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Учредительная активация MAVS Inhibits ВИЧ-1 Оплодотворение через Interferon Secretion и ввод в действие факторов ограничения ВИЧ-1.

Известно, что интерферон типа I препятствует репродукции ВИЧ-1 за счет впрыскивания генных интерферонов (ИПГ), включая ряд факторов ограничения ВИЧ-1. Чтобы лучше понять интерферонально-посредованное ограничение ВИЧ-1, мы создали учредительно активную форму адаптационного белка MAVS. Учредительный MAVS образовался в результате слияния полной длины MAVS в усеченную форму белка вируса Эпштейн Барра LMP1 (ΔLMP1). Супернавигационный от ΔLMP1-MAVS трансформированные 293T клетки содержали высокие уровни интерферонов типа I и блокировали воспроизведение ВИЧ как в TZM-bl, так и в первичных человечески

Совпадение в аннотации оригинала
Type I interferon is known to inhibit HIV-1 replication through the induction of interferon stimulated genes (ISG), including a number of HI … d HIV restriction factors Viperin, Tetherin, MxB, and ISG56. Interferon blockade studies implicated interferon-beta in this response. In addition to direct viral inhibition, ΔLMP1-MAVS markedly enhanced secretion of IFN-β and IL-12p70 by dendritic cells and the activation and maturation of dendritic cells. Based on this immunostimulatory activity, an adenoviral v …

Present role and future potential of type I interferons in adjuvant therapy of high-risk operable melanoma.

Few molecular therapeutic approaches have been so rigorously investigated in relation to the pathophysiology and outcome of human diseases as type I interferons. Historically, IFNs were discovered after the phenomenon of 'interference' was first described by Isaacs and Lindenmann in 1957, and for years IFNs (IFNalpha) were considered as potential "antiviral penicillins" until the broader spectrum of effects upon normal cell physiology, the natural and adaptive immune systems, and tumor growth and proliferation were described. Interferon beta (IFNbeta) was the second human gene after insulin to

The ORF6, ORF8 and nucleocapsid proteins of SARS-CoV-2 inhibit type I interferon signaling pathway.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel human coronavirus causing the pandemic of severe pneumonia (Coronavirus Disease 2019, COVID-19). SARS-CoV-2 is highly pathogenic in human, having posed immeasurable public health challenges to the world. Innate immune response is critical for the host defense against viral infection and the dysregulation of the host innate immune responses probably aggravates SARS-CoV-2 infection, contributing to the high morbidity and lethality of COVID-19. It has been reported that some coronavirus proteins play an important role in

Pharmacokinetics/pharmacodynamics by race: Analysis of a peginterferon β-1a phase 1 study.

BACKGROUND: Black/African American participants are underrepresented in clinical trials for multiple sclerosis but can experience a greater burden of disease than other racial groups in the United States. A phase 1, open-label, crossover study that demonstrated bioequivalence of subcutaneous and intramuscular injection of peginterferon β-1a in healthy volunteers enrolled similar proportions of Black and White participants, enabling a post hoc subgroup analysis comparing these groups. METHODS: Peginterferon β-1a (125 μg) was administered by subcutaneous or intramuscular injection, followed by

Therapeutic effect of human fibroblast interferon on premalignant lesions arising in oral mucosa. A pilot study.

Human fibroblast interferon (HuIFN-beta) was topically administered to 20 premalignant lesions histopathologically showing epithelial dysplasia such as leukoplakia and lichen planus which arose in the oral mucosa. HuIFN-beta was prepared in the water-soluble gel form containing 2% carboxymethylcellulose, 45% glycelin, 0.1 M citrate buffer (pH 4.5) and 0.2% SDS as stabilizing agents. This preparation was found to be effective for herpetic gingivostomatitis and zostal lesions arising along the intercostal nerve. Thus, the HuIFN-beta preparation (10(4) to 5 X 10(3) IU) was applied to the oral muc

Interferons regulate the phenotype of wild-type and mutant herpes simplex viruses in vivo.

Mechanisms responsible for neuroattenuation of herpes simplex virus (HSV) have been defined previously by studies of mutant viruses in cultured cells. The hypothesis that null mutations in host genes can override the attenuated phenotype of null mutations in certain viral genes was tested. Mutants such as those in infected cell protein (ICP) 0, thymidine kinase, ribonucleotide reductase, virion host shutoff, and ICP34.5 are reduced in their capacity to replicate in nondividing cells in culture and in vivo. The replication of these viruses was examined in eyes and trigeminal ganglia for 1-7 d a

The predominance of beta (CC) chemokine transcripts in idiopathic inflammatory muscle diseases.

