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Microorganisms
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Enterovirus and Type 1 Diabetes
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Enterovirus and Type 1 Diabetes

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 44881

Special Issue Editor

Prof. Dr. Didier Hober

E-Mail Website
Guest Editor
University of Lille and CHU Lille, 59000 Lille, France
Interests: viral pathogenesis; enterovirus; coxsackieviruses B; persistence; virus inactivation; virus detection; antiviral drugs; type 1 diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fifty years ago, Taylor et al. reported the presence of neutralizing anti-coxsackievirus B4 antibodies in serum of patients with type 1 diabetes (T1D). Since this pioneering work in the field of enteroviruses and T1D, epidemiological studies have been carried out to display an association between enterovirus infections and the disease. The presence of markers of enteroviral infection (infectious particles, viral RNA and protein and antibodies) has been investigated in various biological samples of patients: blood, saliva, stools, gut, pancreas necropsies, and, more recently, pancreas biopsies. Moreover, the hypothesis of the role of enteroviruses, especially coxsackieviruses B (CV-B), in the pathogenesis of T1D has been a driving force to improve the knowledge about the cellular and molecular mechanisms of enterovirus infection and about the impact of enteroviruses on cells that are possibly involved in the development of the disease. Since the disease is a result of the disturbance of pancreas islet beta cells, the interaction between enteroviruses and these insulin-producing cells and other pancreas cells has been studied. Thus, the persistence of these viruses in cells has been observed. In addition, a possible disturbing effect of CV-B on the central tolerance, through the impact of viruses on the thymus, has been investigated. It has been reported that antibodies enhance the infection of immune cells with CV-B, which results in an activation of interferon alpha that can induce autoimmunity. The identification of enteroviruses as agents possibly involved in the development of T1D has driven forward research to fight these viruses through various strategies based on antiviral molecules and vaccines. The enteroviral pathogenesis of T1D can be conceived in a form of the result of a complex interplay between enteroviruses and the host. This topic, “Enterovirus and Type 1 Diabetes”, deserves a Special Issue in Microorganisms.

Prof. Didier Hober
Guest Editor

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Keywords

  • enterovirus
  • coxsackieviruses B
  • type 1 diabetes (T1D)

Published Papers (14 papers)

