Relevant bibliographies by topics / Type I interferons

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Academic literature on the topic 'Type I interferons'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 June 2025

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Journal articles on the topic "Type I interferons"

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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 (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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Sozaeva, L. S. "The new immunological methods for diagnostics of type 1 autoimmune polyendocrine syndrome." Problems of Endocrinology 61, no. 3 (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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Le-Thi-Phuong, Thao, Gaëtan Thirion, and Jean-Paul Coutelier. "Distinct gamma interferon-production pathways in mice infected with lactate dehydrogenase-elevating virus." Journal of General Virology 88, no. 11 (2007): 3063–66. http://dx.doi.org/10.1099/vir.0.83242-0.

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Two distinct pathways of gamma interferon (IFN-γ) production have been found in mice infected with lactate dehydrogenase-elevating virus. Both pathways involve natural killer cells. The first is mostly interleukin-12-independent and is not controlled by type I interferons. The second, which is suppressed by type I interferons, leads to increased levels of IFN-γ production and requires the secretion of interleukin-12. This regulation of IFN-γ production by type I interferons may help to control indirect pathogenesis induced by this cytokine.
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Crow, Mary K., Mikhail Olferiev, and Kyriakos A. Kirou. "Type I Interferons in Autoimmune Disease." Annual Review of Pathology: Mechanisms of Disease 14, no. 1 (2019): 369–93. http://dx.doi.org/10.1146/annurev-pathol-020117-043952.

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Type I interferons, which make up the first cytokine family to be described and are the essential mediators of antivirus host defense, have emerged as central elements in the immunopathology of systemic autoimmune diseases, with systemic lupus erythematosus as the prototype. Lessons from investigation of interferon regulation following virus infection can be applied to lupus, with the conclusion that sustained production of type I interferon shifts nearly all components of the immune system toward pathologic functions that result in tissue damage and disease. We review recent data, mainly from studies of patients with systemic lupus erythematosus, that provide new insights into the mechanisms of induction and the immunologic consequences of chronic activation of the type I interferon pathway. Current concepts implicate endogenous nucleic acids, driving both cytosolic sensors and endosomal Toll-like receptors, in interferon pathway activation and suggest targets for development of novel therapeutics that may restore the immune system to health.
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Joyce, Margaret M., Robert C. Burghardt, Rodney D. Geisert, et al. "Pig Conceptuses Secrete Estrogen and Interferons to Differentially Regulate Uterine STAT1 in a Temporal and Cell Type-Specific Manner." Endocrinology 148, no. 9 (2007): 4420–31. http://dx.doi.org/10.1210/en.2007-0505.

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Conceptus trophectoderm and uterine luminal epithelial cells interact via endocrine, paracrine, and autocrine modulators to mediate pregnancy recognition and implantation. Pig conceptuses not only release estrogens for pregnancy recognition but also secrete interferons during implantation. Because interferon-stimulated genes are increased by interferons secreted for pregnancy recognition in ruminants, we asked whether the interferon-stimulated gene, STAT1, is up-regulated in pig endometrium by conceptus estrogens and/or interferons. STAT1 expression in response to day of pregnancy, estrogen injection, and intrauterine infusion of conceptus secretory proteins in pigs indicated 1) estrogen increases STAT1 in luminal epithelial cells, 2) conceptus secretory proteins that contain interferons increase STAT1 in stroma, 3) STAT1 increases in close proximity to the conceptus, and 4) early estrogen results in conceptus death and no STAT1 in stroma. The interactions of estrogen and interferons to regulate cell-type-specific expression of STAT1 highlight the complex interplay between endometrium and conceptus for pregnancy recognition and implantation.
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Pisanelli, Giuseppe, Ugo Pagnini, Giuseppe Iovane, and Adolfo García-Sastre. "Type I and Type II Interferon Antagonism Strategies Used by Paramyxoviridae: Previous and New Discoveries, in Comparison." Viruses 14, no. 5 (2022): 1107. http://dx.doi.org/10.3390/v14051107.

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Paramyxoviridae is a viral family within the order of Mononegavirales; they are negative single-strand RNA viruses that can cause significant diseases in both humans and animals. In order to replicate, paramyxoviruses–as any other viruses–have to bypass an important protective mechanism developed by the host’s cells: the defensive line driven by interferon. Once the viruses are recognized, the cells start the production of type I and type III interferons, which leads to the activation of hundreds of genes, many of which encode proteins with the specific function to reduce viral replication. Type II interferon is produced by active immune cells through a different signaling pathway, and activates a diverse range of genes with the same objective to block viral replication. As a result of this selective pressure, viruses have evolved different strategies to avoid the defensive function of interferons. The strategies employed by the different viral species to fight the interferon system include a number of sophisticated mechanisms. Here we analyzed the current status of the various strategies used by paramyxoviruses to subvert type I, II, and III interferon responses.
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He, Buyuan, James T. Tran, and David Jesse Sanchez. "Manipulation of Type I Interferon Signaling by HIV and AIDS-Associated Viruses." Journal of Immunology Research 2019 (April 4, 2019): 1–10. http://dx.doi.org/10.1155/2019/8685312.

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Type I Interferons were first described for their profound antiviral abilities in cell culture and animal models, and later, they were translated into potent antiviral therapeutics. However, as additional studies into the function of Type I Interferons progressed, it was also seen that pathogenic viruses have coevolved to encode potent mechanisms allowing them to evade or suppress the impact of Type I Interferons on their replication. For chronic viral infections, such as HIV and many of the AIDS-associated viruses, including HTLV, HCV, KSHV, and EBV, the clinical efficacy of Type I Interferons is limited by these mechanisms. Here, we review some of the ways that HIV and AIDS-associated viruses thrive in Type I Interferon-rich environments via mechanisms that block the function of this important antiviral cytokine. Overall, a better understanding of these mechanisms creates avenues to better understand the innate immune response to these viruses as well as plan the development of antivirals that would allow the natural antiviral effect of Type I Interferons to manifest during these infections.
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Domeier, Phillip P., and Ziaur S. M. Rahman. "Regulation of B Cell Responses in SLE by Three Classes of Interferons." International Journal of Molecular Sciences 22, no. 19 (2021): 10464. http://dx.doi.org/10.3390/ijms221910464.

