Journal articles: 'Interferon'

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Simpson, S. "Interfering with Interferon." Science's STKE 2007, no. 376 (February 28, 2007): tw81. http://dx.doi.org/10.1126/stke.3762007tw81.

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Polyak, Stephen J. "Interfering with interferon." Trends in Microbiology 7, no. 10 (October 1999): 401. http://dx.doi.org/10.1016/s0966-842x(99)01592-9.

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Bucci, Mirella. "Interfering with Interferon." Nature Chemical Biology 10, no. 5 (April 17, 2014): 324. http://dx.doi.org/10.1038/nchembio.1511.

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Martz, Lauren. "Interfering with interferon." Science-Business eXchange 6, no. 16 (April 2013): 381. http://dx.doi.org/10.1038/scibx.2013.381.

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Harris, Bethany D., Srilalitha Kuruganti, Ashlesha Deshpande, Paul A. Goepfert, W. Winn Chatham, and Mark R. Walter. "Characterization of Type-I IFN subtype autoantibodies and activity in SLE serum and urine." Lupus 29, no. 9 (July 1, 2020): 1095–105. http://dx.doi.org/10.1177/0961203320935976.

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Background/objective Type-I interferons contribute to pathogenesis in systemic lupus erythematosus, including nephritis. Interferons consist of a family of 16 proteins yet are often characterized in patients without knowledge of the specific interferon subtypes involved. Different interferons may function in the kidneys, and other organs, relative to what is often measured in patient blood. Moreover, antibodies to interferons may potentially modulate systemic or organ-specific interferon activity. The aim of this study was to characterize global interferon activity levels and identify autoantibodies to the 12 interferon α subtypes in patient serum and urine. Methods Interferon activity levels in serum and urine were measured using an interferon bioassay. Anti-interferon and anti-cytokine autoantibodies were measured by ELISA. Serum and urine samples were also characterized for their ability to neutralize the biological activity of exogenously added interferons. Results Serum interferon activity was increased in 62% of systemic lupus erythematosus patient samples, relative to healthy donor controls, whereas binding interferon α autoantibodies to at least one interferon α subtype were found in 68% of the samples evaluated. High Systemic Lupus Erythematosus Disease Activity Index scores were significantly ( p = 0.001) associated with patient samples containing interferon α autoantibodies to three or more interferon α subtypes in their serum. Interferon α autoantibodies that potently block interferon activity were rare (∼5% of samples), but collectively bound to all 12 interferon α subtypes. Urine interferon activity and interferon α autoantibody profiles did not correlate with their serum counterparts, suggesting immune responses in systemic lupus erythematosus kidneys can be distinct from those measured in serum. Analysis of autoantibodies to 15 additional cytokines in serum identified higher frequencies of granulocyte-macrophage colony-stimulating factor and interleukin 17A autoantibodies, suggesting these signaling pathways may potentially contribute, with interferons, to systemic lupus erythematosus pathogenesis. Conclusions The measurement of autoantibodies to multiple interferon subtypes in serum and urine may provide an alternative method for following interferon-mediated systemic lupus erythematosus disease activity. The results suggest autoantibodies might be used for patient monitoring and/or identifying additional cytokine signaling pathways that are functioning in different systemic lupus erythematosus patients.

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Barinaga, M. "Immunology. Interfering with interferon." Science 259, no. 5102 (March 19, 1993): 1693–94. http://dx.doi.org/10.1126/science.8456294.

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Smith, Geoffrey L., Julian A. Symons, and Antonio Alcamı́. "Poxviruses: Interfering with Interferon." Seminars in Virology 8, no. 5 (April 1998): 409–18. http://dx.doi.org/10.1006/smvy.1997.0145.

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REVEL, MICHEL, ASHER ZILBERSTEIN, ROSE MARIA RUGGIERI, MENACHEM RUBINSTEIN, and LUISA CHEN. "Autocrine Interferons and Interferon-β2." Journal of Interferon Research 7, no. 5 (October 1987): 529–36. http://dx.doi.org/10.1089/jir.1987.7.529.

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MENKES, DAVID B., and JAMES A. MacDONALD. "Interferons, serotonin and neurotoxicity." Psychological Medicine 30, no. 2 (March 2000): 259–68. http://dx.doi.org/10.1017/s0033291799001774.

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Background. Interferons are a class of cytokines profoundly affecting immune function. Several interferons are now synthesized and used clinically, notably for viral diseases and cancer. In addition to their desired immune effects, interferons cause a number of toxicities, including prominent effects on the nervous system.Methods. This literature review focused on the incidence of depression associated with interferon treatment. Possible neurochemical mechanisms and remedial strategies were also considered.Results. Interferon treatment, particularly with the alpha subtype, is unquestionably linked with depression, but the strength of association is uncertain because of erratic ascertainment and pre- treatment co-morbidity. A likely pathogenic mechanism has been described, involving interferon suppression of serotonin synthesis. Controlled treatment trials of interferon-induced depression are not yet available.Conclusions. Neurotoxicity substantially limits the use of interferons. At least some of the risk of depression appears to derive from their anti-serotonergic effects, consistent with the large body of evidence pointing to a general link between serotonin and affective illness. Vigilant detection and aggressive treatment of depression is necessary to optimize interferon treatment of many patients.

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de Lemos, Livia Pires, Augusto Guerra, Ramon Pereira, Rosangela Gomes, Isabella Godói, Isabela Diniz, Ivan Zimmermann, et al. "OP40 First Case Of Disinvestment Using Real-World Evidence In Brazil." International Journal of Technology Assessment in Health Care 33, S1 (2017): 18–19. http://dx.doi.org/10.1017/s0266462317001349.