Cytokines and chemokines that upregulate major histocompatibility complex class I antigens, recruit lymphocytes, and enhance T-cell-mediated myotoxicity may be important in the pathogenesis of dermatomyositis and polymyositis. We searched for cytokine and chemokine transcripts in inflammatory muscle specimens from 14 newly diagnosed or treated patients. Control specimens from six patients without inflammatory muscle disease were analyzed for transcripts of interleukins-1 beta, -2, -4, -6, -10, and -15, and interferon-gamma, tumor necrosis factor-alpha, transforming growth factor-beta 1, macrop

Characterization of Shuni viruses detected in Israel.

Shuni virus (SHUV) was recently identified in Israel in several brains of ovine, bovine, and goat fetuses and newborn animals with congenital arthrogryposis-hydranencephaly syndrome. In the present study, the sequences of several Israeli SHUV strains were analyzed in detail; based on the small genome segment which encodes the nucleocapsid protein and the small nonstructural protein (NSs), a very high similarity of 99-100 % among each other was found. In contrast to the highly conserved N protein, several mutations were found within the NSs-coding sequence of SHUVs present in brain samples of m

Current status of melanoma treatment with interferon, cytokines and other biologic response modifiers in Japan.

This paper introduces the current status of melanoma treatment with various biologic response modifiers (BRMs) in Japan, with an emphasis on the clinical results of Interferon therapies. The authors also refer briefly to the current situation of interleukin-2 (IL-2) and tumor necrosis factor (TNF) in Japan. Many BRMs have been used in treatment of melanoma, e.g., IFN, IL-2, TNFs, BCG, MY-1 (DNA extracted from BCG), WPG (CWs of Bifidobacterium infantis, ATCC 15697), OK-432 (Picibanil, Streptococcus pyogenes preparation), bestatin, and forphenicinol. Some of these have completed clinical trials,

Effect of interferon therapy in a patient with chronic active hepatitis type C associated with interstitial pneumonia and rheumatoid arthritis: a case report.

Interferon (IFN) is widely used to treat patients with chronic hepatitis types B and C but has been found to occasionally aggravate rheumatoid arthritis (RA) or cause interstitial pneumonia. We administered 6 MIU/d IFN-beta by intravenous injection for 6 weeks to a 55-year-old man with chronic active hepatitis type C associated with RA and interstitial pneumonia. Transaminase levels rapidly returned to normal after treatment and hepatitis C virus-RNA (nested RT-PCR method) was negative on completion of treatment. No significant adverse reactions or aggravation of RA or interstitial pneumonia o

Human peripheral gammadelta T cells potentiate the early proinflammatory cytokine response to staphylococcal toxic shock syndrome toxin-1.

Toxic shock syndrome toxin (TSST)-1 is a superantigen known to profoundly induce proinflammatory cytokines by activation of V beta -specific alpha beta T cells, but its effect on gamma delta T cells, which normally constitute 1%-5% of peripheral blood mononuclear cells (PBMCs), is unclear. Here, we demonstrate that TSST-1 induced significantly higher levels of interferon (IFN)- gamma, tumor necrosis factor (TNF)- alpha, and interleukin (IL)-2, and a lower level of IL-10 in human PBMCs when the gamma delta subpopulation has been primed by isopentylpyrophosphate, compared with that in control PB

Biological and molecular characterization of PNH-like lymphocytes emerging after Campath-1H therapy.

Campath-1H, an anti-CD52 monoclonal antibody, is therapeutically active in lymphoproliferative and autoimmune diseases. After Campath-1H therapy, lymphocytes with a paroxysmal nocturnal haemoglobinuria (PNH) phenotype have been reported to emerge. We characterized a PNH-like lymphocyte population emerging after Campath-1H therapy, in a patient with fludarabine refractory B-cell chronic lymphocytic leukaemia (B-CLL). We demonstrated a reduction in PIG-A mRNA levels compared with controls, and of all cytokines tested [interleukin (IL)-4, IL-13, IL-2, interferon(IFN)-gamma, IL-6, IL-10, and tumou

Pharmacological treatment other than corticosteroids, intravenous immunoglobulin and plasma exchange for Guillain Barré syndrome.