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There are three classes of interferons (type 1, 2, and 3) that can contribute to the development and maintenance of various autoimmune diseases, including systemic lupus erythematosus (SLE). Each class of interferons promotes the generation of autoreactive B cells and SLE-associated autoantibodies by distinct signaling mechanisms. SLE patients treated with various type 1 interferon-blocking biologics have diverse outcomes, suggesting that additional environmental and genetic factors may dictate how these cytokines contribute to the development of autoreactive B cells and SLE. Understanding how each class of interferons controls B cell responses in SLE is necessary for developing optimized B cell- and interferon-targeted therapeutics. In this review, we will discuss how each class of interferons differentially promotes the loss of peripheral B cell tolerance and leads to the development of autoreactive B cells, autoantibodies, and SLE.
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De Maeyer, Edward, and Jaqueline De Maeyer-Guignard. "Type I Interferons." International Reviews of Immunology 17, no. 1-4 (1998): 53–73. http://dx.doi.org/10.3109/08830189809084487.

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Doehn, Jan-Moritz, Christoph Tabeling, Robert Biesen, et al. "CD169/SIGLEC1 is expressed on circulating monocytes in COVID-19 and expression levels are associated with disease severity." Infection 49, no. 4 (2021): 757–62. http://dx.doi.org/10.1007/s15010-021-01606-9.

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AbstractCoronavirus disease 2019 (COVID-19) is caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Type I interferons are important in the defense of viral infections. Recently, neutralizing IgG auto-antibodies against type I interferons were found in patients with severe COVID-19 infection. Here, we analyzed expression of CD169/SIGLEC1, a well described downstream molecule in interferon signaling, and found increased monocytic CD169/SIGLEC1 expression levels in patients with mild, acute COVID-19, compared to patients with severe disease. We recommend further clinical studies to evaluate the value of CD169/SIGLEC1 expression in patients with COVID-19 with or without auto-antibodies against type I interferons.
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Dissertations / Theses on the topic "Type I interferons"

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Shabman, Reed Solomon Heise Mark T. "Alphavirus evasion of type I interferons." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1879.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.<br>Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.
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Ching, Yee-Man. "Regulation of type 2 inflammation by type I interferons." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/43755.

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Rhinovirus-induced asthma exacerbations are a major cause of morbidity and mortality in patients. Experimental clinical infection studies indicate rhinovirus augments type 2 inflammation in asthma. Additionally, asthmatic lung cells have impaired type I interferon production in response to rhinovirus stimulation. Evidence suggests co-regulation of type I interferon signalling and type 2 immunity exists; therefore, we hypothesised that type I interferon deficiency in asthma leads to the reduced regulation of type 2 immunity, resulting in exacerbation of allergen-induced type 2 inflammation during rhinovirus infection. To investigate the role of type I interferon signalling, type I interferon receptor (IFNAR1) knockout mice, an anti-IFNAR1 blocking antibody and recombinant interferon-β therapy were used in mouse models of rhinovirus-induced airways disease. Impaired IFNAR1 signalling resulted in enhanced eosinophilic inflammation in response to allergen challenge and rhinovirus infection, which was associated with increased CCL24 and Th2 chemokines CCL17 and CCL22. Recombinant interferon-β treatment had limited effects on responses to the combination of allergen and rhinovirus, but suppressed allergen-induced CCL17. In THP1-derived macrophages, interferon-β co-treatment and pre-treatment suppressed IL-4 and TNFα-induced Th2 chemokine production. Microarray analysis was performed on these cells to help identify the regulatory mechanism of type I interferon on Th2 chemokine expression. Interferon-β pre-treatment significantly upregulated PTPN6 (encoding SHP1, a phosphatase that regulates STAT6 activity) expression compared with IL-4 and TNFα-stimulated cells. Western blot analysis did not identify differences in STAT6 phosphorylation following interferon-β treatment, or differences in SHP1 protein levels. These findings support a role for type I interferon in the negative regulation of type 2 inflammation in both the presence and absence of rhinovirus; however, this mechanism has yet to be identified. Impaired interferon responses in asthma may contribute to enhanced type 2 immunity that is considered pathological in allergic airways inflammation and virus-induced asthma exacerbations.
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Platis, Dimitris. "Structure/function analysis of Type I interferons." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397783.

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Cooles, Faye Anisa Hogarth. "Type 1 interferons in early rheumatoid arthritis." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3733.

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Rheumatoid arthritis (RA) is a heterogeneous autoimmune disease predominantly causing synovial inflammation. Early and established RA exhibit both overlapping and distinct pathological processes. Early treatment improves clinical outcomes and delineating early disease pathology can inform novel therapeutic pathways. Type 1 interferons have diverse effects on immune function and relative exposure can be recorded using an interferon gene signature (IGS). The IGS is positive in 20-30% of established RA patients where it does not associate with disease activity but can predict response to some biological therapies. However, glucocorticoids and potentially other immunomodulatory therapies can modify the IGS. I therefore examined the IGS in early, drug naïve RA focusing on prevalence, association with clinical phenotype, and impact on disease progression. I additionally attempted to identify the source of type 1 interferons and triggers for their production. I demonstrated the IGS is increased in early RA, falls with treatment/time and appears to predict clinical response to initial therapies. In this latter capacity it out-performed baseline CRP, ESR and DAS-28. The IGS also positively associated with disease activity and IgM rheumatoid factor titres. The latter association was supported by an analysis of the B cell transcriptome of IGS+ early RA patients, where there was increased gene expression in pathways related to B cell activation; increased plasma cell differentiation; and propensity to produce IgM. Genes were also upregulated that are usually expressed in B cell malignancies, further emphasising a potentially pathologically activated state. Retroelements (SINE, LINE-1 and ERV), are putative triggers of type 1 interferons in autoimmunity. However early RA whole blood LINE-1 activity was comparable to healthy controls and was actually reduced in IGS+ patients. Furthermore pDCs showed uniformly reduced retroelement activity in early RA compared with healthy controls. Indeed there was differential retroelement expression across lymphocyte subsets in early RA; expression was highest in B and T cells and comparatively lower in DCs and monocytes. Finally despite being a major source of type 1 interferons, pDCs in IGS+ early RA patients had comparable interferon-α expression to other lymphocytes. In conclusion I demonstrate that type 1 interferons may play a pathogenic role in early RA and disease progression - although their source and triggers remain unclear. Nonetheless I hypothesise that therapies that target type 1 interferons could have clinical benefit in early RA.
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Hidmark, Åsa. "Induction of type I interferons and viral immunity /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-227-9/.