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INTRODUCTION:Beta-interferons are used as first-line therapy for relapsing-remitting multiple sclerosis in Brazil. In order to evaluate the possible inferiority of one of the beta-interferons available and support a guideline update, we conducted an eleven-year (January 2000 to December 2010) nationwide real-world performance assessment using the Unified Health System (SUS) databases.METHODS:We assessed whether patients using subcutaneous beta-interferon switched treatment, relapsed or died (composite event) earlier than patients using intramuscular beta-interferons. Patients without a dispensing registry longer than three months were censored. We used the Kaplan-Meier method to estimate the cumulative probability of persistence on initial treatment, and compared groups with the Log-rank test. The influence of the drug on the occurrence of event was assessed with Cox proportional hazards analysis.RESULTS:The number of patients included was 12,154, and the majority started treatment with subcutaneous beta-interferon-1a (45.7 percent), followed by subcutaneous beta-interferon-1b (27.7 percent) and by intramuscular beta-interferon (26.6 percent). Women represented 73.1 percent and the mean age was 38.93±11.34 years old. The group of patients who used intramuscular beta-interferon switched treatment, relapsed or died earlier (median 47 months; 95 percent Confidence Interval, CI 44–52) than patients using the subcutaneous beta-interferons, (69 months (95 percent CI 64–76) for beta- interferon 1a and 73 (95 percent CI 66–84) months for beta-interferon 1b) (p< .0001 for both comparisons). Accordingly, the use of intramuscular beta-interferon was associated with a higher probability of event (Hazard ratio, HR 1.38; 95 percent CI 1.29-1.48), while the use of the other beta-interferons had a protective effect (1a: HR .86; 95 percent CI .81-.92; 1b: HR .89; 95 percent CI .83-.95).CONCLUSIONS:The inferiority of intramuscular beta-interferon found in the real-world corroborates findings from head-to-head studies and systematic reviews conducted by Cochrane and the National Commission for Technology Incorporation in SUS (CONITEC/Brazil). This result led to disinvestment in intramuscular beta-interferon and was the first case of clinical guideline update using real-world evidence in Brazil.

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Zimring, James C., Stephen Goodbourn, and Margaret K. Offermann. "Human Herpesvirus 8 Encodes an Interferon Regulatory Factor (IRF) Homolog That Represses IRF-1-Mediated Transcription." Journal of Virology 72, no. 1 (January 1, 1998): 701–7. http://dx.doi.org/10.1128/jvi.72.1.701-707.1998.

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ABSTRACT Human herpesvirus 8 (HHV-8) is the probable viral etiologic agent for Kaposi’s sarcoma. The HHV-8 genome encodes viral interferon regulatory factor (vIRF), a gene product that has homology to the IRF family of transcription factors. We demonstrate that vIRF inhibits responses to type I and type II interferons and blocks IRF-1-mediated transcription. vIRF does not compete with IRF-1 for binding to DNA or complex directly with IRF-1. The ability of vIRF to block IRF-1-mediated transcription is independent of the DNA binding domains of both vIRF and IRF-1. These data suggest that vIRF may contribute to viral pathogenesis and cellular transformation by interfering with interferon- and IRF-1-mediated gene expression through a novel mechanism.

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Sozaeva, L. S. "The new immunological methods for diagnostics of type 1 autoimmune polyendocrine syndrome." Problems of Endocrinology 61, no. 3 (June 15, 2015): 43–46. http://dx.doi.org/10.14341/probl201561343-46.

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Type 1 autoimmune polyglandular syndrome (type 1APS) is a rare genetic disease resulting from mutations in the AIRE gene. Diagnostics of this pathology is based not only on the results of genetic studies but also on the measurement of the level of antibodies against type 1 interferons, such as interferon-ω and interferon-α2. The present review of the literature is focused on type 1 interferons, anti-interferon antibodies, and pathophysiological characteristics of the processes induced by these antibodies.

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&NA;. "Interferon-??/interferon-??-2b/interferon-??" Reactions Weekly &NA;, no. 981 (December 2003): 13. http://dx.doi.org/10.2165/00128415-200309810-00042.

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Gizinger, O. A. "Interferons and interferon therapy. Literature review." Terapevt (General Physician), no. 7 (May 19, 2021): 46–59. http://dx.doi.org/10.33920/med-12-2107-07.

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The article describes the types and biological characteristics of interferons, which are an integral part of the antiviral defense of the body. The possibilities of using interferons, interferon inducers in the complex treatment of acute respiratory viral infections are shown. The validity and possible risks of using interferon preparations for the treatment and prevention of acute respiratory viral infections are analyzed, taking into account information about their mechanisms of action.

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Ramaswamy, Madhu, Raj Tummala, Katie Streicher, Andre Nogueira da Costa, and Philip Z. Brohawn. "The Pathogenesis, Molecular Mechanisms, and Therapeutic Potential of the Interferon Pathway in Systemic Lupus Erythematosus and Other Autoimmune Diseases." International Journal of Molecular Sciences 22, no. 20 (October 19, 2021): 11286. http://dx.doi.org/10.3390/ijms222011286.

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Therapeutic success in treating patients with systemic lupus erythematosus (SLE) is limited by the multivariate disease etiology, multi-organ presentation, systemic involvement, and complex immunopathogenesis. Agents targeting B-cell differentiation and survival are not efficacious for all patients, indicating a need to target other inflammatory mediators. One such target is the type I interferon pathway. Type I interferons upregulate interferon gene signatures and mediate critical antiviral responses. Dysregulated type I interferon signaling is detectable in many patients with SLE and other autoimmune diseases, and the extent of this dysregulation is associated with disease severity, making type I interferons therapeutically tangible targets. The recent approval of the type I interferon-blocking antibody, anifrolumab, by the US Food and Drug Administration for the treatment of patients with SLE demonstrates the value of targeting this pathway. Nevertheless, the interferon pathway has pleiotropic biology, with multiple cellular targets and signaling components that are incompletely understood. Deconvoluting the complexity of the type I interferon pathway and its intersection with lupus disease pathology will be valuable for further development of targeted SLE therapeutics. This review summarizes the immune mediators of the interferon pathway, its association with disease pathogenesis, and therapeutic modalities targeting the dysregulated interferon pathway.