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21 pages, 2595 KiB  
Article
Modulation of IGF2 Expression in the Murine Thymus and Thymic Epithelial Cells Following Coxsackievirus-B4 Infection
by Hélène Michaux, Aymen Halouani, Charlotte Trussart, Chantal Renard, Hela Jaïdane, Henri Martens, Vincent Geenen and Didier Hober
Microorganisms 2021, 9(2), 402; https://doi.org/10.3390/microorganisms9020402 - 15 Feb 2021
Cited by 3 | Viewed by 1967
Abstract
Coxsackievirus B4 (CV-B4) can infect human and murine thymic epithelial cells (TECs). In a murine TEC cell line, CV-B4 can downregulate the transcription of the insulin-like growth factor 2 (Igf2) gene coding for the self-peptide of the insulin family. In this [...] Read more.
Coxsackievirus B4 (CV-B4) can infect human and murine thymic epithelial cells (TECs). In a murine TEC cell line, CV-B4 can downregulate the transcription of the insulin-like growth factor 2 (Igf2) gene coding for the self-peptide of the insulin family. In this study, we show that CV-B4 infections of a murine TEC cell line decreased Igf2 P3 promoter activity by targeting a region near the transcription start site; however, the stability of Igf2 transcripts remained unchanged, indicating a regulation of Igf2 transcription. Furthermore, CV-B4 infections decreased STAT3 phosphorylation in vitro. We also showed that mice infected with CV-B4 had an altered expression of Igf2 isoforms as detected in TECs, followed by a decrease in the pro-IGF2 precursor in the thymus. Our study sheds new light on the intrathymic regulation of Igf2 transcription during CV-B4 infections and supports the hypothesis that a viral infection can disrupt central self-tolerance to insulin by decreasing Igf2 transcription in the thymic epithelium. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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13 pages, 1730 KiB  
Article
Extracellular Vesicles Released by Enterovirus-Infected EndoC-βH1 Cells Mediate Non-Lytic Viral Spread
by Eitan Netanyah, Matteo Calafatti, Jeanette Arvastsson, Eduardo Cabrera-Rode, Corrado M. Cilio and Luis Sarmiento
Microorganisms 2020, 8(11), 1753; https://doi.org/10.3390/microorganisms8111753 - 8 Nov 2020
Cited by 13 | Viewed by 2974
Abstract
While human enteroviruses are generally regarded as a lytic virus, and persistent non-cytolytic enterovirus infection in pancreatic beta cells has been suspected of playing a role in type 1 diabetes pathogenesis. However, it is still unclear how enteroviruses could exit the pancreatic beta [...] Read more.
While human enteroviruses are generally regarded as a lytic virus, and persistent non-cytolytic enterovirus infection in pancreatic beta cells has been suspected of playing a role in type 1 diabetes pathogenesis. However, it is still unclear how enteroviruses could exit the pancreatic beta cell in a non-lytic manner. This study aimed to investigate the role of beta cell-derived extracellular vesicles (EVs) in the non-lytic enteroviral spread and infection. Size-exclusion chromatography and antibody-based immunoaffinity purification were used to isolate EVs from echovirus 16-infected human beta EndoC-βH1 cells. EVs were then characterized using transmission electron microscopy and Multiplex Bead-Based Flow Cytometry Assay. Virus production and release were quantified by 50% cell culture infectious dose (CCID50) assay and qRT-PCR. Our results showed that EVs from echovirus 16-infected EndoC-βH1 cells harbor infectious viruses and promote their spread during the pre-lytic phase of infection. Furthermore, the EVs-mediated infection was not inhibited by virus-specific neutralizing antibodies. In summary, this study demonstrated that enteroviruses could exit beta cells non-lytically within infectious EVs, thereby thwarting the access of neutralizing antibodies to viral particles. These data suggest that enterovirus transmission through EVs may contribute to viral dissemination and immune evasion in persistently infected beta cells. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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16 pages, 2637 KiB  
Article
Coxsackievirus-B4 Infection Can Induce the Expression of Human Endogenous Retrovirus W in Primary Cells
by Arthur Dechaumes, Antoine Bertin, Famara Sane, Sandrine Levet, Jennifer Varghese, Benjamin Charvet, Valéry Gmyr, Julie Kerr-Conte, Justine Pierquin, Govindakarnavar Arunkumar, François Pattou, Hervé Perron and Didier Hober
Microorganisms 2020, 8(9), 1335; https://doi.org/10.3390/microorganisms8091335 - 1 Sep 2020
Cited by 13 | Viewed by 2540
Abstract
Human Endogenous Retrovirus W Envelope (HERV-W ENV) mRNA or protein can be found in peripheral blood mononuclear cells (PBMCs) and exocrine pancreas of patients with type 1 diabetes (T1D). Further, previous observations have shown an association between enteroviral infection and development of T1D; [...] Read more.
Human Endogenous Retrovirus W Envelope (HERV-W ENV) mRNA or protein can be found in peripheral blood mononuclear cells (PBMCs) and exocrine pancreas of patients with type 1 diabetes (T1D). Further, previous observations have shown an association between enteroviral infection and development of T1D; specifically, coxsackievirus-B (CV-B) has been detected in the blood and pancreas of patients with T1D. Notably, viruses can activate HERV-W expression. Hence, we evaluated the effect of CV-B4 infection on HERV-W ENV mRNA expression. Primary human pancreatic ductal cells were obtained from five brain-dead donors. In the pancreatic cells of three donors, the HERV-W ENV mRNA level measured using RT-qPCR was upregulated upon CV-B4 infection. The HERV-W ENV protein was detected in the infected cells using the immunoblot assay. In human PBMCs inoculated with CV-B4 or when CV-B4 was incubated with an enhancing serum, the HERV-W ENV mRNA level was higher than the background RNA level. In monocyte-derived macrophages obtained from 5 of 13 donors, the HERV-W ENV mRNA level was higher in cultures inoculated with CV-B4 than in the control. Therefore, CV-B4 can upregulate or induce the transcription of a certain HERV-W ENV copy (or copies) in primary cell cultures, such as monocytes, macrophages, and pancreatic cells. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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16 pages, 1659 KiB  
Article
Immune Transcriptome of Cells Infected with Enterovirus Strains Obtained from Cases of Type 1 Diabetes