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Wahlund, Casper. "Detection And Quantification Of Equine Type I Interferons." Thesis, Uppsala universitet, Medicinska fakulteten, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-159198.

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Type I interferons (IFNs), perhaps the most important of cytokines in fighting viral infections, have been target for detailed research only the past few decades and much is yet to be investigated. Hidden in the mysteries of IFNs might be powerful anti-viral and anti-tumor therapies, alongside greatly increased understanding of vertebrate immunology. This project aims at investigating IFN expression of in vitro stimulated equine cell lines and studies of IFN expression in horses, both healthy and a number of horses diagnosed with inflammatory bowel disease (IBD). Amongst equine diseases, IBD is of increasing concern and scientific progressions within the project are, in several aspects, also applicable for human medicine.
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SPOSITO, BENEDETTA. "Type III Interferons: Running Interference with Mucosal Repair." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/402377.

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Gli interferoni (IFN) sono mediatori e regolatori fondamentali della risposta immunitaria dell'ospite a virus e ad altri agenti microbici. Gli IFN di tipo I e di tipo III (o IFN-λ) sono tra le prime citochine ad essere indotte in seguito a infezioni virali. Il legame tra gli IFN e i rispettivi recettori attiva vie di trasduzione del segnale simili tra loro che inducono l'espressione di geni stimolati dagli IFN (ISG) con funzioni antivirali. La caratteristica principale che rende ciascuna di queste famiglie di IFN unica e non ridondante è l'esistenza di recettori distinti che fanno sì che gli IFN-I attivino una risposta ubiquitaria e che gli IFN-III agiscano esclusivamente sulle cellule epiteliali e su un sottoinsieme di cellule immunitarie. Ulteriori distinzioni riguardano la natura meno infiammatoria degli IFN-III e la loro induzione solitamente anticipata rispetto a quella degli IFN-I. Pertanto gli IFN-III sono considerati i difensori di prima linea delle mucose con la capacità di attivare una risposta antivirale precoce senza causare danno tissutale. Se la loro azione risulta insufficiente a contenere l’infezione, il sistema passa all’induzione degli IFN-I, i quali generano una risposta antivirale e infiammatoria più potente e a livello sistemico, che tuttavia può portare ad immunopatologia. Nel corso della mia tesi ho verificato l'ipotesi secondo cui anche gli IFN-III possano causare immunopatologia, in particolare durante infezioni virali delle vie respiratorie e in contesti di danno all’epitelio gastrointestinale in malattie infiammatorie croniche intestinali e lesioni da radiazioni. In primo luogo, io e i miei colleghi abbiamo dimostrato che in un polmone in cui è stata indotta una risposta antivirale, gli IFN-III prodotti dalle cellule dendritiche inibiscono la proliferazione delle cellule epiteliali portando ad una compromissione del rigenerazione della barriera e ad un aumento della suscettibilità ad infezioni batteriche. In seguito abbiamo analizzato la produzione di IFN lungo il tratto respiratorio di pazienti affetti da COVID-19. Abbiamo trovato che, nelle alte vie aeree, l'espressione di IFN-I/III correla con la carica virale e che negli anziani, che presentano un maggiore rischio di sviluppare una patologia severa, questa correlazione è più debole o assente. Una forte espressione di IFN-λ1, IFN-λ3 e ISG caratterizza le alte vie aeree di pazienti con sintomatologia lieve, mentre risultano fortemente espressi gli IFN-I, IFN-λ2 e un insieme di geni antiproliferativi e proapoptotici lungo tutto il tratto respiratorio di pazienti ospedalizzati, suggerendo che possano ostacolare il processo di riparazione dell’epitelio. Infine, abbiamo dimostrato che gli IFN-III ritardano la rigenerazione dell'intestino tenue e del colon in seguito a danno da radiazioni o da colite indotta da destrano sodio solfato, poiché contribuiscono a indurre la morte cellulare delle cellule epiteliali tramite la formazione di un complesso proteico costituito da Z-DNA binding protein (ZBP1) e gasdermin C (GSDMC). I nostri risultati mettono in discussione il ruolo degli IFN-III come protettori delle mucose poiché indicano che quando non propriamente regolati possono causare immunopatologia. Queste evidenze portano alla necessità di progettare l’uso clinico degli IFN di tipo III in modo da evitare le loro funzioni dannose per i tessuti e massimizzarne gli effetti benefici.<br>Interferons (IFNs) are fundamental mediators and regulators of the host immune response to viruses and other microbial agents. Type I and type III IFNs (also known as IFN-λ) are some of the first cytokines to be induced upon detection of viral infections. Signaling through their specific receptors leads to the activation of a similar signaling cascade that triggers the expression of a common set of IFN-stimulated genes (ISGs) with antiviral effector functions. The main feature that makes each of these families of IFNs unique and nonredundant is the existence of distinct receptors that differentiate them in their ability to act on virtually every cell type (type I IFNs) or exclusively on epithelial cells and a subset of immune cells (type III IFNs). Despite inducing a widely overlapping set of genes, IFN-I can mount a stronger proinflammatory response compared to IFN-III. This, coupled with the earlier induction of IFN-III upon infection, has led to the classification of IFN-III as front-line defenders of mucosal surfaces with the ability to initiate an early antiviral response with minimal tissue-damaging effects. If their response is insufficient the system shifts to the more potent and broader-acting antiviral and inflammatory IFN-I response that can cause immunopathology. In the course of my thesis, I have tested the hypothesis that also IFN-III contribute to immunopathology at barrier sites such as the respiratory and gastrointestinal epithelia during viral infections and inflammatory bowel disease/radiation-induced injury respectively. First, my colleagues and I found that in a mouse model where we mimicked the induction of antiviral responses in the respiratory tract, IFN-III produced by lung dendritic cells inhibited the proliferation of lung epithelial cells leading to an impairment in barrier restoration and an increase in susceptibility to bacterial infections. Then we measured IFN responses along the respiratory tract of COVID-19 patients. We uncovered that in the upper airways expression of IFN-I/III correlated with viral load and elderly patients, that have a higher risk of developing severe COVID-19, had a dysregulation in the IFN response. A strong expression of IFN-λ1, IFN-λ3 and ISGs characterized the upper airways of mild patients. IFN-I and IFN-λ2 together with antiproliferative and proapoptotic genes were upregulated along all the respiratory tract of severe COVID-19 patients, suggesting that they might contribute to the impairment of epithelium restitution. Finally, we demonstrated that IFN-III delayed colon and small intestine repair after dextran sulfate sodium-induced colitis and radiation-induced injury by triggering cell death of epithelial cells via the formation of a novel protein complex that includes Z-DNA binding protein (ZBP1) and gasdermin C (GSDMC). Our findings challenge the role of IFN-III as protectors of mucosal barriers as they indicate that a dysregulated IFN-III response holds the potential to contribute to immunopathology. Therefore, the clinical use of type III IFNs should be designed in such a way that their tissue-damaging functions are avoided and their beneficial effects are maximized.
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Goritzka, Michelle. "Regulation of virus induced inflammation by type I interferons." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/49786.

