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Rabies virus nucleoprotein functions to evade activation of the RIG-I-mediated antiviral response.

The rabies virus Ni-CE strain causes nonlethal infection in adult mice after intracerebral inoculation, whereas the parental Nishigahara (Ni) strain kills mice. We previously reported that the chimeric CE(NiN) strain with the N gene from the Ni strain in the genetic background of the Ni-CE strain kills adult mice, indicating that the N gene is related to the different pathogenicities of Ni and Ni-CE strains. In the present study, to obtain an insight into the mechanism by which the N gene determines viral pathogenicity, we compared the effects of Ni, Ni-CE, and CE(NiN) infections on host gene

Diabetogenic potential of human pathogens uncovered in experimentally permissive beta-cells.

Pancreatic beta-cell antiviral defense plays a critical role in protection from coxsackievirus B4 (CVB4)-induced diabetes. In the present study, we tested the hypothesis that interferon (IFN)-induced antiviral defense determines beta-cell survival after infection by the human pathogen CVB3, cytomegalovirus (CMV), and lymphocytic choriomeningitis virus (LCMV). We demonstrated that mice harboring beta-cells that do not respond to IFN because of the expression of the suppressor of cytokine signaling-1 (SOCS-1) succumb to an acute form of type 1 diabetes after infection with CVB3. Interestingly, t

РНК-Сек, базирующаяся на RNA-Seq, обнаруживает воспаление олигодендроглиевой линии в аутоиммунном энцефаломиелите.

Клетки олигодендроглиевой линии (ООК) имеют решающее значение для нейронных функций поддержки, включая минелинирование и воспоминание. Появляющиеся данные свидетельствуют об их активной роли в нейроинфламмации, особенно в таких условиях, как Множественный склероз (MS). В рамках этого исследования изучается возбудительный транслатом ОРЦ в начале экспериментального аутоиммунного энцефаломиелита (EAE), который представляет собой установленную модель НР. Использование последовательности РНК на основе RiboTag в генетически модифицированных системах Olig2-Cre Мыши RiboTag, мы опознали 1,556 Регулиру

Совпадение в аннотации оригинала
Oligodendroglial lineage cells (OLCs) are critical for neuronal support functions, including myelination and remyelination. Emerging evidenc … OLCs exacerbates EAE pathology by enhancing antigen presentation and chemokine production, whereas interferon-beta (IFN-β) signaling showed minimal impact. These findings provide novel insights into the inflammatory role of OLCs in EAE and suggest therapeutic potential in targeting OLC-mediated neuroinflammation for MS and related disorders.

Type-III interferon, not type-I, is the predominant interferon induced by respiratory viruses in nasal epithelial cells.

As an innate immune response against diverse viral infections, a host induces two types of interferon (IFN), type-I (IFN-β/α) and type-III (IFN-λ). We investigated IFN inductions by respiratory viruses, including respiratory syncytial virus (RSV), measles virus and mumps virus in human nasal epithelial cells (NECs). IFN-λ, but not IFN-β/α, was induced by respiratory virus infection in primary NECs and immortalized NECs through transfection with the human telomerase reverse transcriptase gene (hTERT-NECs). In contrast, both IFN-λ and IFN-β/α were induced by RSV infection in human bronchiolar ca

Type I Interferon, Induced by Adenovirus or Adenoviral Vector Infection, Regulates the Cytokine Response to Lipopolysaccharide in a Macrophage Type-Specific Manner.

INTRODUCTION: While TLR ligands derived from microbial flora and pathogens are important activators of the innate immune system, a variety of factors such as intracellular bacteria, viruses, and parasites can induce a state of hyperreactivity, causing a dysregulated and potentially life-threatening cytokine over-response upon TLR ligand exposure. Type I interferon (IFN-αβ) is a central mediator in the induction of hypersensitivity and is strongly expressed in splenic conventional dendritic cells (cDC) and marginal zone macrophages (MZM) when mice are infected with adenovirus. This study invest

[Cytokines in vaccines and interferon preparations].