by Anello Marcello Poma, Angelo Genoni, Francesco Broccolo, Maria Denaro, Alberto Pugliese, Fulvio Basolo and Antonio Toniolo
Microorganisms 2020, 8(7), 1031; https://doi.org/10.3390/microorganisms8071031 - 12 Jul 2020
Cited by 12 | Viewed by 2993
Abstract
Enterovirus (EV) infection of insulin-producing pancreatic beta cells is associated with type 1 diabetes (T1D), but little is known about the mechanisms that lead the virus to cause a persistent infection and, possibly, to induce beta cell autoimmunity. A cell line susceptible to [...] Read more.
Enterovirus (EV) infection of insulin-producing pancreatic beta cells is associated with type 1 diabetes (T1D), but little is known about the mechanisms that lead the virus to cause a persistent infection and, possibly, to induce beta cell autoimmunity. A cell line susceptible to most enterovirus types was infected with EV isolates from cases of T1D and, for comparison, with a replication-competent strain of coxsackievirus B3. The transcription of immune-related genes and secretion of cytokines was evaluated in infected vs. uninfected cells. Acutely infected cells showed the preserved transcription of type I interferon (IFN) pathways and the enhanced transcription/secretion of IL6, IL8, LIF, MCP1, and TGFB1. On the other hand, infection by defective EV strains obtained from diabetic subjects suppressed IFN pathways and the transcription of most cytokines, while enhancing the expression of IL8, IL18, IL32, and MCP1. IL18 and IL32 are known for their pathogenic role in autoimmune diabetes. Thus, the cytokine profile of AV3 cells infected by diabetes-derived EV strains closely matches that observed in patients at the early stages of T1D. The concordance of our results with clinically verified information reinforces the hypothesis that the immune changes observed in type 1 diabetic patients are due to a hardly noticeable virus infection. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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16 pages, 6676 KiB  
Article
Multiplexed High-Throughput Serological Assay for Human Enteroviruses
by Niila V. V. Saarinen, Jussi Lehtonen, Riitta Veijola, Johanna Lempainen, Mikael Knip, Heikki Hyöty, Olli H. Laitinen and Vesa P. Hytönen
Microorganisms 2020, 8(6), 963; https://doi.org/10.3390/microorganisms8060963 - 26 Jun 2020
Cited by 5 | Viewed by 3829 | Correction
Abstract
Immunological assays detecting antibodies against enteroviruses typically use a single enterovirus serotype as antigen. This limits the ability of such assays to detect antibodies against different enterovirus types and to detect possible type-specific variation in antibody responses. We set out to develop a [...] Read more.
Immunological assays detecting antibodies against enteroviruses typically use a single enterovirus serotype as antigen. This limits the ability of such assays to detect antibodies against different enterovirus types and to detect possible type-specific variation in antibody responses. We set out to develop a multiplexed assay for simultaneous detection of antibodies against multiple enterovirus and rhinovirus types encompassing all human infecting species. Seven recombinant VP1 proteins from enteroviruses EV-A to EV-D and rhinoviruses RV-A to RV-C species were produced. Using Meso Scale Diagnostics U-PLEX platform we were able to study antibody reactions against these proteins as well as non-structural enterovirus proteins in a single well with 140 human serum samples. Adults had on average 33-fold stronger antibody responses to these antigens (p < 10−11) compared to children, but children had less cross-reactivity between different enterovirus types. The results suggest that this new high-throughput assay offers clear benefits in the evaluation of humoral enterovirus immunity in children, giving more exact information than assays that are based on a single enterovirus type as antigen. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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14 pages, 3987 KiB  
Article
Proteomic and Transcriptional Profiles of Human Stem Cell-Derived β Cells Following Enteroviral Challenge
by Julius O. Nyalwidhe, Agata Jurczyk, Basanthi Satish, Sambra Redick, Natasha Qaisar, Melanie I. Trombly, Pranitha Vangala, Riccardo Racicot, Rita Bortell, David M. Harlan, Dale L. Greiner, Michael A. Brehm, Jerry L. Nadler and Jennifer P. Wang
Microorganisms 2020, 8(2), 295; https://doi.org/10.3390/microorganisms8020295 - 20 Feb 2020
Cited by 6 | Viewed by 3488
Abstract
Enteroviral infections are implicated in islet autoimmunity and type 1 diabetes (T1D) pathogenesis. Significant β-cell stress and damage occur with viral infection, leading to cells that are dysfunctional and vulnerable to destruction. Human stem cell-derived β (SC-β) cells are insulin-producing cell clusters that [...] Read more.
Enteroviral infections are implicated in islet autoimmunity and type 1 diabetes (T1D) pathogenesis. Significant β-cell stress and damage occur with viral infection, leading to cells that are dysfunctional and vulnerable to destruction. Human stem cell-derived β (SC-β) cells are insulin-producing cell clusters that closely resemble native β cells. To better understand the events precipitated by enteroviral infection of β cells, we investigated transcriptional and proteomic changes in SC-β cells challenged with coxsackie B virus (CVB). We confirmed infection by demonstrating that viral protein colocalized with insulin-positive SC-β cells by immunostaining. Transcriptome analysis showed a decrease in insulin gene expression following infection, and combined transcriptional and proteomic analysis revealed activation of innate immune pathways, including type I interferon (IFN), IFN-stimulated genes, nuclear factor-kappa B (NF-κB) and downstream inflammatory cytokines, and major histocompatibility complex (MHC) class I. Finally, insulin release by CVB4-infected SC-β cells was impaired. These transcriptional, proteomic, and functional findings are in agreement with responses in primary human islets infected with CVB ex vivo. Human SC-β cells may serve as a surrogate for primary human islets in virus-induced diabetes models. Because human SC-β cells are more genetically tractable and accessible than primary islets, they may provide a preferred platform for investigating T1D pathogenesis and developing new treatments. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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Review