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Type I interferons (IFNs) are the first line of defence against viral pathogens. They play a crucial role in activating antiviral responses to limit viral replication and viral spread. Human respiratory syncytial virus (RSV) can cause severe lung inflammation and this has been associated with polymorphisms in several innate immune response genes, including many that control the IFN system. In order to elucidate the importance of type I IFNs in regulating local inflammatory responses in the lung, their role in pulmonary immune responses to RSV infection was assessed in mice lacking the type I IFN receptor (Ifnar1-/-). Levels of proinflammatory cytokines and chemokines were markedly reduced during RSV infection. Similar results were obtained when in Ifnar1-/- mice were challenged with non-infectious innate stimuli such as Toll-like receptor agonists. It was further shown that the administration of recombinant IFN-α together with innate stimuli was sufficient to potentiate the proinflammatory cytokine production. Exploiting a reporter mouse strain expressing GFP under the control of the Ifna6 promoter, alveolar macrophages (AMs) were identified as the predominant source of type I IFNs during RSV infection. This type I IFN production solely relied on signalling through the cytosolic RIG-I-like receptors (RLRs), as AMs lacking MAVS, the adaptor downstream of RLRs, were unable to produce type I IFNs. Furthermore, Mavs-/- mice showed compromised production of proinflammatory cytokines and chemokines, and as a consequence had an increased viral burden and RSV-induced pathology. Interestingly, Mavs-/- mice had a marked deficiency in the production of monocyte chemoattractants and recruitment of inflammatory monocytes (infMo). The administration of recombinant CCL2 during RSV infection permitted monocyte recruitment into the lung of Mavs-/- mice and mediated an unexpected antiviral activity and reduced disease severity. This work emphasises a role for type I IFNs in antiviral immune responses by driving early proinflammatory cytokine responses and recruitment of antiviral monocytes, a yet underappreciated novel cell type responsible for dampening RSV-disease burden in vivo.
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Wang, Ling, and Shunbin Ning. ""Toll-Free" Pathways for Production of Type I Interferons." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/6540.

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Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) are recognized by different cellular pathogen recognition receptors (PRRs), which are expressed on cell membrane or in the cytoplasm of cells of the innate immune system. Nucleic acids derived from pathogens or from certain cellular conditions represent a large category of PAMPs/DAMPs that trigger production of type I interferons (IFN-I) in addition to pro-inflammatory cytokines, by specifically binding to intracellular Toll-like receptors or cytosolic receptors. These cytosolic receptors, which are not related to TLRs and we call them "Toll-free" receptors, include the RNA-sensing RIG-I like receptors (RLRs), the DNA-sensing HIN200 family, and cGAS, amongst others. Viruses have evolved myriad strategies to evoke both host cellular and viral factors to evade IFN-I-mediated innate immune responses, to facilitate their infection, replication, and establishment of latency. This review outlines these "Toll-free" innate immune pathways and recent updates on their regulation, with focus on cellular and viral factors with enzyme activities.
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Koppe, Uwe Moritz Eberhard. "Role of type I interferons in Streptococcus pneumoniae pneumonia." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16532.

