoma.

Functional inaccessibility of quiescent herpes simplex virus genomes.

ICP0 prevents RNase L-independent rRNA cleavage in herpes simplex virus type 1-infected cells.

Identification of a novel pathway essential for the immediate-early, interferon-independent antiviral response to enveloped virions.

Induction of innate immunity against herpes simplex virus type 2 infection via local delivery of Toll-like receptor ligands correlates with beta interferon production.

The IFN-independent response to virus particle entry provides a first line of antiviral defense that is independent of TLRs and retinoic acid-inducible gene I.

Distinct functional motifs within the IL-17 receptor regulate signal transduction and target gene expression.

Antigen presentation by exosomes released from peptide-pulsed dendritic cells is not suppressed by the presence of active CTL.

Impairment of human NK cell cytotoxic activity and cytokine release by cigarette smoke.

Cigarette smoke suppresses type I interferon-mediated antiviral immunity in lung fibroblast and epithelial cells.

Restoration of vitamin C synthesis in transgenic Gulo-/- mice by helper-dependent adenovirus-based expression of gulonolactone oxidase.

Cigarette smoke attenuation of poly I:C-induced innate antiviral responses in human PBMC is mainly due to inhibition of IFN-beta production.

Cutting edge: FimH adhesin of type 1 fimbriae is a novel TLR4 ligand.

Characterization of the interferon regulatory factor 3-mediated antiviral response in a cell line deficient for IFN production.

FimH adhesin of type 1 fimbriae is a potent inducer of innate antimicrobial responses which requires TLR4 and type 1 interferon signalling.

Differential modification of interferon regulatory factor 3 following virus particle entry.

Cell fusion-induced activation of interferon-stimulated genes is not required for restriction of a herpes simplex virus VP16/ICP0 mutant in heterokarya formed between permissive and restrictive cells.

Exposure to cigarette smoke suppresses IL-15 generation and its regulatory NK cell functions in poly I:C-augmented human PBMCs.

Mechanisms employed by herpes simplex virus 1 to inhibit the interferon response.

Long double-stranded RNA induces an antiviral response independent of IFN regulatory factor 3, IFN-beta promoter stimulator 1, and IFN.

An accessory to the 'Trinity': SR-As are essential pathogen sensors of extracellular dsRNA, mediating entry and leading to subsequent type I IFN responses.

Cellular localization of the herpes simplex virus ICP0 protein dictates its ability to block IRF3-mediated innate immune responses.

Recognition of virus infection and innate host responses to viral gene therapy vectors.

Replication of subgenomic hepatitis C virus replicons in mouse fibroblasts is facilitated by deletion of interferon regulatory factor 3 and expression of liver-specific microRNA 122.

Treating viral exacerbations of chronic obstructive pulmonary disease: insights from a mouse model of cigarette smoke and H1N1 influenza infection.

Adaptive antiviral immunity is a determinant of the therapeutic success of oncolytic virotherapy.

IL-15 and type I interferon are required for activation of tumoricidal NK cells by virus-infected dendritic cells.

A critical role for IL-15 in TLR-mediated innate antiviral immunity against genital HSV-2 infection.

Retroviral expression of MIR2 decreases both surface MHC class I and the alloimmune CTL response.

Membrane perturbation elicits an IRF3-dependent, interferon-independent antiviral response.

Varicella-zoster virus immediate-early protein ORF61 abrogates the IRF3-mediated innate immune response through degradation of activated IRF3.

Innate and adaptive immune responses to herpes simplex virus.

Methods related to molecular virology.

Herpes simplex virus 1 tegument protein US11 downmodulates the RLR signaling pathway via direct interaction with RIG-I and MDA-5.

The nitric oxide pathway provides innate antiviral protection in conjunction with the type I interferon pathway in fibroblasts.

Anti-NMDA receptor encephalitis. The disorder, the diagnosis and the immunobiology.

Comparative functional evaluation of immunocompetent mouse breast cancer models established from PyMT-tumors using small animal PET with [(18)F]FDG and [(18)F]FLT.

Recent advances in understanding viral evasion of type I interferon.

MARCO is required for TLR2- and Nod2-mediated responses to Streptococcus pneumoniae and clearance of pneumococcal colonization in the murine nasopharynx.

The herpes simplex virus 1-encoded envelope glycoprotein B activates NF-κB through the Toll-like receptor 2 and MyD88/TRAF6-dependent signaling pathway.

Proinflammatory cytokines and chemokines - but not interferon-β - produced in response to HSV-2 in primary human genital epithelial cells are associated with viral replication and the presence of the virion host shutoff protein.

Novel paradigms of innate immune sensing of viral infections.

HIV-1 gp120 induces TLR2- and TLR4-mediated innate immune activation in human female genital epithelium.

Oncolytic virotherapy and immunogenic cancer cell death: sharpening the sword for improved cancer treatment strategies.

Immunogenic HSV-mediated oncolysis shapes the antitumor immune response and contributes to therapeutic efficacy.

Rewiring cancer cell death to enhance oncolytic viro-immunotherapy.

Permissiveness of human cancer cells to oncolytic bovine herpesvirus 1 is mediated in part by KRAS activity.

Combining oncolytic HSV-1 with immunogenic cell death-inducing drug mitoxantrone breaks cancer immune tolerance and improves therapeutic efficacy.

Novel roles of cytoplasmic ICP0: proteasome-independent functions of the RING finger are required to block interferon-stimulated gene production but not to promote viral replication.

Extracellular dsRNA: its function and mechanism of cellular uptake.

Type-I interferon signaling through ISGF3 complex is required for sustained Rip3 activation and necroptosis in macrophages.

Danger, diversity and priming in innate antiviral immunity.