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14 pages, 1194 KiB  
Review
Enteroviruses and Type 1 Diabetes Mellitus: An Overlooked Relationship in Some Regions
by Abdulaziz Alhazmi, Famara Sane, Mouna Lazrek, Magloire Pandoua Nekoua, Francis Badia-Boungou, Ilka Engelmann, Enagnon Kazali Alidjinou and Didier Hober
Microorganisms 2020, 8(10), 1458; https://doi.org/10.3390/microorganisms8101458 - 23 Sep 2020
Cited by 14 | Viewed by 3089
Abstract
Enteroviruses (EVs) infect millions of people annually. EV infections can be asymptomatic or symptomatic with conditions ranging from mild illnesses to serious diseases such as dilated cardiomyopathy. A causal relationship between EV infections and type 1 diabetes mellitus (T1DM) has been heavily debated, [...] Read more.
Enteroviruses (EVs) infect millions of people annually. EV infections can be asymptomatic or symptomatic with conditions ranging from mild illnesses to serious diseases such as dilated cardiomyopathy. A causal relationship between EV infections and type 1 diabetes mellitus (T1DM) has been heavily debated, with some studies suggesting that this relationship is not yet conclusive and requires additional evidence, whereas others strongly argue for this correlation. While this relationship is well investigated in some developed countries like the USA and Finland, it is understudied or neglected in other countries like Russia for many reasons such as the low incidence of T1DM. Although the Middle East and North Africa (MENA) are highly affected by T1DM, the role of EVs in the disease in MENA has not been investigated extensively. Therefore, we aimed to address the relationship between T1DM and EVs in MENA and other regions globally. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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18 pages, 718 KiB  
Review
Type 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infection
by Pouria Akhbari, Sarah J Richardson and Noel G Morgan
Microorganisms 2020, 8(9), 1419; https://doi.org/10.3390/microorganisms8091419 - 15 Sep 2020
Cited by 17 | Viewed by 4052
Abstract
Enteroviruses (EVs) have long been implicated in the pathogenesis of type 1 diabetes (T1D), and accumulating evidence has associated virus-induced autoimmunity with the loss of pancreatic beta cells in T1D. Inflammatory cytokines including interferons (IFN) form a primary line of defence against viral [...] Read more.
Enteroviruses (EVs) have long been implicated in the pathogenesis of type 1 diabetes (T1D), and accumulating evidence has associated virus-induced autoimmunity with the loss of pancreatic beta cells in T1D. Inflammatory cytokines including interferons (IFN) form a primary line of defence against viral infections, and their chronic elevation is a hallmark feature of many autoimmune diseases. IFNs play a key role in activating and regulating innate and adaptive immune responses, and to do so they modulate the expression of networks of genes and transcription factors known generically as IFN stimulated genes (ISGs). ISGs in turn modulate critical cellular processes ranging from cellular metabolism and growth regulation to endoplasmic reticulum (ER) stress and apoptosis. More recent studies have revealed that IFNs also modulate gene expression at an epigenetic as well as post-transcriptional and post-translational levels. As such, IFNs form a key link connecting the various genetic, environmental and immunological factors involved in the initiation and progression of T1D. Therefore, gaining an improved understanding of the mechanisms by which IFNs modulate beta cell function and survival is crucial in explaining the pathogenesis of virally-induced T1D. This should provide the means to prevent, decelerate or even reverse beta cell impairment. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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8 pages, 207 KiB  
Review
Extending the Enterovirus Lead: Could a Related Picornavirus be Responsible for Diabetes in Humans?
by William Klitz and Bo Niklasson
Microorganisms 2020, 8(9), 1382; https://doi.org/10.3390/microorganisms8091382 - 10 Sep 2020
Cited by 3 | Viewed by 1783
Abstract
We found an association between the abundance of rodents in the wild and onset of type 1 diabetes (T1D) in humans. A picornavirus named Ljungan virus (LV) was subsequently isolated from wild bank voles. Both picornavirus-like particles detected by electron microscopy and LV [...] Read more.