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Streptococcus pneumoniae ist die häufigste Ursache für ambulant erworbene Pneumonien weltweit. Daher müssen die Wirts-Pathogen-Interaktionen erforscht werden, um neue Therapiestrategien zu entwickeln. In dieser Studie habe ich 1. den Typ I Interferon (IFN)-stimulierenden Signalweg des angeborenen Immunsystems in Pneumokokken-infizierten Wirtszellen sowie 2. dessen Bedeutung in der Pneumokokkenpneumonie untersucht. Humane und murine Makrophagen, aber nicht alveolare Epithelzellen, produzierten Typ I IFNs nach Infektion mit S. pneumoniae. Dieses war abhängig vom Virulenzfaktor Pneumolysin und erforderte sowohl die Phagozytose der Bakterien als auch die Ansäuerung der Endosomen. Die Induktion der Typ I IFNs wird durch einen zytosolischen Signalweg vermittelt, welcher wahrscheinlich DNA erkennt und sowohl das Adapterprotein STING als auch den Transkriptionsfaktor IRF3 aktiviert. Typ I IFNs, welche von infizierten Makrophagen gebildet wurden, regulierten die Expression von IFN-stimulierten Genen (ISGs) und Chemokinen in Makrophagen und co-kultivierten alveolaren Epithelzellen in vitro und in Mauslungen in vivo. In einem murinen Pneumoniemodell hatten die Typ I IFNs jedoch einen negativen Effekt für den Wirt. Mäuse mit einem Defekt im Typ I IFN-Rezeptor oder mit einem Knockout im Typ I und Typ II IFN-Rezeptor hatten eine signifikant geringere Bakterienlast in der Lunge und eine verminderte Reduktion der Körpertemperatur und des Körpergewichtes als wild-typ Mäuse. Diese Effekte waren nicht durch Änderungen in der Zellrekrutierung oder durch Änderungen der Zytokin-/Chemokinexpression erklärbar. Zusammenfassend lässt sich feststellen, dass Typ I IFNs durch Pneumokokken induziert werden, aber dass sie trotz einiger positiver Effekte auf die Expression von ISGs einen negativen Gesamteffekt in einem murinen Pneumoniemodell aufweisen. Ein detailliertes Verständnis der Typ I IFN-Antwort während der Pneumokokkeninfektion kann die Entwicklung neuer Therapiestrategien unterstützen.<br>Streptococcus pneumoniae is the leading cause of community-acquired pneumonia world-wide. A detailed understanding of the host-pathogen interactions is required in order to foster the development of new therapeutic strategies. Here, I (I) characterized an innate immune recognition pathway that senses pneumococcal infection and triggers the production of type I interferons (IFNs), and (II) examined the role of type I IFNs in pneumococcal pneumonia in mice. Human and murine macrophages, but not alveolar epithelial cells, produced type I IFNs after infection with S. pneumoniae. This induction was dependent on the virulence factor pneumolysin, the phagocytosis of the bacteria, and the acidification of the endosome. Moreover, it appeared to be mediated by a cytosolic DNA-sensing pathway involving the adaptor molecule STING and the transcription factor IRF3. Type I IFNs produced by S. pneumoniae-infected macrophages positively regulated the expression of IFN-stimulated genes (ISGs) and chemokines in macrophages and co-cultured alveolar epithelial cells in vitro and in mouse lungs in vivo. However, in a murine model of pneumococcal pneumonia, type I IFN signaling was detrimental to the host defense. Mice deficient in the type I IFN signaling or double deficient in type I and type II IFN signaling had a significantly reduced bacterial load in the lung and a diminished reduction of body temperature and body weight compared to wild-type mice. The decreased susceptibility of the knockout mice was unlikely to be attributable to alterations in cell recruitment or cytokine/chemokine production. In conclusion, type I IFNs are induced during pneumococcal infection. However, despite their positive effects on the expression of some ISGs and chemokines, they negatively affect the outcome of pneumococcal pneumonia in an in vivo mouse model. Targeting the type I IFN system could potentially be an effective way in enhancing the immune response in patients with S. pneumoniae pneumonia.
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Books on the topic "Type I interferons"

1

Parker, Dane, ed. Bacterial Activation of Type I Interferons. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09498-4.

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Ghislain, Julien Johannes. Type I interferon signal transduction. National Library of Canada = Bibliothèque nationale du Canada, 1997.

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1959-, Karupiah Gunasegaran, ed. Gamma interferon in antiviral defense. R.G. Landes, 1997.

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Kumaran, Jyothi. The role of the SD100A domain in IFNAR1 in type I interferon signaling. National Library of Canada, 1999.

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D, Kisner, Smyth John F, and International Conference on Malignant Lymphoma (2nd : 1984 : Lugano, Switzerland), eds. Interferon alpha-2: Pre-clinical and clinical evaluation : proceedings of the symposium held in adjunction with the Second International Conference on Malignant Lymphoma, Lugano, Switzerland, June 13, 1984. Nijhoff, 1985.

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Zemskov, Vladimir, and Veronika Zemskova. Immunotropic effects of therapeutic factors. INFRA-M Academic Publishing LLC., 2020. http://dx.doi.org/10.12737/1039485.

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Data on the immunotropic effects of traditional drugs - antibiotics, antihistamines, anti-inflammatory, and metabolic agents-are summarized. The profile properties of cytostatics, immune globulins, cytokines, vaccines, interferons and their ability to develop General organizational effects are analyzed. Data on the types, blocks, principles of immunotherapy administration, and ways to prevent complications are highlighted.&#x0D; For students and teachers, as well as employees of medical universities.
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International Cancer Congress. (15th 1990 Hamburg, Germany). Intron A: The role of biologics in cancer and AIDS : abstracts and posters. Pennine Press on behalf of Schering-Plough International, 1990.

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E, Kalyuzhny Alexander, ed. Handbook of ELISPOT: Methods and protocols. Humana Press, 2005.

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Károly, Lapis, Eckhardt S, and International Union against Cancer, eds. Biological response modifiers, leukaemias and lymphomas. Akadémiai Kiadó, 1987.

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Virology, Conference on. HIV and other highly pathogenic viruses. Academic Press, 1988.

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Book chapters on the topic "Type I interferons"

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Kotenko, Sergei V., and Raymond P. Donnelly. "Type III Interferons: The Interferon-λ Family." In The Interferons. Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608206.ch6.

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Samarajiwa, Shamith A., William Wilson, and Paul J. Hertzog. "Type I Interferons: Genetics and Structure." In The Interferons. Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608206.ch1.

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Brierley, Melissa M., Jyothi Kumaran, and Eleanor N. Fish. "Biological Actions of Type I Interferons." In The Interferons. Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608206.ch7.

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Langer, Jerome A. "Type I Interferons." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101827.

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Resch, Theresa K., Gabriele Reichmann, and Zoe Waibler. "Type I Interferons." In Compendium of Inflammatory Diseases. Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_125.

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Langer, Jerome A. "Type I Interferons." In Encyclopedia of Signaling Molecules. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101827-1.

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Resch, Theresa K., Gabriele Reichmann, and Zoe Waibler. "Type I Interferons." In Encyclopedia of Inflammatory Diseases. Springer Basel, 2014. http://dx.doi.org/10.1007/978-3-0348-0620-6_125-1.

