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Regulation of Viral Infection in Diabetes
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Regulation of Viral Infection in Diabetes

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 20593

Special Issue Editor

Prof. Dr. Seiho Nagafuchi

E-Mail Website
Guest Editor
Division of Metabolism and Endocrinology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga 849-8501, Japan
Interests: virus; diabetes; immunity; susceptibility gene; vaccine; ß-cell; insulin; enterovirus; COVID-19

Special Issue Information

Dear Colleagues,

Although there is no “Diabetes Virus”, many viruses have been known to cause diabetes. The recent world-threating COVID-19 pandemic has also been reported to be associated with the induction of diabetes, as well as increased clinical severity in patients with diabetes infected with SARS-CoV-2 virus. The means by which the virus infection causes type 1 diabetes is associated with the high growth rate of the virus in pancreatic β-cells, inflammatory reactions around islets and induction of autoimmunity to β-cells, leading to extensive damage of those cells, resulting in the loss of insulin-secreting activity, and development of type 1 diabetes. The regulatory mechanisms to control virus infection are influenced by the infectivity of the virus to attach the host cells via virus receptors, affecting growth in infected cells and spread of the proliferated virus to surrounding uninfected cells. To resist viral infection, many host factors are operative, mainly the induction of innate and adoptive immunity, such as the interferon and Th1 type immune response. In this Special Issue of Biology, we describe historical, present and future aspects of viral infection in type 1 diabetes and regulatory mechanisms of viral infection in type 1 diabetes, aiming to develop an anti-diabetogenic virus vaccine to prevent virus-induced type 1 diabetes in the near future.

Prof. Dr. Seiho Nagafuchi
Guest Editor

Manuscript Submission Information

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Keywords

  • virus
  • diabetes
  • immunity
  • vaccine
  • COVID-19

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

2 pages, 198 KiB  
Editorial
Regulation of Viral Infection in Diabetes
by Seiho Nagafuchi
Biology 2021, 10(6), 529; https://doi.org/10.3390/biology10060529 - 13 Jun 2021
Cited by 1 | Viewed by 2025
Abstract
Though there is no ‘Diabetes Virus’, multiple agents such as mumps virus, rubella virus, influenza virus, type A hepatitis virus, enterovirus, rotavirus, cytomegalovirus, varicella-zoster virus, human herpesvirus 6, Epstein-Barr virus, and also SARS-CoV-2 have been reported to be associated to diabetes [...] Full article
(This article belongs to the Special Issue Regulation of Viral Infection in Diabetes)

Research

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16 pages, 1867 KiB  
Article
Pre-Existing Diabetes and COVID-Associated Hyperglycaemia in Patients with COVID-19 Pneumonia
by Andrea Laurenzi, Amelia Caretto, Chiara Molinari, Elena Bazzigaluppi, Cristina Brigatti, Ilaria Marzinotto, Alessia Mercalli, Raffaella Melzi, Rita Nano, Cristina Tresoldi, Giovanni Landoni, Fabio Ciceri, Vito Lampasona, Marina Scavini and Lorenzo Piemonti
Biology 2021, 10(8), 754; https://doi.org/10.3390/biology10080754 - 05 Aug 2021
Cited by 6 | Viewed by 3538
Abstract
Aim. The aim of the current study was to compare clinical characteristics, laboratory findings, and major outcomes of patients hospitalized for COVID-19 pneumonia with COVID-associated hyperglycaemia or pre-existing diabetes. Methods. A cohort of 176 adult patients with a diagnosis of pre-existing diabetes ( [...] Read more.
Aim. The aim of the current study was to compare clinical characteristics, laboratory findings, and major outcomes of patients hospitalized for COVID-19 pneumonia with COVID-associated hyperglycaemia or pre-existing diabetes. Methods. A cohort of 176 adult patients with a diagnosis of pre-existing diabetes (n = 112) or COVID-associated hyperglycaemia (n = 55) was studied. Results. Patients with COVID-associated hyperglycaemia had lower BMI, significantly less comorbidities, and higher levels of inflammatory markers and indicators of multi-organ injury than those with pre-existing diabetes. No differences between pre-existing diabetes and COVID-associated hyperglycaemia were evident for symptoms at admission, the humoral response against SARS-CoV-2, or autoantibodies to glutamic acid decarboxylase or interferon alpha-4. COVID-associated hyperglycaemia was independently associated with the risk of adverse clinical outcome, which was defined as ICU admission or death (HR 2.11, 95% CI 1.34–3.31; p = 0.001), even after adjustment for age, sex, and other selected variables associated with COVID-19 severity. Furthermore, at the same time, we documented a negative association (HR 0.661, 95% CI 0.43–1.02; p = 0.063) between COVID-associated hyperglycaemia to swab negativization. Conclusions. Recognizing hyperglycaemia as a specific clinical entity associated with COVID-19 pneumonia is relevant for early and appropriate patient management and close monitoring for the progression of disease severity. Full article
(This article belongs to the Special Issue Regulation of Viral Infection in Diabetes)
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Review

