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Microorganisms
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Coxsackievirus Infection and Associated Diseases
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Coxsackievirus Infection and Associated Diseases

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

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 17516

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,

In the late 1940s, viruses were isolated from the feces of boys suffering from paralysis who lived in the village of Coxsackie (New York, USA). It was the first step in the discovery of the coxsackieviruses, which were classified into group A and B by the nature of the disease induced in mice: flaccid paralysis by group A viruses and spastic paralysis by those of group B. Since this time, the knowledge of these viruses has progressed. The molecular biology of coxsackieviruses, epidemiological and clinical aspects, host response, virus–host interaction, and immunopathology have been investigated. The sum of knowledge regarding the virulence of these agents, the mechanisms of pathogenesis, and their role in human diseases (acute and chronic) has increased considerably in recent years. The role of coxsackieviruses A (CV-A) in hand, foot, and mouth disease has been a driving force to improve the knowledge about these viruses. The hypothesis of the role of coxsackieviruses B (CV-B) in the pathogenesis of chronic myocarditis and dilated cardiomyopathy and in the pathogenesis of T1D have helped in improving knowledge about the cellular and molecular mechanisms of CV-B infection and about the impact of these viruses on cells that are possibly involved in the development of diseases. The concept of persistence of these viruses was developed. It was observed that antibodies enhance the infection of immune cells with CV-B. Various strategies based on antiviral molecules and vaccines were developed to fight CV-A and CV-B. Thus, this topic, “Coxsackievirus Infection and Associated Diseases” deserves a Special Issue in Microorganisms.

Prof. Didier Hober
Guest Editor

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Keywords

  • coxsackievirus B
  • coxsackievirus A

Published Papers (7 papers)

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Editorial

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2 pages, 182 KiB  
Editorial
Coxsackievirus Infection and Associated Diseases
by Magloire Pandoua Nekoua and Didier Hober
Microorganisms 2022, 10(8), 1566; https://doi.org/10.3390/microorganisms10081566 - 04 Aug 2022
Cited by 1 | Viewed by 1129
Abstract
Coxsackieviruses (CV) are ubiquitous and widespread single-stranded RNA viruses belonging to the Picornaviridae family and the genus Enterovirus, which also includes poliovirus (PV), the best known of the enteroviruses (EV) [...] Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)