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Müller, Frank. "Overview of Clinical Applications of Type I Interferons." In The Interferons. Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608206.ch10.

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Dhariwala, Miqdad O., and Deborah M. Anderson. "Yersinia Activation of Type I Interferon." In Bacterial Activation of Type I Interferons. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09498-4_8.

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Hertzog, Paul J. "Production and Action of Type I Interferons in Host Defense." In Bacterial Activation of Type I Interferons. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09498-4_1.

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Conference papers on the topic "Type I interferons"

1

Batoroev, A. S., A. A. Maltuguev, and D. B. Dugarzhapova. "Slot-Type Diffraction Screens for Interfering Field Suppression." In EMC_1986_Wroclaw. IEEE, 1986. https://doi.org/10.23919/emc.1986.10828477.

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"01 Targeting type I interferons." In 8th ANNUAL MEETING OF THE LUPUS ACADEMY, Warsaw, Poland, September 6–8, 2019. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-la.13.

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Chung, Yooyun, Hio Lam Phoebe Tsou, Michael A. Heneghan, Shilpa Chokshi, and Antonio Riva. "P33 The role of type II and III interferons in primary biliary cholangitis." In Abstracts of the British Association for the Study of the Liver Annual Meeting, 19–22 September 2023. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2023. http://dx.doi.org/10.1136/gutjnl-2023-basl.49.

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Moneta, Gian Marco, Claudia Bracaglia, Ivan Caiello та ін. "AB0185 INTERFERON-Γ AMPLIFIES IMMUNE RESPONSE MEDIATED BY TYPE I INTERFERONS IN PAEDIATRIC SYSTEMIC LUPUS ERYTHEMATOSUS AND CORRELATES WITH DISEASE ACTIVITY". У Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7613.

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Ehrlich, S., K. Wild, M. Smits, et al. "Type I Interferons promote maintenance and function of follicular T helper cells in vitro." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677255.

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Ka, Na-Lee, Ga Young Lim, and Mi-Ock Lee. "Abstract 2565: Type I interferons enhance chemosensitivity of breast cancer by inhibiting DNA repair." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2565.

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Ka, Na-Lee, Ga Young Lim, and Mi-Ock Lee. "Abstract 2565: Type I interferons enhance chemosensitivity of breast cancer by inhibiting DNA repair." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2565.

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Rafael Vidal, C., S. Martínez Ramos, B. Malvar Fernández, et al. "S12.3 Type I interferons induce TIE2-mediated endothelial cell dysfunction in systemic lupus erythematosus." In 13th European Lupus Meeting, Stockholm (October 5–8, 2022). Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-elm2022.27.

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Haljasmägi, L., H. Bradford, M. Menon, et al. "S12.2 Type I interferons and their autoantibodies in the context of systemic lupus erythematosus." In 13th European Lupus Meeting, Stockholm (October 5–8, 2022). Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-elm2022.26.

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Lim, Joanne Y. H., Scott A. Gerber, and Edith M. Lord. "Abstract A95: Distinct roles of type I and type II interferons in radiation-induced antitumor immunity against B16 melanoma." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a95.

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Reports on the topic "Type I interferons"

1

Kozina, Carol L., Matthew Wallace Moorman, Catherine Branda, et al. Investigation of type-I interferon dysregulation by arenaviruses : a multidisciplinary approach. Office of Scientific and Technical Information (OSTI), 2011. http://dx.doi.org/10.2172/1029825.

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Pilitkul, Trairak, Prapaporn Pisitkun, Asada Leelahavanichkul, and Poorichaya Somparn. Systems-investigation of aberrant signaling in immune cells of SLE mouse model. Faculty of Medicine, Chulalongkorn University, 2020. https://doi.org/10.58837/chula.res.2020.21.

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Autoimmune diseases occur when the immune cells react against self antigens and subsequently lead to inflammation in the tissues. The interactions between genetics and environmental triggers regulate the phenotypes and outcome of the diseases. Type I interferon has been shown as one of the most crucial cytokines involving in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic systemic autoimmune disease which can result in autoantibody production and fatal glomerulonephritis. Activation via nucleic acid sensors can induce the production of type I interferon from dendritic cells and promote SLE severity. Stimulator of interferon genes (Sting) is a cytoplasmic DNA sensor that signals downstream to enhance type I interferon production after its activation. Recently, it was shown that a gain mutation in the STING gene resulting in over activity of the IFN pathway can cause familial inflammatory syndrome with lupus like manifestations in humans. However, the functional studies of Sting in different autoimmune mouse models suggest the conflicting roles of Sting in the pathogenesis of autoimmune diseases. In order to determine if Sting participates in lupus pathogenesis, the Fcgr2b deficienct mice (lupus mouse model) were bred with Sting deficient mice to create the double deficient mice. In the absence of Sting, the Fcgr2b deficient mice do not develop fatal glomerulonephritis and autoantibodies. The original knowledge from this study is a proof of concept for targeting Sting as a future promising treatment in autoimmune diseases.
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Pisitkun, Trairak, Prapaporn Pisitkun, Asada Leelahavanichkul, and Poorichaya Somparn. Systems biology investigation of immune cell regulation at the molecular level in SLE. Faculty of Medicine, Chulalongkorn University, 2018. https://doi.org/10.58837/chula.res.2018.24.

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Autoimmune diseases occur when the immune cells react against self-antigens and subsequently lead to inflammation in the tissues. The interactions between genetics and environmental triggers regulate the phenotypes and outcome of the diseases. Type I interferon has been shown as one of the most crucial cytokines involving in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic systemic autoimmune disease which can result in autoantibody production and fatal glomerulonephritis. Activation via nucleic acid sensors can induce the production of type I interferon from dendritic cells and promote SLE severity. Stimulator of interferon genes (Sting) is a cytoplasmic DNA sensor that signals downstream to enhance type I interferon production after its activation. Recently, it was shown that a gain mutation in the STING gene resulting in over-activity of the IFN pathway can cause familial inflammatory syndrome with lupus-like manifestations in humans. However, the functional studies of Sting in different autoimmune mouse models suggest the conflicting roles of Sting in the pathogenesis of autoimmune diseases. In order to determine if Sting participates in lupus pathogenesis, the Fcgr2b-deficienct mice (lupus mouse model) were bred with Sting-deficient mice to create the double-deficient mice. In the absence of Sting, the Fcgr2b-deficient mice do not develop fatal glomerulonephritis and autoantibodies. The original knowledge from this study is a proof of concept for targeting Sting as a future promising treatment in autoimmune diseases.
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Pilitkul, Trairak, Prapaporn Pisitkun, and Asada Leelahavanichkul. Systems-investigation of aberrant signaling in immune cells of SLE mouse model. Faculty of Medicine, Chulalongkorn University, 2015. https://doi.org/10.58837/chula.res.2015.22.