We found an association between the abundance of rodents in the wild and onset of type 1 diabetes (T1D) in humans. A picornavirus named Ljungan virus (LV) was subsequently isolated from wild bank voles. Both picornavirus-like particles detected by electron microscopy and LV antigen visualized by immunohistochemistry was seen in islets of Langerhans in diabetic wild bank voles. LV antigen has also been found in islets of Langerhans in a patient with recent onset of T1D and in the commonly used Bio Breeding (BB) T1D rat model. We discuss the possibility of T1D and type 2 diabetes (T2D) as parts of a single disease entity. Antiviral compounds directed against picornavirus have been found to be an effective treatment of diabetes in BB rats. We propose using the same currently available antiviral compounds in clinical trials in humans. Antiviral treatment would have the potential to be both proof of concept for involvement of a picornavirus in diabetes pathogenesis and also present a first-generation therapy. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
20 pages, 971 KiB  
Review
Genetic Susceptibility of the Host in Virus-Induced Diabetes
by Keiichiro Mine, Yasunobu Yoshikai, Hirokazu Takahashi, Hitoe Mori, Keizo Anzai and Seiho Nagafuchi
Microorganisms 2020, 8(8), 1133; https://doi.org/10.3390/microorganisms8081133 - 27 Jul 2020
Cited by 14 | Viewed by 3260
Abstract
Enteroviruses, especially Coxsackie B viruses, are among the candidate environmental factors causative of type 1 diabetes. Host genetic factors have an impact on the development of virus-induced diabetes (VID). Host background, in terms of whether the host is prone to autoimmunity, should also [...] Read more.
Enteroviruses, especially Coxsackie B viruses, are among the candidate environmental factors causative of type 1 diabetes. Host genetic factors have an impact on the development of virus-induced diabetes (VID). Host background, in terms of whether the host is prone to autoimmunity, should also be considered when analyzing the role of target genes in VID. In this review, we describe the genetic susceptibility of the host based on studies in humans and VID animal models. Understanding the host genetic factors should contribute not only to revealing the mechanisms of VID development, but also in taking measures to prevent VID. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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20 pages, 3536 KiB  
Review
Enteroviruses and T1D: Is It the Virus, the Genes or Both which Cause T1D
by Shirin Geravandi, Huan Liu and Kathrin Maedler
Microorganisms 2020, 8(7), 1017; https://doi.org/10.3390/microorganisms8071017 - 8 Jul 2020
Cited by 24 | Viewed by 4982
Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disorder that results from the selective destruction of insulin-producing β-cells in the pancreas. Up to now, the mechanisms triggering the initiation and progression of the disease are, in their complexity, not fully understood and imply [...] Read more.
Type 1 diabetes (T1D) is a chronic autoimmune disorder that results from the selective destruction of insulin-producing β-cells in the pancreas. Up to now, the mechanisms triggering the initiation and progression of the disease are, in their complexity, not fully understood and imply the disruption of several tolerance networks. Viral infection is one of the environmental factors triggering diabetes, which is initially based on the observation that the disease’s incidence follows a periodic pattern within the population. Moreover, the strong correlation of genetic susceptibility is a prerequisite for enteroviral infection associated islet autoimmunity. Epidemiological data and clinical findings indicate enteroviral infections, mainly of the coxsackie B virus family, as potential pathogenic mechanisms to trigger the autoimmune reaction towards β-cells, resulting in the boost of inflammation following β-cell destruction and the onset of T1D. This review discusses previously identified virus-associated genetics and pathways of β-cell destruction. Is it the virus itself which leads to β-cell destruction and T1D progression? Or is it genetic, so that the virus may activate auto-immunity and β-cell destruction only in genetically predisposed individuals? Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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23 pages, 1083 KiB  
Review
Innate Viral Sensor MDA5 and Coxsackievirus Interplay in Type 1 Diabetes Development
by Samuel I. Blum and Hubert M. Tse
Microorganisms 2020, 8(7), 993; https://doi.org/10.3390/microorganisms8070993 - 3 Jul 2020
Cited by 24 | Viewed by 3937