Virus vaccines prepared on the basis of cells of mammals (rabies, poliomyelitis, measles and hepatitis A vaccines) contain cytokines (IL-1 beta, IL-6, TNF-alpha), whose concentration depends on the kind of the vaccine. Cell lines (green monkey kidney cells, VERO, 4647), used for the preparation of commercial and experimental vaccines, do not produce spontaneously any of the above cytokines. Cell line L-68, used for the manufacture of experimental measles vaccine, is capable of the spontaneous synthesis of IL-6. In Russian and foreign preparations of interferon the presence of IL-1 beta and TNF

Cytoadhesion of Plasmodium falciparum-Infected Red Blood Cells Changes the Expression of Cytokine-, Histone- and Antiviral Protein-Encoding Genes in Brain Endothelial Cells.

Malaria remains a significant global health problem, mainly due to Plasmodium falciparum, which is responsible for most fatal infections. Infected red blood cells (iRBCs) evade spleen clearance by adhering to endothelial cells (ECs), triggering capillary blockage, inflammation, endothelial dysfunction and altered vascular permeability, prompting an endothelial transcriptional response. The iRBCIT4var04/HBEC-5i model, where iRBCs present IT4var04 (VAR2CSA) on their surface, was used to analyze the effects of iRBC binding on ECs at different temperature (37°C vs. 40°C). Binding of non-infected R

Natalizumab (TYSABRI) and multiple sclerosis. With longer follow-up: even more toxic than suspected.

The standard disease-modifying treatment for patients with relapsing-remitting multiple sclerosis is interferon beta injection, in the absence of a better alternative. In 2007, natalizumab had an unfavourable harm-benefit balance in patients with severe multiple sclerosis in whom interferon beta was ineffective, due to insufficient evidence of efficacy and a risk of life-threatening progressive multifocal leukoencephalopathy. In 2014, we found no new comparative trials focusing on the efficacy of natalizumab monotherapy in its authorised indications in the EU. Post-marketing data confirm the a

Modulation of fibronectin gene expression in inflammatory mononuclear phagocytes of rat liver after acute liver injury.

BACKGROUND/AIMS: In acute liver injury, fibronectin (FN) is deposited at the site of hepatocellular necrosis. We have previously shown that liver inflammatory mononuclear phagocytes (MNP), in contrast to quiescent hepatic macrophages, synthesize abundant amounts of FN. We now analyzed effects of agents known to influence macrophage functions to better understand liver damage and repair. METHODS: Acute rat liver injury was induced by CCl(4). Liver cellular FN (cFN) expression was analyzed by in situ-hybridization. Liver MNP were isolated and characterized immunocytochemically. Protein synthesi

Macrophage activation for cytolysis of virally infected target cells.

Bone-marrow-culture-derived macrophages killed virally infected cells but not uninfected cells. This activity could be enhanced by preexposure of the macrophages to lipopolysaccharide (LPS), and/or purified interferons. The ability to kill virally infected targets was not restricted to a single cell type or virus. Comparing the ability of activators to induce activity against virally infected targets or tumor (P815) targets, it was found that much lower levels of LPS or alpha/beta-interferon were able to induce cytolytic activity for virally infected cells than were needed for tumor targets. F

Interferon regulates c-myc gene expression in Daudi cells at the post-transcriptional level.

c-myc gene mRNA is reduced by greater than 75% in the human lymphoblastoid cell line Daudi when growth is inhibited by treatment with human interferon beta (IFN-beta). In the present communication, we describe the effect of IFN-beta treatment on transcription of the c-myc gene and on the steady-state level of c-myc mRNA in the cytoplasm of Daudi cells. The results show that, although the rate of c-myc transcription is not significantly different in nuclei isolated either from untreated cells or from those treated with IFN-beta for 3 or 24 hr, the level of c-myc mRNA in the cytoplasm is reduced

Pathogenicity and Transcriptomic Profiling Revealed Activation of Apoptosis and Pyroptosis in Brain of Mice Infected with the Beta Variant of SARS-CoV-2.

OBJECTIVE: Patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection frequently develop central nervous system damage, yet the mechanisms driving this pathology remain unclear. This study investigated the primary pathways and key factors underlying brain tissue damage induced by the SARS-CoV-2 beta variant (lineage B.1.351). METHODS: K18-hACE2 and C57BL/6 mice were intranasally infected with the SARS-CoV-2 beta variant. Viral replication, pathological phenotypes, and brain transcriptomes were analyzed. Gene Ontology (GO) analysis was performed to identify altered pa

Effect of teriflunomide on QuantiFERON-TB Gold results.