BACKGROUND: Plasma exchange and intravenous immunoglobulin, but not corticosteroids, are beneficial in Guillain-Barré syndrome (GBS). The efficacy of other pharmacological agents is unknown. OBJECTIVES: To review systematically the evidence from randomised controlled trials for pharmacological agents other than plasma exchange, intravenous immunoglobulin and corticosteroids. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Specialized Register (5 July 2010), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2010, Issue 2), MEDLINE (Januar

Self-injection anxiety training: a treatment for patients unable to self-inject injectable medications.

Anxiety and phobia frequently prevent patients with multiple sclerosis (MS) from self-injecting their injectable disease-modifying medications. This small, randomized, controlled trial tested the efficacy of a six-session nurse-administered programme to teach self-injection to patients with MS, who, due to anxiety or phobia, were unable to self-inject their injectable medications. Participants were 30 patients with MS who were prescribed interferon beta-1a (IFNbeta-1a) administered via weekly intramuscular injection. All patients were unable to self-inject due to anxiety or phobia. Patients we

An Interferon-Response Transcriptomic Signature of Lymphovascular Invasion in Prostate Cancer.

Lymphovascular invasion is an adverse pathologic feature in prostate cancer, but its independent molecular drivers remain unclear due to strong confounding by tumor grade and stage. We performed a confounder-adjusted transcriptomic analysis of 403 TCGA-PRAD samples. Differential expression was adjusted for Gleason score and pathological T stage. A transcriptional profile associated with LVI was derived and tested in multivariable logistic and Cox proportional hazards models for biochemical recurrence-free survival, with bootstrap internal validation. After multivariable adjustment, 129 genes w

RNF213 regulates blood‒brain barrier integrity by targeting TRAF3 for type I interferon activation during A. baumannii infection.

RNF213 is the first identified susceptibility gene for moyamoya disease, and the encoded protein was recently recognized as a key antimicrobial protein. However, the function of RNF213 in host defense against brain infection remains unclear. Here, we show that increased expression of Rnf213 is significantly regulated by interferon alpha/beta receptor (IFNAR) signaling during bacterial infection and ligand stimulation. RNF213 deficiency impairs type I interferon (IFN-I) production and decreases the expression of interferon-stimulated genes (ISGs) in response to IFN-β stimulation and Acinetobact

Inhibition of pseudorabies virus replication via upregulated interferon response by targeting 7-dehydrocholesterol reductase.

Pseudorabies virus (PRV) is an alpha-herpesvirus capable of infecting a range of animal species, particularly its natural host, pigs, result … hibits the phosphorylation of interferon regulatory factor 3 (IRF3), resulting in reduced levels of interferon-beta (IFN-β) and interferon-stimulated genes (ISGs). Finally, we revealed that the DHCR7 inhibitor, trans-1,4-bis(2-chlorobenzylaminomethyl) cyclohexane dihydrochloride (AY9944), significantly suppresses PRV replication both in vitro and in vivo. Taken t …

Impact of warm compresses on local injection-site reactions with self-administered glatiramer acetate.

Patients with multiple sclerosis (MS) report a number of adverse events related to immunomodulator injections, including local injection-site reactions (LISRs). Reactions characterized by pain, swelling, redness, or inflammation have been experienced by patients who self-inject glatiramer acetate, interferon beta-1b, or interferon beta-1a. Although these reactions rarely are serious, they can foster negative attitudes about self-injection and undermine a patient's commitment to treatment, especially in the early stages of therapy. This randomized crossover study of 50 patients who had initiate

Glucocorticoid regulation of transforming growth factor-beta activation in urogenital sinus mesenchymal cells.

The transforming growth factors-beta (TGF-beta s) regulate many aspects of cell proliferation and differentiation. The TGF-beta isoforms are produced by most cell types in the biologically inactive, latent form. The physiological relevance of latent TGF-beta and the regulation of activation to the biologically active form are not well understood. Although expression of TGF-beta messenger RNA is regulated by the steroid hormone family, the mechanisms of hormonal regulation of TGF-beta activation have not been well studied. Fetal rat urogenital sinus organ cultures and derived mesenchymal cell l