Research

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9 pages, 2740 KiB  
Communication
Primary Site of Coxsackievirus B Replication in the Small Intestines: No Proof of Peyer’s Patches Involvement
by Shubhada Bopegamage, Katarina Berakova, Pavol Gomocak, Renata Baksova, Jochem Galama, Heikki Hyoty and Sisko Tauriainen
Microorganisms 2021, 9(12), 2600; https://doi.org/10.3390/microorganisms9122600 - 16 Dec 2021
Cited by 3 | Viewed by 2245
Abstract
Background: Enterovirus (EV) infections are associated with a broad range of diseases. Since the first experimental infection of primates with poliovirus (PV), tonsils and the Peyer’s patches (PPs) have been believed to be the primary replication sites of EVs. Our aim was to [...] Read more.
Background: Enterovirus (EV) infections are associated with a broad range of diseases. Since the first experimental infection of primates with poliovirus (PV), tonsils and the Peyer’s patches (PPs) have been believed to be the primary replication sites of EVs. Our aim was to localize different viral markers in the small intestines (SI) of coxsackievirus B (CVB) orally and intraperitoneally (i.p.) infected mice. Methods: Transverse sections of SIs of both infected and control male outbred mice were collected at different intervals post-infection (p.i) and analyzed for presence of interferon-alpha (IFN-α) and viral protein VP1 by immunohistochemistry and in situ hybridization (ISH). Fluorescent marker, eGFP, was identified in cryosections of mice infected with eGFP-CVB3. Results: In the infected SIs, we observed enlarged germinating centers (GCs) in the PPs; IFN-α was detected in the PPs and mucosal layer of the SIs. However, VP1, viral RNA and the eGFP were absent in the GCs of PPs at all stages of infection irrespective of the virus strains used. Conclusions: Virus was present in the epithelial cells but not in GCs of the PPs of the murine SIs. Our results do not support the hypothesis of EV replication in the PP especially in the GCs. Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
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17 pages, 3621 KiB  
Article
Consequences of Both Coxsackievirus B4 and Type 1 Diabetes on Female Non-Obese Diabetic Mouse Kidneys
by Debra L. Walter, Jean R. Thuma, Ramiro Malgor, Frank L. Schwartz, Kelly D. McCall and Karen T. Coschigano
Microorganisms 2021, 9(11), 2357; https://doi.org/10.3390/microorganisms9112357 - 15 Nov 2021
Cited by 2 | Viewed by 1449
Abstract
Despite the 2019 Executive Order on Advancing American Kidney Health Initiative, kidney disease has moved up in rank from the 9th to the 8th leading cause of death in the United States. A recent push in the field of nephrology has been to [...] Read more.
Despite the 2019 Executive Order on Advancing American Kidney Health Initiative, kidney disease has moved up in rank from the 9th to the 8th leading cause of death in the United States. A recent push in the field of nephrology has been to identify molecular markers and/or molecular profiles involved in kidney disease process or injury that can help identify the cause of injury and predict patient outcomes. While these studies have had moderate success, they have not yet considered that many of the health conditions that cause kidney disease (diabetes, hypertension, etc.) can also be caused by environmental factors (such as viruses), which in and of themselves can cause kidney disease. Thus, the goal of this study was to identify molecular and phenotypic profiles that can differentiate kidney injury caused by diabetes (a health condition resulting in kidney disease) and coxsackievirus B4 (CVB4) exposure (which can cause diabetes and/or kidney disease), both alone and together. Non-obese diabetic (NOD) mice were used for this study due to their susceptibility to both type 1 diabetes (T1D)- and CVB4-mediated kidney injury, in order to glean a better understanding of how hyperglycemia and viral exposure, when occurring on their own and in combination, may alter the kidneys’ molecular and phenotypic profiles. While no changes in kidney function were observed, molecular biomarkers of kidney injury were significantly up- and downregulated based on T1D and CVB4 exposure, both alone and together, but not in a predictable pattern. By combining individual biomarkers with function and phenotypic measurements (i.e., urinary albumin creatinine ratio, serum creatinine, kidney weight, and body weight), we were able to perform an unbiased separation of injury group based on the type of injury. This study provides evidence that unique kidney injury profiles within a kidney disease health condition are identifiable, and will help us to identify the causes of kidney injury in the future. Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
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17 pages, 4633 KiB  
Article
Mt10-CVB3 Vaccine Virus Protects against CVB4 Infection by Inducing Cross-Reactive, Antigen-Specific Immune Responses
by Ninaad Lasrado, Rajkumar Arumugam, Mahima T. Rasquinha, Meghna Sur, David Steffen and Jay Reddy
Microorganisms 2021, 9(11), 2323; https://doi.org/10.3390/microorganisms9112323 - 10 Nov 2021
Cited by 7 | Viewed by 2358
Abstract
Group B coxsackieviruses (CVB) containing six serotypes, B1–B6, affect various organs, and multiple serotypes can induce similar diseases such as myocarditis and pancreatitis. Yet, no vaccines are currently available to prevent these infections. Translationally, the derivation of vaccines that offer protection against multiple [...] Read more.
Group B coxsackieviruses (CVB) containing six serotypes, B1–B6, affect various organs, and multiple serotypes can induce similar diseases such as myocarditis and pancreatitis. Yet, no vaccines are currently available to prevent these infections. Translationally, the derivation of vaccines that offer protection against multiple serotypes is highly desired. In that direction, we recently reported the generation of an attenuated strain of CVB3, termed Mt10, which completely protects against both myocarditis and pancreatitis induced by the homologous wild-type CVB3 strain. Here, we report that the Mt10 vaccine can induce cross-protection against multiple CVB serotypes as demonstrated with CVB4. We note that the Mt10 vaccine could induce cross-reactive neutralizing antibodies (nABs) against both CVB1 and CVB4. In challenge studies with CVB4, the efficacy of the Mt10 vaccine was found to be 92%, as determined by histological evaluation of the heart and pancreas. Antibody responses induced in Mt10/CVB4 challenged animals indicated the persistence of cross-reactive nABs against CVB1, CVB3, and CVB4. Evaluation of antigen-specific immune responses revealed viral protein 1 (VP1)-reactive antibodies, predominantly IgG2a, IgG2b, IgG3, and IgG1. Similarly, by using major histocompatibility complex class II tetramers, we noted induction of VP1-specific CD4 T cells capable of producing multiple T cell cytokines, with interferon-γ being predominant. Finally, none of the vaccine recipients challenged with CVB4 revealed the presence of viral nucleic acid in the heart or pancreas. Taken together, our data suggest that the Mt10 vaccine can prevent infections caused by multiple CVB serotypes, paving the way for the development of monovalent CVB vaccines to prevent heart and pancreatic diseases of enteroviral origin. Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
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20 pages, 3830 KiB  
Article
Coxsackievirus B4 Transplacental Infection Severely Disturbs Central Tolerogenic Mechanisms in the Fetal Thymus
by Aymen Halouani, Hélène Michaux, Habib Jmii, Charlotte Trussart, Ahlem Chahbi, Henri Martens, Chantal Renard, Mahjoub Aouni, Didier Hober, Vincent Geenen and Hela Jaïdane
Microorganisms 2021, 9(7), 1537; https://doi.org/10.3390/microorganisms9071537 - 19 Jul 2021
Cited by 3 | Viewed by 2581
Abstract
Thymus plays a fundamental role in central tolerance establishment, especially during fetal life, through the generation of self-tolerant T cells. This process consists in T cells education by presenting them tissue-restricted autoantigens promiscuously expressed by thymic epithelial cells (TECs), thus preventing autoimmunity. Thymus [...] Read more.
Thymus plays a fundamental role in central tolerance establishment, especially during fetal life, through the generation of self-tolerant T cells. This process consists in T cells education by presenting them tissue-restricted autoantigens promiscuously expressed by thymic epithelial cells (TECs), thus preventing autoimmunity. Thymus infection by Coxsackievirus B (CV-B) during fetal life is supposed to disturb thymic functions and, hence, to be an inducing or accelerating factor in the genesis of autoimmunity. To further investigate this hypothesis, in our current study, we analyzed thymic expression of autoantigens, at the transcriptional and protein level, following in utero infection by CV-B4. mRNA expression levels of Igf2 and Myo7, major autoantigens of pancreas and heart, respectively, were analyzed in whole thymus and in enriched TECs together along with both transcription factors, Aire and Fezf2, involved in autoantigens expression in the thymus. Results show that in utero infection by CV-B4 induces a significant decrease in Igf2 and Myo7 expression at both mRNA and protein level in whole thymus and in enriched TECs as well. Moreover, a correlation between viral load and autoantigens expression can be observed in the whole thymus, indicating a direct effect of in utero infection by CV-B4 on autoantigens expression. Together, these results indicate that an in utero infection of the thymus by CV-B4 may interfere with self-tolerance establishment in TECs by decreasing autoantigen expression at both mRNA and protein level and thereby increase the risk of autoimmunity onset. Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
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16 pages, 2678 KiB  
Article
Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection?
by Virginia M. Stone, Emma E. Ringqvist, Pär G. Larsson, Erna Domsgen, Ulrika Holmlund, Eva Sverremark-Ekström and Malin Flodström-Tullberg
Microorganisms 2021, 9(1), 105; https://doi.org/10.3390/microorganisms9010105 - 05 Jan 2021
Cited by 7 | Viewed by 2956
Abstract
Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFNλs; IL-28A, IL-28B, IL29, and IFNλ4) in the intestine. However, many viruses have developed strategies to counteract these defense mechanisms by preventing the production of IFNs. Here we use [...] Read more.
Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFNλs; IL-28A, IL-28B, IL29, and IFNλ4) in the intestine. However, many viruses have developed strategies to counteract these defense mechanisms by preventing the production of IFNs. Here we use infection models, a clinical virus isolate, and several molecular biology techniques to demonstrate that both type I and III IFNs induce an antiviral state and attenuate Coxsackievirus group B (CVB) replication in human intestinal epithelial cells (IECs). While treatment of IECs with a viral mimic (poly (I:C)) induced a robust expression of both type I and III IFNs, no such up-regulation was observed after CVB infection. The blunted IFN response was paralleled by a reduction in the abundance of proteins involved in the induction of interferon gene transcription, including TIR-domain-containing adapter-inducing interferon-β (TRIF), mitochondrial antiviral-signaling protein (MAVS), and the global protein translation initiator eukaryotic translation initiation factor 4G (eIF4G). Taken together, this study highlights a potent anti-Coxsackieviral effect of both type I and III IFNs in cells located at the primary site of infection. Furthermore, we show for the first time that the production of type I and III IFNs in IECs is blocked by CVBs. These findings suggest that CVBs evade the host immune response in order to successfully infect the intestine. Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
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Review