Multiple sclerosis is a chronic inflammatory disease of the central nervous system characterized by damage to myelin and axons, over time leading to progressive neuronal degeneration and microglial activation. There is still no curative treatment, but during the last 20 years eight different therapies have become available including interferon beta, glatiramer acetate, teriflunomide, dimethyl fumarate, natalizumab, fingolimod, alemtuzumab, mitoxantrone and teriflunomide. Teriflunomide is an immunomodulatory drug that exerts an inhibitory effect on T cell activation in central nervous system of

Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.

Severe acute respiratory syndrome (SARS) is a life-threatening infectious disease which has been difficult to study and treat because of the lack of a readily available animal model. Intranasal infection of A/J mice with the coronavirus murine hepatitis virus strain 1 (MHV-1) produced pulmonary pathological features of SARS. All MHV-1-infected A/J mice developed progressive interstitial pneumonitis, including dense macrophage infiltrates, giant cells, and hyaline membranes, resulting in death of all animals. In contrast, other mouse strains developed only mild transitory disease. Infected A/J

Regulation of collagen synthesis and messenger RNA levels in normal and hypertrophic scar fibroblasts in vitro by interferon alfa-2b.

Hypertrophic scars, which commonly occur after thermal and traumatic injury of the skin, are a fibroproliferative disorder of the dermal matrix wherein components of the inflammatory process, including the fibrotic growth factor, transforming growth factor-beta, appear to activate dormant fibroblasts leading to cellular proliferation and excessive matrix synthesis. To investigate the potential beneficial role and mechanism of interferon alfa-2b in controlling excessive collagen production in hypertrophic scar, we measured dose response, time of onset, and duration of action in hypertrophic sca

Culture of human amniotic cells: a system to study interferon production.

This study investigated whether primary culture of human amniotic membrane cells (PCHAM) could be used as an in vitro model system for the study of interferon (IFN) production. PCHAM cells infected with Newcastle disease virus (NDV) produced the two antigenic types of IFN, previously shown in a amniotic membrane cells (HAM) system. PCHAM IFN was detected as early as 2 h after NDV infection and was composed by two antigenically distinct fractions, one neutralized with anti-HuIFN beta antibody and another that is not related to IFN beta, -alpha and -gamma. These fractions correspond respectively

Human IP-9: A keratinocyte-derived high affinity CXC-chemokine ligand for the IP-10/Mig receptor (CXCR3).

Chemokines and their receptors play a crucial part in the recruitment of leukocytes into inflammatory sites. The CXC chemokines IP-10 and Mig are selective attractants for activated (memory) T cells, the predominant cell type in skin infiltrates in many inflammatory dermatoses. The selectivity for activated T cells can be explained by the fact that both chemokines exert their effects through a common receptor, CXCR3, which is nearly exclusively expressed on activated T cells. The aim of this study was to identify biologically active CXCR3 ligands produced by keratinocytes. To that end, Chinese

Primary malignant melanoma of the female urethra: a case report.

A case of primary malignant melanoma of the female urethra is presented. A 65-year-old Japanese woman was referred with dysuria and urethral bleeding. A hemorrhagic blue-black tumor, 3 cm in diameter, was diagnosed as a malignant melanoma by urinary cytology and biopsy. In spite of radical surgery followed by adjuvant immunochemotherapy with beta interferon, dacarbazine, nimustine and vincristine (IFN beta-DAV), the patient died of the disease one year after surgery because of lung metastasis which developed six months after diagnosis. The regional lymph nodes were not involved. In the present

Successful treatment of co-morbid schizophrenia and multiple sclerosis.

Multiple sclerosis (MS) has both neurological and psychiatric manifestations. Though depression, bipolar disorder and la belle indifference are commonly described, schizophrenia-like-psychosis is not widely reported with MS. Drug interactions and side effects make treatment, in such scenario, challenging. We, for the first time, report a patient with MS and paranoid schizophrenia successfully treated with concurrent use of clozapine and risperidone with interferon-beta-1a.

Interferon induces natural killer cell blastogenesis in vivo.

Interferon (IFN), types beta and gamma, and IFN inducers polyinosinic-polycytidylic acid and lymphocytic choriomeningitis virus all stimulated the generation of blast-NK cells in mouse spleens. Blast-NK cells were characterized on the basis of size, 3H-thymidine uptake, and NK cell markers. These data indicate that in addition to augmenting NK cell-mediated lysis, IFN may regulate NK cell proliferation in vivo.