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Samuel, Charles E. "Interferons, Interferon Receptors, Signal Transducer and Transcriptional Activators, and Interferon Regulatory Factors." Journal of Biological Chemistry 282, no. 28 (May 14, 2007): 20045–46. http://dx.doi.org/10.1074/jbc.r700025200.

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Galik, P. K., J. A. Gard, T. S. Spencer, M. S. Marley, D. A. Stringfellow, M. D. Givens, and M. A. Edmondson. "153 EFFECTS OF OVINE INTERFERON-β ON REPLICATION OF BOVINE VIRAL DIARRHEA VIRUS AND BOVINE HERPESVIRUS-1." Reproduction, Fertility and Development 20, no. 1 (2008): 156. http://dx.doi.org/10.1071/rdv20n1ab153.

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Bovine viral diarrhea virus (BVDV) and bovine herpesvirus-1 (BHV-1) are the most commonly isolated viruses from abattoir-origin materials utilized in embryo production and known to associate with zona pellucida-intact (ZP-I) embryos after exposure and washing. Some evidence indicates that developing embryos may produce substances that are able to inhibit viral replication in adjacent cells. Interferons such as recombinant human interferon-α are known to have anti-BVDV activity but no effect against BHV-1. In some preliminary studies, bovine interferon-τ has shown antiviral activities against BVDV but not against BHV-1. However, interferon-τ in other species has not been evaluated for anti-BVDV and anti-BHV-1 effects. Thus, the objective of this study was to evaluate the cytotoxicity and anti-viral effect of ovine interferon-τ against a non-cytopathic high affinity strain of BVDV (SD-1) and BHV-1 (Colorado) in cell culture. Serial dilutions (1:10) beginning with an initial concentration of 1 mg mL–1 of interferon-τ were made in 96-well plates and then Madin Darby bovine kidney (MDBK) cells were seeded in the wells. Cells and interferon-τ were incubated at 37.5�C in 5% CO2 and air for 24 h prior to addition of virus. The following concentrations of BVDV were added to the wells: 6000, 3500, 1000, 625, and 350 cell culture infective doses (CCID50) (50% endpoint) per well. In addition, four viral concentrations of BHV-1, 1000, 500, 250, and 100 CCID50/mL were evaluated in separate cell cultures. Virus isolation was utilized to determine if the addition of interferon-τ decreased the amount of infective virus. Ovine interferon-τ produced no observable cytotoxicity in MDBK cells in any of the assays. Also, the three highest concentrations of interferon-τ significantly decreased the amount of BVDV in all of the concentrations of BVDV tested but had no apparent effect on the concentration of BHV-1 in cell cultures. Therefore ovine interferon-τ has anti-BVDV effects similar to those seen with bovine interferont-τ and neither has any apparent antiviral activity on BHV-1 in cell culture. Additionally, ovine and bovine interferon-τ might serve to limit or prevent the transmission of BVDV and curtail the negative effects of BVDV on oocyte and embryo development. However, a similar effect is not expected for BHV-1.

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Nason-Burchenal, K., D. Gandini, M. Botto, J. Allopenna, JR Seale, NC Cross, JM Goldman, E. Dmitrovsky, and PP Pandolfi. "Interferon augments PML and PML/RAR alpha expression in normal myeloid and acute promyelocytic cells and cooperates with all-trans retinoic acid to induce maturation of a retinoid-resistant promyelocytic cell line." Blood 88, no. 10 (November 15, 1996): 3926–36. http://dx.doi.org/10.1182/blood.v88.10.3926.bloodjournal88103926.

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The PML gene is fused to the retinoic acid receptor alpha gene (RAR alpha) in the acute promyelocytic leukemia (APL) 15; 17 translocation. PML is expressed in diverse tissues and cell lines and localized in the nucleus with a typical speckled pattern. In the bone marrow, it is preferentially expressed in myeloid cells. PML appears to be transcriptionally regulated by class I and II interferons, which raises the possibility that interferons modulate the function and growth and differentiation potential of normal myeloid cells and precursors by activating PML-dependent pathways. Similarly, interferons could act on APL cells, alone or in combination with all-trans retinoic acid (RA), especially if the PML/RAR alpha fusion transcript that results from the t(15; 17) is induced by interferon. We report here that PML is expressed at low levels or not expressed in normal circulating human monocytes, lymphocytes, and polymorphonucleate cells, but is markedly induced by interferon; that PML and PML/RAR alpha expression is augmented by interferon in the NB4 APL cell line, which carries the t(15; 17), and in APL blasts from patients; that interferon inhibits growth and survival of NB4 APL cells in cooperation with RA; that interferons alone have minimal maturation effect on NB4 cells; and, finally, that interferon gamma, but not alpha or beta, induces maturation and growth suppression of NB4 cells with de novo retinoid resistance, and partially restores RA response.

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Puoti, Massimo, Sergio Babudieri, Giovanni Rezza, Pierluigi Viale, Maria Giulia Antonini, Ivana Maida, Stefania Rossi, et al. "Use of Pegylated Interferons is Associated with An Increased Incidence of Infections during Combination Treatment of Chronic Hepatitis C: A Side Effect of Pegylation?" Antiviral Therapy 9, no. 4 (May 2004): 627–30. http://dx.doi.org/10.1177/135965350400900417.