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12 pages, 1631 KiB  
Review
Effect of Coxsackievirus B4 Infection on the Thymus: Elucidating Its Role in the Pathogenesis of Type 1 Diabetes
by Abdulaziz Alhazmi, Magloire Pandoua Nekoua, Hélène Michaux, Famara Sane, Aymen Halouani, Ilka Engelmann, Enagnon Kazali Alidjinou, Henri Martens, Hela Jaidane, Vincent Geenen and Didier Hober
Microorganisms 2021, 9(6), 1177; https://doi.org/10.3390/microorganisms9061177 - 29 May 2021
Cited by 11 | Viewed by 3700
Abstract
The thymus gland is a primary lymphoid organ for T-cell development. Various viral infections can result in disturbance of thymic functions. Medullary thymic epithelial cells (mTECs) are important for the negative selection of self-reactive T-cells to ensure central tolerance. Insulin-like growth factor 2 [...] Read more.
The thymus gland is a primary lymphoid organ for T-cell development. Various viral infections can result in disturbance of thymic functions. Medullary thymic epithelial cells (mTECs) are important for the negative selection of self-reactive T-cells to ensure central tolerance. Insulin-like growth factor 2 (IGF2) is the dominant self-peptide of the insulin family expressed in mTECs and plays a crucial role in the intra-thymic programing of central tolerance to insulin-secreting islet β-cells. Coxsackievirus B4 (CVB4) can infect and persist in the thymus of humans and mice, thus hampering the T-cell maturation and differentiation process. The modulation of IGF2 expression and protein synthesis during a CVB4 infection has been observed in vitro and in vivo in mouse models. The effect of CVB4 infections on human and mouse fetal thymus has been studied in vitro. Moreover, following the inoculation of CVB4 in pregnant mice, the thymic function in the fetus and offspring was disturbed. A defect in the intra-thymic expression of self-peptides by mTECs may be triggered by CVB4. The effects of viral infections, especially CVB4 infection, on thymic cells and functions and their possible role in the pathogenesis of type 1 diabetes (T1D) are presented. Full article
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
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