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21 pages, 1021 KiB  
Review
Re-Enlightenment of Fulminant Type 1 Diabetes under the COVID-19 Pandemic
by Hiroyuki Sano and Akihisa Imagawa
Biology 2022, 11(11), 1662; https://doi.org/10.3390/biology11111662 - 15 Nov 2022
Cited by 3 | Viewed by 2431
Abstract
Fulminant type 1 diabetes (FT1D) is a subtype of type 1 diabetes (T1D) that is characterized by the rapid progression to diabetic ketoacidosis against the background of rapid and almost complete pancreatic islet destruction. The HbA1c level at FT1D onset remains normal or [...] Read more.
Fulminant type 1 diabetes (FT1D) is a subtype of type 1 diabetes (T1D) that is characterized by the rapid progression to diabetic ketoacidosis against the background of rapid and almost complete pancreatic islet destruction. The HbA1c level at FT1D onset remains normal or slightly elevated despite marked hyperglycemia, reflecting the rapid clinical course of the disease, and is an important marker for diagnosis. FT1D often appears following flu-like symptoms, and there are many reports of its onset being linked to viral infections. In addition, disease-susceptibility genes have been identified in FT1D, suggesting the involvement of host factors in disease development. In most cases, islet-related autoantibodies are not detected, and histology of pancreatic tissue reveals macrophage and T cell infiltration of the islets in the early stages of FT1D, suggesting that islet destruction occurs via an immune response different from that occurring in autoimmune type 1 diabetes. From 2019, coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) spread worldwide and became a serious problem. Reports on the association between SARS-CoV-2 and T1D are mixed, with some suggesting an increase in T1D incidence due to the COVID-19 pandemic. When discussing the association between COVID-19 and T1D, it is also necessary to focus on FT1D. However, it is not easy to diagnose this subtype without understanding the concept. Therefore, authors hereby review the concept and the latest findings of FT1D, hoping that the association between COVID-19 and T1D will be adequately evaluated in the future. Full article
(This article belongs to the Special Issue Regulation of Viral Infection in Diabetes)
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22 pages, 742 KiB  
Review
Environmental Factors and the Risk of Developing Type 1 Diabetes—Old Disease and New Data
by Katarzyna Zorena, Małgorzata Michalska, Monika Kurpas, Marta Jaskulak, Anna Murawska and Saeid Rostami
Biology 2022, 11(4), 608; https://doi.org/10.3390/biology11040608 - 16 Apr 2022
Cited by 13 | Viewed by 5063
Abstract
The incidence of type 1 diabetes (T1D) is increasing worldwide. The onset of T1D usually occurs in childhood and is caused by the selective destruction of insulin-producing pancreatic islet cells (β-cells) by autoreactive T cells, leading to insulin deficiency. Despite advanced research and [...] Read more.
The incidence of type 1 diabetes (T1D) is increasing worldwide. The onset of T1D usually occurs in childhood and is caused by the selective destruction of insulin-producing pancreatic islet cells (β-cells) by autoreactive T cells, leading to insulin deficiency. Despite advanced research and enormous progress in medicine, the causes of T1D are still not fully understood. Therefore, an extensive online search for scientific research on environmental factors associated with diabetes and the identification of new factors of unexplained etiology has been carried out using the PubMed, Cochrane, and Embase databases. The search results were limited to the past 11 years of research and discovered 143 manuscripts published between 2011 and 2022. Additionally, 21 manuscripts from between 2000 and 2010 and 3 manuscripts from 1974 to 2000 were referenced for historical reference as the first studies showcasing a certain phenomenon or mechanism. More and more scientists are inclined to believe that environmental factors are responsible for the increased incidence of diabetes. Research results show that higher T1D incidence is associated with vitamin D deficiency, a colder climate, and pollution of the environment, as well as the influence of