Abstract
Type 1 diabetes (T1D) is a polygenic autoimmune disease characterized by immune-mediated destruction of insulin-producing β-cells. The concordance rate for T1D in monozygotic twins is ≈30–50%, indicating that environmental factors also play a role in T1D development. Previous studies have demonstrated that enterovirus [...] Read more.
Type 1 diabetes (T1D) is a polygenic autoimmune disease characterized by immune-mediated destruction of insulin-producing β-cells. The concordance rate for T1D in monozygotic twins is ≈30–50%, indicating that environmental factors also play a role in T1D development. Previous studies have demonstrated that enterovirus infections such as coxsackievirus type B (CVB) are associated with triggering T1D. Prior to autoantibody development in T1D, viral RNA and antibodies against CVB can be detected within the blood, stool, and pancreata. An innate pathogen recognition receptor, melanoma differentiation-associated protein 5 (MDA5), which is encoded by the IFIH1 gene, has been associated with T1D onset. It is unclear how single nucleotide polymorphisms in IFIH1 alter the structure and function of MDA5 that may lead to exacerbated antiviral responses contributing to increased T1D-susceptibility. Binding of viral dsRNA via MDA5 induces synthesis of antiviral proteins such as interferon-alpha and -beta (IFN-α/β). Viral infection and subsequent IFN-α/β synthesis can lead to ER stress within insulin-producing β-cells causing neo-epitope generation, activation of β-cell-specific autoreactive T cells, and β-cell destruction. Therefore, an interplay between genetics, enteroviral infections, and antiviral responses may be critical for T1D development. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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17 pages, 1617 KiB  
Review
Enteroviral Pathogenesis of Type 1 Diabetes: The Role of Natural Killer Cells
by Magloire Pandoua Nekoua, Arthur Dechaumes, Famara Sane, Enagnon Kazali Alidjinou, Kabirou Moutairou, Akadiri Yessoufou and Didier Hober
Microorganisms 2020, 8(7), 989; https://doi.org/10.3390/microorganisms8070989 - 1 Jul 2020
Cited by 15 | Viewed by 3384
Abstract
Enteroviruses, especially group B coxsackieviruses (CV-B), have been associated with the development of chronic diseases such as type 1 diabetes (T1D). The pathological mechanisms that trigger virus-induced autoimmunity against islet antigens in T1D are not fully elucidated. Animal and human studies suggest that [...] Read more.
Enteroviruses, especially group B coxsackieviruses (CV-B), have been associated with the development of chronic diseases such as type 1 diabetes (T1D). The pathological mechanisms that trigger virus-induced autoimmunity against islet antigens in T1D are not fully elucidated. Animal and human studies suggest that NK cells response to CV-B infection play a crucial role in the enteroviral pathogenesis of T1D. Indeed, CV-B-infected cells can escape from cytotoxic T cells recognition and destruction by inhibition of cell surface expression of HLA class I antigen through non-structural viral proteins, but they can nevertheless be killed by NK cells. Cytolytic activity of NK cells towards pancreatic beta cells persistently-infected with CV-B has been reported and defective viral clearance by NK cells of patients with T1D has been suggested as a mechanism leading to persistence of CV-B and triggering autoimmunity reported in these patients. The knowledge about host antiviral defense against CV-B infection is not only crucial to understand the susceptibility to virus-induced T1D but could also contribute to the design of new preventive or therapeutic approaches for individuals at risk for T1D or newly diagnosed patients. Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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Other

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4 pages, 162 KiB  
Correction
Correction: Saarinen, N.V.V., et al. Multiplexed High-Throughput Serological Assay for Human Enteroviruses. Microorganismis 2020, 8, 963
by Niila V. V. Saarinen, Jussi Lehtonen, Riitta Veijola, Johanna Lempainen, Mikael Knip, Heikki Hyöty, Olli H. Laitinen and Vesa P. Hytönen
Microorganisms 2020, 8(9), 1426; https://doi.org/10.3390/microorganisms8091426 - 17 Sep 2020
Cited by 1 | Viewed by 1638
Abstract
The authors wish to make the following corrections to this paper [...] Full article
(This article belongs to the Special Issue Enterovirus and Type 1 Diabetes)
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