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Standard interferon treatment is known to increase the risk of infections; this risk also needs to be evaluated in clinical practice for pegylated interferon. To this end, we studied 255 patients treated with standard (103) or pegylated (152) interferon, in combination with ribavirin, for hepatitis C. Overall, 31 anti-hepatitis C virus treatment-related infections were observed. Neutropenia (neutrophil counts below 1x103 cells/ml) was observed in a significantly higher proportion of patients treated with pegylated interferons (48% vs 9%; P=0.0009). Of the 31 infections, eight were respiratory infections and were observed only in patients with neutropenia. None of the non-respiratory infections was observed in patients with neutropenia. Multivariate analysis, using Cox's proportional hazards regression model, found a higher risk of all infections associated with both use of pegylated interferons [hazard ratio (HR) 4.6] and neutropenia (HR 2.46). However, neutropenia was independently associated with acute respiratory infections only and use of pegylated interferons with non-respiratory infections. In summary, use of pegylated interferon appears to increase the risk of non-respiratory infections independently from neutropenia.

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Bojic, Ivanko, Ljubisa Dokic, and Svetlana Minic. "Effects of interferons on hepatitis C virus infection." Medical review 59, no. 9-10 (2006): 482–86. http://dx.doi.org/10.2298/mpns0610482b.

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Introduction. The consequences of hepatitis C virus infections (chronic hepatitis, liver cirrhosis and hepatocellular carcinoma) are one of the major problems in clinical medicine. The persistence of infection in spite of high specific antibody titre suggests that the virus has the ability to "escape" the immunological response. Interferon therapy. Interferons are important components of the early host response to infection. They have antiviral, antiproliferative, and immunomodulatory activities. Many viruses have developed the ability to "annul" or alleviate the action of interferon by preventing its synthesis or by interfering with signaling pathways in the cells. During acute infection some of the non-structural proteins of HCV block regulatory factors that are responsible for the synthesis of endogenous infection. Within a cell, interferon induces a number of genes to produce proteins that prevent virus replication. Among them, the most important are RNA-dependent protein kinase and the eukaryotic initiation factor. However, viral proteins, especially viral envelope proteins and nonstructural protein 5A, prevent their phosphorylation and activation which enhance virus replication. These are the facts that have to be considered when using IFN in chronic hepatitis C patients. .

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Chang, Xiaobo, Xibao Shi, Xiaozhuan Zhang, Li Wang, Xuewu Li, Aiping Wang, Ruiguang Deng, Enmin Zhou, and Gaiping Zhang. "IFI16 Inhibits Porcine Reproductive and Respiratory Syndrome Virus 2 Replication in a MAVS-Dependent Manner in MARC-145 Cells." Viruses 11, no. 12 (December 16, 2019): 1160. http://dx.doi.org/10.3390/v11121160.

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Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded positive-sense RNA virus, and the current strategies for controlling PRRSV are limited. Interferon gamma-inducible protein 16 (IFI16) has been reported to have a broader role in the regulation of the type I interferons (IFNs) response to RNA and DNA viruses. However, the function of IFI16 in PRRSV infection is unclear. Here, we revealed that IFI16 acts as a novel antiviral protein against PRRSV-2. IFI16 could be induced by interferon-beta (IFN-β). Overexpression of IFI16 could significantly suppress PRRSV-2 replication, and silencing the expression of endogenous IFI16 by small interfering RNAs led to the promotion of PRRSV-2 replication in MARC-145 cells. Additionally, IFI16 could promote mitochondrial antiviral signaling protein (MAVS)-mediated production of type I interferon and interact with MAVS. More importantly, IFI16 exerted anti-PRRSV effects in a MAVS-dependent manner. In conclusion, our data demonstrated that IFI16 has an inhibitory effect on PRRSV-2, and these findings contribute to understanding the role of cellular proteins in regulating PRRSV replication and may have implications for the future antiviral strategies.

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Matthys, Valery, and Erich R. Mackow. "Hantavirus Regulation of Type I Interferon Responses." Advances in Virology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/524024.

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Hantaviruses primarily infect human endothelial cells (ECs) and cause two highly lethal human diseases. Early addition of Type I interferon (IFN) to ECs blocks hantavirus replication and thus for hantaviruses to be pathogenic they need to prevent early interferon induction. PHV replication is blocked in human ECs, but not inhibited in IFN deficient VeroE6 cells and consistent with this, infecting ECs with PHV results in the early induction of IFNβand an array of interferon stimulated genes (ISGs). In contrast, ANDV, HTNV, NY-1V and TULV hantaviruses, inhibit early ISG induction and successfully replicate within human ECs. Hantavirus inhibition of IFN responses has been attributed to several viral proteins including regulation by the Gn proteins cytoplasmic tail (Gn-T). The Gn-T interferes with the formation of STING-TBK1-TRAF3 complexes required for IRF3 activation and IFN induction, while the PHV Gn-T fails to alter this complex or regulate IFN induction. These findings indicate that interfering with early IFN induction is necessary for hantaviruses to replicate in human ECs, and suggest that additional determinants are required for hantaviruses to be pathogenic. The mechanism by which Gn-Ts disrupt IFN signaling is likely to reveal potential therapeutic interventions and suggest protein targets for attenuating hantaviruses.

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Adolf, G. R. "Antigenic Structure of Human Interferon 1 (Interferon II1): Comparison with Other Human Interferons." Journal of General Virology 68, no. 6 (June 1, 1987): 1669–76. http://dx.doi.org/10.1099/0022-1317-68-6-1669.

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Aschacher, Thomas, Artem Krokhin, Irina Kuznetsova, Johannes Langle, Vladimir Nebolsin, Andrey Egorov, and Michael Bergmann. "Effect of the preparation Ingavirin® (imidazolyl ethanamide pentandioic acid) on the interferon status of cells under conditions of viral infection." Epidemiology and Infectious Diseases 21, no. 4 (August 15, 2016): 196–205. http://dx.doi.org/10.17816/eid40907.

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Ingavirin® (imidazolyl ethanamide pentandioic acid) is an original antiviral drug, which is used in Russia for treatment and profilaxis of influenza and other acute viral infections. We confirmed that imidazolyl ethanamide pentandioic acid (IEPA), not being interferon inducer itself, enhances synthesis of both interferon-a/fi receptors (IFNAR) to interferone and cell sensitivity to interferone signalling, which was suppressed by NS1 protein - pathogen factor of influenza virus. IEPA is able to promote antiviral effector proteins PKR and MxA in infected cells, in opposition to interferon system suppression by influenza virus. Theoretical ground of clinical efficacy of Ingavirine® could be confirmed by obtained data of influence to innate immune system during viral infection.