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Autoimmune diseases occur when the immune cells react against self-antigens and subsequently lead to inflammation in the tissues. The interactions between genetics and environmental triggers regulate the phenotypes and outcome of the diseases. Type I interferon has been shown as one of the most crucial cytokines involving in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic systemic autoimmune disease which can result in autoantibody production and fatal glomerulonephritis. Activation via nucleic acid sensors can induce the production of type I interferon from dendritic cells and promote SLE severity. Stimulator of interferon genes (Sting) is a cytoplasmic DNA sensor that signals downstream to enhance type I interferon production after its activation. Recently, it was shown that a gain mutation in the STING gene resulting in over-activity of the IFN pathway can cause familial inflammatory syndrome with lupus-like manifestations in humans. However, the functional studies of Sting in different autoimmune mouse models suggest the conflicting roles of Sting in the pathogenesis ofautoimmune diseases. In order to determine if Sting participates in lupus pathogenesis, the Fcgr2b-deficienct mice (lupus mouse model) were bred with Sting-deficient mice to create the double-deficient mice. In the absence of Sting, the Fcgr2b-deficient mice do not develop fatal glomerulonephritis and autoantibodies. The original knowledge from this study is a proof of concept for targeting Sting as a future promising treatment in autoimmune diseases.
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Lin, Hongwei, Yanjun Gao, Kang Sun, and Faguang Jin. Association between PM2.5 pollution and outpatient visits for respiratory diseases in China: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0144.

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Review question / Objective: Previous epidemiological studies on the association between PM2.5 pollution and outpatient visits for respiratory diseases in China were mostly limited to one region， and the different papers have no coherent results. Our objective is to perform a systematic review and meta-analysis of the relevant literature in order to summarize the association between PM2.5 pollution and outpatient visits for respiratory diseases in multiple cities in China. Condition being studied: As an important component of air pollutants, particulate matter 2.5 (PM2.5) can float in the atmosphere for a long time with a small aerodynamic size (≤2.5μm) and large specific surface area which is attached to a variety of toxic and harmful substances . PM2.5 can deposite under the trachea of the respiratory tract, reaching deep into the alveolar area, damaging alveolar macrophages and type Ⅱ alveolar epithelial cells, inducing alveolar inflammation, resulting in decreased immunity of the respiratory tract and interfering with normal physiological functions of the lungs.
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Chen, Ziying, Zefei Jiang, Ziyun Guo, Mengchao Wang, Zhen Wang, and Liwei Chen. Comparative efficacy of different types of acupuncture for cancer-related fatigue: a protocol for systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.7.0012.

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Review question / Objective: To evaluate the efficacy and safety of all current acupuncture therapies for the treatment of CRF through network meta-analysis. Condition being studied: Cancer-related fatigue (CRF) has been defined as a distressing, persistent, subjective sense of physical, emotional, and/or cognitive tiredness or exhaustion related to cancer and/or cancer treatment that is not proportional to recent activity and interferes with usual functioning, as one of the most common symptoms in cancer and related therapies, presents a huge challenge to the quality of life for cancer patients. Unlike general fatigue that can be relieved with rest, CRF is more debilitating, more persistent, and manifests itself in various ways, both physically and mentally. The estimated prevalence of CRF varies widely by various fatigue evaluation indicators, types of cancer, and cancer treatments, ranging from 14.03% to 100%, however, the latest systematic review show that it can have a pooled prevalence of up to 52%, this deserves our attention. But there has been no gold standard treatment for CRF.
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Delineau, Valeska, Ligia Passos, Ana Rita Ferreira, and Lia Fernandes. The role of behavioral and psychological symptoms of dementia (BPSD) in patient’s autonomy. A scoping review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0008.

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Review question / Objective: This scoping review study aims to identify, summarize, and appraise available literature regarding the role of (BPSD)/neuropsychiatric symptoms in patients’ autonomy with all types of dementia diagnoses. To accomplish this objective, this scoping review will address the following question: What is the role of behavioral and psychological symptoms of dementia in the patient’s autonomy? This review will comprise the terms capacity, functional abilities, and competence in the autonomy concept. Background: Dementia is a neurodegenerative syndrome characterized by the development of multiple cognitive deficits and behavioral changes that interferes with multiple aspects of life, including cognition, daily functioning, and behavioral. With the progress of the disease, the patients lose their capacity, functional abilities, competence, and autonomy (Barbas &amp; Wilde, 2001; Darby &amp; Dickerson, 2017; Irastorza, Corujo, &amp; Bañuelos, 2011; Lee, Jang, &amp; Chang, 2019; Marson, 2013).
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Lekhanya, Portia Keabetswe, and Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.
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Davidson, Irit, Hsing-Jien Kung, and Richard L. Witter. Molecular Interactions between Herpes and Retroviruses in Dually Infected Chickens and Turkeys. United States Department of Agriculture, 2002. http://dx.doi.org/10.32747/2002.7575275.bard.