viral, bacterial, and yeast-like fungi infections. The key viral infections affecting the risk of developing T1DM are rubella virus, mumps virus, Coxsackie virus, cytomegalovirus, and enterovirus. Since 2020, i.e., from the beginning of the COVID-19 pandemic, more and more studies have been looking for a link between Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and diabetes development. A better understanding of the role of viral, bacterial, and yeast-like fungi infections related to the risk of T1DM in children and adolescents and the identification of new risk factors, especially those spread by the droplet route, is of great importance for people and families with diabetes. Full article
(This article belongs to the Special Issue Regulation of Viral Infection in Diabetes)
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18 pages, 386 KiB  
Review
Clinical Significance of COVID-19 and Diabetes: In the Pandemic Situation of SARS-CoV-2 Variants including Omicron (B.1.1.529)
by Akiko Yonekawa and Nobuyuki Shimono
Biology 2022, 11(3), 400; https://doi.org/10.3390/biology11030400 - 04 Mar 2022
Cited by 10 | Viewed by 2697
Abstract
The coronavirus disease 2019 (COVID-19) global pandemic, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains uncontrolled, with the spread of emerging variants. According to accumulating evidence, diabetes is one of the leading risk factors for a severe COVID-19 clinical [...] Read more.
The coronavirus disease 2019 (COVID-19) global pandemic, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains uncontrolled, with the spread of emerging variants. According to accumulating evidence, diabetes is one of the leading risk factors for a severe COVID-19 clinical course, depending on the glycemic state before admission and during COVID-19 hospitalization. Multiple factors are thought to be responsible, including an altered immune response, coexisting comorbidity, and disruption of the renin-angiotensin system through the virus–host interaction. However, the precise underlying mechanisms remain under investigation. Alternatively, the focus is currently on the diabetogenic and ketosis-prone potential of SARS-CoV-2 itself, even for probable triggers of stress and steroid-induced hyperglycemia in COVID-19. In this article, we present a comprehensive review of the recent literature on the clinical and experimental findings associated with diabetes and COVID-19, and we discuss their bidirectional relationship, i.e., the risk for an adverse prognosis and the deleterious effects on glycometabolism. Accurate assessments of the incidence of new-onset diabetes induced by COVID-19 and its pathogenicity are still unknown, especially in the context of the circulation of SARS-CoV-2 variants, such as Omicron (B.1.1.529), which is a major challenge for the future. Full article
(This article belongs to the Special Issue Regulation of Viral Infection in Diabetes)
16 pages, 653 KiB  
Review
SARS-CoV-2 Infection and Pancreatic β Cell Failure
by Keiichiro Mine, Seiho Nagafuchi, Hitoe Mori, Hirokazu Takahashi and Keizo Anzai
Biology 2022, 11(1), 22; https://doi.org/10.3390/biology11010022 - 24 Dec 2021
Cited by 18 | Viewed by 3457
Abstract
SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 infection may also be a causal factor for diabetes mellitus in [...] Read more.
SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 infection may also be a causal factor for diabetes mellitus in patients with COVID-19. According to the research reviewed in this paper, the pancreas and pancreatic β cells appear to be targets of SARS-CoV-2 and are damaged by direct or indirect effects of the infection. However, controversial results have been reported between study groups, mainly due to the limited number of cases with diabetes precipitated by COVID-19. In this review, we comprehensively discuss the published findings on the potential association between SARS-CoV-2 infection or COVID-19 and pancreatic β-cell damage leading to diabetes onset. These findings will further contribute to our understanding of the pathogenesis of diabetes mellitus. Full article
(This article belongs to the Special Issue Regulation of Viral Infection in Diabetes)
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