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Sasseville, Denis, Walid Al Ghamdi, and Sultan Al Khenaizan. "Interferon-Induced Cutaneous Necrosis." Journal of Cutaneous Medicine and Surgery 3, no. 6 (October 1999): 320–23. http://dx.doi.org/10.1177/120347549900300610.

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Background: Due to advances in recombinant DNA technology, interferons are now readily available and are frequently used in all branches of medicine. These potent biologic response modifiers carry a number of systemic and local side effects. These cytokines are usually administered subcutaneously, and recent studies have described the occurrence of inflammation or necrosis at the site of injection. Objective: We report a case of cutaneous necrosis at the sites of interferon injections in a 35-year-old man treated for chronic myeloid leukemia with high, daily doses of interferon alfa. In addition, we review the existing literature on interferon-induced cutaneous necrosis and discuss preventive strategies. Conclusion: Cutaneous inflammation or necrosis at interferon injection sites is not uncommon. Although interferon beta-lb is most commonly responsible for this complication, it is now increasingly reported with interferon alfa. It appears to be secondary to the proinflammatory effects of these cytokines or to their unmasking of a subtle hyper-coagulable state.

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Hamilton, A. O., L. Jones, L. Morrison, and K. Whaley. "Modulation of monocyte complement synthesis by interferons." Biochemical Journal 242, no. 3 (March 15, 1987): 809–15. http://dx.doi.org/10.1042/bj2420809.

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Recombinant Escherichia coli-derived gamma-interferon has been shown to stimulate synthesis of the second component of complement (C2), factor B and C1 inhibitor, but to inhibit synthesis of the third component (C3). alpha- and beta-interferons stimulate synthesis of factor B and C3 inhibitor, inhibit C5 synthesis but do not alter synthesis of C2. alpha- and beta-interferons act synergistically with gamma-interferon to enhance both factor B and C1-inhibitor synthesis.

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Ruiz-Moreno, Mercedes, Maria Jose Rúa, Gloria Moraleda, Leonor Guardia, Alberto Moreno, and Vicente Carreño. "Treatment With Interferon Gamma Versus Interferons Alfa and Gamma in Children With Chronic Hepatitis B." Pediatrics 90, no. 2 (August 1, 1992): 254–58. http://dx.doi.org/10.1542/peds.90.2.254.

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Thirty-five children with chronic hepatitis B were randomly assigned to three groups: group 1 (n = 12), untreated group 2 (n = 11), treated with 1 million units of Interferon gamma per square meter of body surface (MU/m2), three times a week for 24 weeks; and group 3 (n = 12), treated with interferon alfa at a dose of 5 MU/m2, three times a week for 12 weeks followed by 1 MU/m2 of interferon gamma with the same schedule. At the end of the treatment (6th month), hepatitis B virus DNA was negative in 16.5% of the control group, in 9% of the children treated with interferon gamma, and in 16.5% of those treated with interferons alfa and gamma. No child had lost the hepatitis B e antigen by this time. No basal differences in the serum hepatitis B virus DNA concentration among the groups were observed. At follow-up (15th month), viral genome was negative in 25% of the untreated children, in 36% of the group treated with interferon gamma, and in 41.5% of the children who had received interferons alfa and gamma. Hepatitis B e antigen was negative in 25% of the children who belonged to groups 1 and 3 and in 27% of the children treated with interferon gamma only. These data suggest that interferon gamma does not have a powerful antiviral effect on chronic hepatitis B in children. However, it is well tolerated.

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Ahmad, Imran, Araceli Valverde, Hasan Siddiqui, Samantha Schaller, and Afsar R. Naqvi. "Viral MicroRNAs: Interfering the Interferon Signaling." Current Pharmaceutical Design 26, no. 4 (March 18, 2020): 446–54. http://dx.doi.org/10.2174/1381612826666200109181238.

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Interferons are secreted cytokines with potent antiviral, antitumor and immunomodulatory functions. As the first line of defense against viruses, this pathway restricts virus infection and spread. On the contrary, viruses have evolved ingenious strategies to evade host immune responses including the interferon pathway. Multiple families of viruses, in particular, DNA viruses, encode microRNA (miR) that are small, non-protein coding, regulatory RNAs. Virus-derived miRNAs (v-miR) function by targeting host and virus-encoded transcripts and are critical in shaping host-pathogen interaction. The role of v-miRs in viral pathogenesis is emerging as demonstrated by their function in subverting host defense mechanisms and regulating fundamental biological processes such as cell survival, proliferation, modulation of viral life-cycle phase. In this review, we will discuss the role of v-miRs in the suppression of host genes involved in the viral nucleic acid detection, JAK-STAT pathway, and cytokine-mediated antiviral gene activation to favor viral replication and persistence. This information has yielded new insights into our understanding of how v-miRs promote viral evasion of host immunity and likely provide novel antiviral therapeutic targets.

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Becker, Christian, Tobias Bopp, and Kerstin Steinbrink. "Interferon α interferes with immunological tolerance." OncoImmunology 2, no. 12 (December 2013): e27528. http://dx.doi.org/10.4161/onci.27528.

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Clynes, Raphael. "IVIG Therapy: Interfering with Interferon-γ." Immunity 26, no. 1 (January 2007): 4–6. http://dx.doi.org/10.1016/j.immuni.2007.01.006.

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Zlotorynski, Eytan. "Interfering with interferon by RNA editing." Nature Reviews Molecular Cell Biology 19, no. 3 (February 7, 2018): 141. http://dx.doi.org/10.1038/nrm.2018.12.