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Tumors in commercial poultry are caused mainly by infection with avian herpes and retroviruses, the herpesvirus Marek's disease virus (MDV) and the retroviruses, reticuloendotheliosis (REV), lymphoid leukosis, subgroups A-I and J (ALV and ALV-J) in chickens, or Iymphoprolipherative disease (LPDV) in turkeys. Infection with one virus aggravates the clinical outcome of birds that are already infected by another oncogenic virus. As these viruses do not interfere for infection, MDV and one or more retroviruses can infect the same flock, the same bird and the same cell. While infecting the same cell, herpes and retroviruses might interact in at least three ways: a) Integration of retrovirus genomes, or genomic fragments (mainly the LTR) into MDV;b) alteration of LTR-driven expression of retroviral genes by MDV immediate- early genes, and c) by herpesvirus induced cellular transcriptional factors. The first type of molecular interaction have been demonstrated to happen efficiently in vitro by Dr. Kung, in cases multiple infection of cell cultures with MDV and REV or MDV and ALV. Moreover, Dr. Witter showed that an in vitro-created recombinant, RM1, had altered in vitro replication and in vivo biological properties. A more comprehensive characterization of RM1 was carried out in the present project. We sought to highlight whether events of such integrations occur also in the bird, in vivo. For that, we had first to determine the prevalence of dually-infected individual birds in commercial flocks, as no systematic survey has been yet reported. Surprisingly, about 25% of the commercial flocks infected with avian oncogenic viruses had a multiple virus infection and 5% of the total samples ana lysed had multiple virus sequences. Then, we aimed to evaluate and characterize biologically and molecularly the resulting recombinants, if formed, and to analyse the factors that affect these events (virus strains, type and age of birds and time interval between the infection with both viruses). The perception of retrovirus insertions into herpesviruses in vivo is not banal, as the in vivo and in vitro systems differ in the viral-target cells, lymphocytes or fibroblasts, in the MDV-replicative type, transforming or productive, and the immune system presence. We realized that previous methods employed to study in vitro created recombinant viruses were not adequate for the study of samples taken directly from the bird. Therefore, the Hot Spot-combined PCR was developed based on the molecularly known RM1 virus. Also, the PFGE that was used for tissue cultured-MDV separation was inefficient for separating MDV from organs, but useful with feather tips as a source of bird original MDV. Much attention was dedicated now to feathers, because if a recombinant virus would be formed in vivo, its biological significance would be evident by horizontal dissemination through the feathers. Major findings were: a) not only in vitro, but also in vivo MDV and retrovirus co-infections lead to LTR integrations into MDV. That was shown by the detection of chimeric molecules. These appeared in low quantities and as quasispecies, thus interfering with sequence analysis of cloned gel-purified chimeric molecules. Mainly inserts were located in the repeat long MDV fragments. In field birds chimeric molecules were detected at a lower frequency (2.5%) than in experimentally infected birds (30-50%). These could be transmitted experimentally to another birds by inoculation with chimeric molecules containing blood. Several types of chimeric molecules were formed, and same types were detected in birds infected by a second round. To reproduce viral integrations, in vivo infection trials were done with field inoculate that contained both viruses, but the chimeric molecule yield was undetectable.
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Whitham, Steven A., Amit Gal-On, and Tzahi Arazi. Functional analysis of virus and host components that mediate potyvirus-induced diseases. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7591732.bard.

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The mechanisms underlying the development of symptoms in response to virus infection remain to be discovered in plants. Insight into symptoms induced by potyviruses comes from evidence implicating the potyviral HC-Pro protein in symptom development. In particular, recent studies link the development of symptoms in infected plants to HC-Pro's ability to interfere with small RNA metabolism and function in plant hosts. Moreover, mutation of the highly conserved FRNK amino acid motif to FINK in the HC-Pro of Zucchini yellow mosaic virus (ZYMV) converts a severe strain into an asymptomatic strain, but does not affect virus accumulation in cucurbit hosts. The ability of this FINK mutation to uncouple symptoms from virus accumulation creates a unique opportunity to study symptom etiology, which is usually confounded by simultaneous attenuation of both symptoms and virus accumulation. Our goal was to determine how mutations in the conserved FRNK motif affect host responses to potyvirus infection in cucurbits and Arabidopsis thaliana. Our first objective was to define those amino acids in the FRNK motif that are required for symptoms by mutating the FRNK motif in ZYMV and Turnip mosaic virus (TuMV). Symptom expression and accumulation of resulting mutant viruses in cucurbits and Arabidopsis was determined. Our second objective was to identify plant genes associated with virus disease symptoms by profiling gene expression in cucurbits and Arabidopsis in response to mutant and wild type ZYMV and TuMV, respectively. Genes from the two host species that are differentially expressed led us to focus on a subset of genes that are expected to be involved in symptom expression. Our third objective was to determine the functions of small RNA species in response to mutant and wild type HC-Pro protein expression by monitoring the accumulation of small RNAs and their targets in Arabidopsis and cucurbit plants infected with wild type and mutant TuMV and ZYMV, respectively. We have found that the maintenance of the charge of the amino acids in the FRNK motif of HC-Pro is required for symptom expression. Reduced charge (FRNA, FRNL) lessen virus symptoms, and maintain the suppression of RNA silencing. The FRNK motif is involved in binding of small RNA species including microRNAs (miRNA) and short interfering RNAs (siRNA). This binding activity mediated by the FRNK motif has a role in protecting the viral genome from degradation by the host RNA silencing system. However, it also provides a mechanism by which the FRNK motif participates in inducing the symptoms of viral infection. Small RNA species, such as miRNA and siRNA, can regulate the functions of plant genes that affect plant growth and development. Thus, this binding activity suggests a mechanism by which ZYMVHC-Pro can interfere with plant development resulting in disease symptoms. Because the host genes regulated by small RNAs are known, we have identified candidate host genes that are expected to play a role in symptoms when their regulation is disrupted during viral infections. As a result of this work, we have a better understanding of the FRNK amino acid motif of HC-Pro and its contribution to the functions of HC-Pro, and we have identified plant genes that potentially contribute to symptoms of virus infected plants when their expression becomes misregulated during potyviral infections. The results set the stage to establish the roles of specific host genes in viral pathogenicity. The potential benefits include the development of novel strategies for controlling diseases caused by viruses, methods to ensure stable expression of transgenes in genetically improved crops, and improved potyvirus vectors for expression of proteins or peptides in plants.
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