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Brzoska, Josef, Harald von Eick, and Manfred Hündgen. "Interferons in the Therapy of Severe Coronavirus Infections: A Critical Analysis and Recollection of a Forgotten Therapeutic Regimen with Interferon Beta." Drug Research 70, no. 07 (May 22, 2020): 291–97. http://dx.doi.org/10.1055/a-1170-4395.

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AbstractThe pharmacological and immunological properties of interferons, especially those of interferon beta, and the corresponding treatment strategies are described, and the results of studies with different interferons in coronavirus infections are analysed. Furthermore, the data obtained with high-dosed native interferon beta in life-threatening acute viral diseases as well as the results of clinical pilot studies with high-dosed recombinant interferon beta-1a are provided because they serve as the rationale for the proposed therapeutic regimen to be applied in acute viral infections. This regimen differs from those approved for treatment of multiple sclerosis and consists of interferon beta-1a administered as a 24 hour intravenous infusion at a daily dose of up to 90 µg for 3–5 consecutive days. Since under this regimen transient severe side effects can occur, it is analysed which patients are suitable for this kind of treatment in general and if patients with severe coronavirus infections could also be treated accordingly.

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Pilna, Hana, Vera Hajkova, Jarmila Knitlova, Jana Liskova, Jana Elsterova, and Zora Melkova. "Vaccinia Virus Expressing Interferon Regulatory Factor 3 Induces Higher Protective Immune Responses against Lethal Poxvirus Challenge in Atopic Organism." Viruses 13, no. 10 (October 3, 2021): 1986. http://dx.doi.org/10.3390/v13101986.

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Vaccinia virus (VACV) is an enveloped DNA virus from the Orthopoxvirus family, various strains of which were used in the successful eradication campaign against smallpox. Both original and newer VACV-based replicating vaccines reveal a risk of serious complications in atopic individuals. VACV encodes various factors interfering with host immune responses at multiple levels. In atopic skin, the production of type I interferon is compromised, while VACV specifically inhibits the phosphorylation of the Interferon Regulatory Factor 3 (IRF-3) and expression of interferons. To overcome this block, we generated a recombinant VACV-expressing murine IRF-3 (WR-IRF3) and characterized its effects on virus growth, cytokine expression and apoptosis in tissue cultures and in spontaneously atopic Nc/Nga and control Balb/c mice. Further, we explored the induction of protective immune responses against a lethal dose of wild-type WR, the surrogate of smallpox. We demonstrate that the overexpression of IRF-3 by WR-IRF3 increases the expression of type I interferon, modulates the expression of several cytokines and induces superior protective immune responses against a lethal poxvirus challenge in both Nc/Nga and Balb/c mice. Additionally, the results may be informative for design of other virus-based vaccines or for therapy of different viral infections.

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Pestka, Sidney, Christopher D. Krause, and Mark R. Walter. "Interferons, interferon-like cytokines, and their receptors." Immunological Reviews 202, no. 1 (December 2004): 8–32. http://dx.doi.org/10.1111/j.0105-2896.2004.00204.x.

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Gun, Sin Yee, Carla Claser, Kevin Shyong Wei Tan, and Laurent Rénia. "Interferons and Interferon Regulatory Factors in Malaria." Mediators of Inflammation 2014 (2014): 1–21. http://dx.doi.org/10.1155/2014/243713.

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Malaria is one of the most serious infectious diseases in humans and responsible for approximately 500 million clinical cases and 500 thousand deaths annually. Acquired adaptive immune responses control parasite replication and infection-induced pathologies. Most infections are clinically silent which reflects on the ability of adaptive immune mechanisms to prevent the disease. However, a minority of these can become severe and life-threatening, manifesting a range of overlapping syndromes of complex origins which could be induced by uncontrolled immune responses. Major players of the innate and adaptive responses are interferons. Here, we review their roles and the signaling pathways involved in their production and protection against infection and induced immunopathologies.

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Samuel, Charles E., and Keiko Ozato. "Induction of interferons and interferon-induced genes." Biotherapy 8, no. 3-4 (September 1996): 183–87. http://dx.doi.org/10.1007/bf01877203.

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&NA;. "Interferon-??/interferon-??-2a." Reactions Weekly &NA;, no. 581 (December 1995): 8. http://dx.doi.org/10.2165/00128415-199505810-00028.

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&NA;. "Interferon-??/interferon-??-2b." Reactions Weekly &NA;, no. 644 (March 1997): 9. http://dx.doi.org/10.2165/00128415-199706440-00026.

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&NA;. "Interferon-??/interferon-??-2b." Reactions Weekly &NA;, no. 687 (February 1998): 9. http://dx.doi.org/10.2165/00128415-199806870-00023.

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&NA;. "Interferon-??/interferon-??-2a." Reactions Weekly &NA;, no. 1084 (January 2006): 15–16. http://dx.doi.org/10.2165/00128415-200610840-00047.

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&NA;. "Interferon-??/interferon-??-2b." Reactions Weekly &NA;, no. 919 (September 2002): 7. http://dx.doi.org/10.2165/00128415-200209190-00020.

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&NA;. "Interferon-??/PEG interferon-??" Reactions Weekly &NA;, no. 1008 (July 2004): 13. http://dx.doi.org/10.2165/00128415-200410080-00041.

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&NA;. "Interferon-??/interferon-??-2b." Reactions Weekly &NA;, no. 1030 (December 2004): 10. http://dx.doi.org/10.2165/00128415-200410300-00030.

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Ghorbani, Amir, Michael C. Abundo, Hana Ji, Kara J. M. Taylor, John M. Ngunjiri, and Chang-Won Lee. "Viral Subpopulation Screening Guides in Designing a High Interferon-Inducing Live Attenuated Influenza Vaccine by Targeting Rare Mutations in NS1 and PB2 Proteins." Journal of Virology 95, no. 2 (October 28, 2020): e01722-20. http://dx.doi.org/10.1128/jvi.01722-20.

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ABSTRACTInfluenza A viruses continue to circulate among wild birds and poultry worldwide, posing constant pandemic threats to humans. Effective control of emerging influenza viruses requires new broadly protective vaccines. Live attenuated influenza vaccines with truncations in nonstructural protein 1 (NS1) have shown broad protective efficacies in birds and mammals, which correlate with the ability to induce elevated interferon responses in the vaccinated hosts. Given the extreme diversity of influenza virus populations, we asked if we could improve an NS1-truncated live attenuated influenza vaccine developed for poultry (PC4) by selecting viral subpopulations with enhanced interferon-inducing capacities. Here, we deconstructed a de novo population of PC4 through plaque isolation, created a large library of clones, and assessed their interferon-inducing phenotypes. While most of the clones displayed the parental interferon-inducing phenotype in cell culture, few clones showed enhanced interferon-inducing phenotypes in cell culture and chickens. The enhanced interferon-inducing phenotypes were linked to either a deletion in NS1 (NS1Δ76-86) or a substitution in polymerase basic 2 protein (PB2-D309N). The NS1Δ76-86 deletion disrupted the putative eukaryotic translation initiation factor 4GI-binding domain and promoted the synthesis of biologically active interferons. The PB2-D309N substitution enhanced the early transcription of interferon mRNA, revealing a novel role for the 309D residue in suppression of interferon responses. We combined these mutations to engineer a novel vaccine candidate that induced additive amounts of interferons and stimulated protective immunity in chickens. Therefore, viral subpopulation screening approaches can guide the design of live vaccines with strong immunostimulatory properties.IMPORTANCE Effectiveness of NS1-truncated live attenuated influenza vaccines relies heavily on their ability to induce elevated interferon responses in vaccinated hosts. Influenza viruses contain diverse particle subpopulations with distinct phenotypes. We show that live influenza vaccines can contain underappreciated subpopulations with enhanced interferon-inducing phenotypes. The genomic traits of such virus subpopulations can be used to further improve the efficacy of the current live vaccines.

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Tiwari, R. K., J. Kusari, R. Kumar, and G. C. Sen. "Gene induction by interferons and double-stranded RNA: selective inhibition by 2-aminopurine." Molecular and Cellular Biology 8, no. 10 (October 1988): 4289–94. http://dx.doi.org/10.1128/mcb.8.10.4289-4294.1988.

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Transcription of several interferon-inducible human genes is also induced by double-stranded RNA. The nature and the mechanism of action of signals generated by interferons and by double-stranded RNA which mediate the induction of these genes are under investigation. Here we report that 2-aminopurine, a known inhibitor of protein kinases, could selectively block this induction process. Induction of mRNAs 561 and 6-16 in HeLaM cells by double-stranded RNA was completely inhibited by 10 mM 2-aminopurine, whereas cellular protein and RNA syntheses as well as the induction of metallothionein mRNA by CdCl2 were unaffected by this inhibitor. In addition, 2-aminopurine blocked the induction of the same two mRNAs and of mRNAs 2-5(A) synthetase, 2A, and 1-8 by alpha interferon and of mRNAs 2A and 1-8 by gamma interferon in HeLaM cells. The observed inhibition was at the level of transcription, and for establishing efficient inhibition, the 2-aminopurine treatment had to begin at early stages of interferon treatment. In GM2767 cells, 2-aminopurine inhibited induction of mRNAs 561 and 6-16 by double-stranded RNA but not by alpha interferon. These results suggest that double-stranded RNA-induced signal 2 is distinct from the interferon-alpha-induced signal 2 (R. K. Tiwari, J. Kusari, and G. C. Sen, EMBO J. 6:3373-3378, 1987) and that 2-aminopurine can block the former but not the latter. Moreover, it appeared that 2-aminopurine could block the production of signal 1 by interferons. This was confirmed by experiments in which we separately tested the effects of 2-aminopurine on signal 1 and signal 2 production by interferons in HeLaM cells. Although no direct experimental evidence is available as yet, our results are consistent with the hypothesis that the functioning of a protein kinase activity may be necessary for transcriptional induction of genes by double-stranded RNA and for gene induction by interferons in those cells in which signal 1 production is needed.

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Tiwari, R. K., J. Kusari, R. Kumar, and G. C. Sen. "Gene induction by interferons and double-stranded RNA: selective inhibition by 2-aminopurine." Molecular and Cellular Biology 8, no. 10 (October 1988): 4289–94. http://dx.doi.org/10.1128/mcb.8.10.4289.

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Transcription of several interferon-inducible human genes is also induced by double-stranded RNA. The nature and the mechanism of action of signals generated by interferons and by double-stranded RNA which mediate the induction of these genes are under investigation. Here we report that 2-aminopurine, a known inhibitor of protein kinases, could selectively block this induction process. Induction of mRNAs 561 and 6-16 in HeLaM cells by double-stranded RNA was completely inhibited by 10 mM 2-aminopurine, whereas cellular protein and RNA syntheses as well as the induction of metallothionein mRNA by CdCl2 were unaffected by this inhibitor. In addition, 2-aminopurine blocked the induction of the same two mRNAs and of mRNAs 2-5(A) synthetase, 2A, and 1-8 by alpha interferon and of mRNAs 2A and 1-8 by gamma interferon in HeLaM cells. The observed inhibition was at the level of transcription, and for establishing efficient inhibition, the 2-aminopurine treatment had to begin at early stages of interferon treatment. In GM2767 cells, 2-aminopurine inhibited induction of mRNAs 561 and 6-16 by double-stranded RNA but not by alpha interferon. These results suggest that double-stranded RNA-induced signal 2 is distinct from the interferon-alpha-induced signal 2 (R. K. Tiwari, J. Kusari, and G. C. Sen, EMBO J. 6:3373-3378, 1987) and that 2-aminopurine can block the former but not the latter. Moreover, it appeared that 2-aminopurine could block the production of signal 1 by interferons. This was confirmed by experiments in which we separately tested the effects of 2-aminopurine on signal 1 and signal 2 production by interferons in HeLaM cells. Although no direct experimental evidence is available as yet, our results are consistent with the hypothesis that the functioning of a protein kinase activity may be necessary for transcriptional induction of genes by double-stranded RNA and for gene induction by interferons in those cells in which signal 1 production is needed.

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Leyssen, Pieter, Christian Drosten, Marcus Paning, Nathalie Charlier, Jan Paeshuyse, Erik De Clercq, and Johan Neyts. "Interferons, Interferon Inducers, and Interferon-Ribavirin in Treatment of Flavivirus-Induced Encephalitis in Mice." Antimicrobial Agents and Chemotherapy 47, no. 2 (February 2003): 777–82. http://dx.doi.org/10.1128/aac.47.2.777-782.2003.

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ABSTRACT We evaluated the prophylactic and therapeutic efficacy of interferon α-2b, pegylated interferon α-2b, poly(I · C), and Ampligen against Modoc virus encephalitis in an animal model for flavivirus infections. All compounds significantly delayed virus-induced morbidity (paralysis) and mortality (due to progressive encephalitis). Viral load (as measured on day 7 postinfection) was significantly reduced by 80 to 100% in the serum, brain, and spleen in mice that had been treated with either interferon α-2b, pegylated interferon α-2b, poly(I · C), or Ampligen. We also studied whether a combination of interferon α-2b and ribavirin (presently the standard therapy for the treatment of infections with hepatitis C virus) would be more effective than treatment with interferon alone. However, ribavirin did not enhance the inhibitory effect of interferon therapy in this animal model for flavivirus infections.

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Tsygankov, Mikhail A., and Marina V. Padkina. "Influence of PDI gene overexpression on heterological proteins production in yeast Pichia pastoris." Ecological genetics 15, no. 2 (June 15, 2017): 21–30. http://dx.doi.org/10.17816/ecogen15221-30.

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Background. The yeast Pichia pastoris is used for synthesis of recombinant secretory proteins. Overexpression of assistant genes, coding proteins involved in secretion, is one of approaches to improve the production of target protein. PpPDI gene encodes P. pastoris yeast protein disulfide isomerase (Pdi). The aim of our study was to evaluate the effect of Pdi overproduction on recombinant interferons (human interferon-alfa16 and chicken interferon-gamma) production. Materials and Methods. PpPDI gene was cloned under the control of the AOX1 gene promoter in plasmid pPICZαA. Primers for AJ302014.1 nucleotide sequence of NCBI data base were used for PpPDI gene cloning. The chromosomal DNA of the GS115 strain was used as a template. To generate strains with PpPDI gene overexpression we used a previously obtained strains producing human interferon-alfa16 and chicken interferon-gamma. Yeast transformation was performed by electroporation. Cultivation was performed using single and two-stage strategies in standard media containing methanol as the sole carbon source to induce the AOX1 gene promoter. Results. We obtained interferon-producing strains with PpPDI gene overexpression. Over-expression of the PpPDI gene in yeast P. pastoris increases the production of interferon-alfa16, a protein containing disulfide bonds, regardless of the mode of cultivation. Effect of PpPDI gene over-expression on the production of interferon-gamma - the protein without disulfide bonds, depends on cultivation mode. Conclusion. PpPDI gene overexpression can be used to enhance the production of interferons and other proteins that contain disulfide bonds. Effect of PpPDI gene overexpression on recombinant proteins without disulfide bonds may depend on cultivation procedure.

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Muttar, A. A. "Cloning and gene expression equine leukocyte α-interferon in cells of Escherichia Coli." Al-Qadisiyah Journal of Veterinary Medicine Sciences 12, no. 1 (June 30, 2013): 82. http://dx.doi.org/10.29079/vol12iss1art234.

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Interferon plays role in innate immune responses through upregulation of costimulatory molecules and induction of proinflammatory cytokines. interferons including interferon alpha (IFNA). The present study characterized IFNA cDNA and predicted protein. The interferon’s play a great role in protection from infections, which have been called by microorganisms, and also have powerful antiproliferation and immunomodulation activity. The purposes of study: cloning and expression of horse leukocyte interferon and purification the product protein. The results and discussion : In the result we isolated (DNA) from equine leukocyte in blood, which was used in the quality of the matrix for amplification of α-interferon gene with PCR HELP, and isolation gene α-interferon and transformation in vector puc18 and expression vector PET24b (+) and recombinant plasmid was transformed into E. coli strain BL21( codon plus 440) induction with IPTG. The results showed the protein having the same molecular weight as horse interferon alpha about 5.81 kDa

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Rhodes, C. J., and K. W. Taylor. "Effect of interferon and double-stranded RNA on B-cell function in mouse islets of Langerhans." Biochemical Journal 228, no. 1 (May 15, 1985): 87–94. http://dx.doi.org/10.1042/bj2280087.

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The direct effects of alpha- and beta-interferons on isolated mouse pancreatic islets were investigated in vitro and found to be similar. After 7 h incubation with interferon concentrations above 350 units/ml, glucose-stimulated (pro)insulin biosynthesis was significantly inhibited, with only a slight inhibition of total protein biosynthesis. Inhibition could be abolished in the additional presence of an anti-interferon antibody. Interferon did not affect insulin release, total insulin content, or glucose oxidation of the islets. The stimulation of (pro)insulin biosynthesis by adenosine, D-glyceraldehyde, mannose, N-acetylglucosamine and leucine was also inhibited by interferon, with no effect on insulin release. At concentrations of dsRNA (double-stranded RNA) said to induce interferon (1-100 micrograms/ml), glucose-stimulated (pro)insulin biosynthesis was inhibited without significantly affecting insulin release. The dsRNA may itself inhibit stimulated (pro)insulin biosynthesis or may function indirectly by the induction of interferon.

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Journal articles on the topic 'Interferon'

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