The roles of Human Cytomegalovirus and Epstein-Barr virus in Type 1 Diabetes Mellitus (original) (raw)
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Diabetic Medicine, 1995
The polymerase chain reaction was used to detect a range of common viruses in the peripheral blood of Type 1 diabetic and non-diabetic control patients in order to identify any abnormal viral presence, with possible roles in the pathogenesis of Type 1 diabetes. Peripheral blood from 17 newly diagnosed Type 1 diabetic patients, 38 Type 1 diabetic patients with disease of longer duration, and 43 age and sex matched non-diabetic controls was obtained. Samples were screened for cytomegalovirus, Epstein-Barr virus, enterovirus (including coxsackie), and mumps virus. Cytomegalovirus was detected in control patients only (5 %), Epstein-Barr virus was detected equally in newly diagnosed and control patients (12 %), and enterovirus was detected slightly more frequently in diabetic than non-diabetic patients (41 Yo and 31 Yo, respectively). Mumps virus was not detected in any of the samples. It is concluded that Type 1 diabetic individuals are neither more prone to persistence of common viruses nor to more frequent acute infections with the viruses tested for than non-diabetic individuals. If common viruses are involved in the pathogenesis of Type 1 diabetes then they act either as non-specific agents to which the host has abnormal immune responses, or, the diabetogenic viruses are eliminated from the body by the time of disease diagnosis.
PLOS ONE, 2019
A microbiota is a complex ecosystem of microorganisms consisting of bacteria, viruses, protozoa, and fungi living in different niches of the human body, which plays an essential role in many metabolic functions. Modifications in the microbiota composition can lead to several diseases, including metabolic disorders. The aim of this study was to analyze the prevalence of four viruses which can cause persistent infections-Epstein-Barr virus (EBV), human papillomavirus (HPV), cytomegalovirus (CMV), and herpes simplex virus type 1 (HSV-1) in patients with diabetes mellitus type 2 (DM2). Blood, saliva and oral swabs were collected from all the study participants. The nested-PCR technique was used to detect the viral DNA. DNA of at least one virus was detected in 71.1% of diabetic patients and in 30% of individuals without diabetes. In patients with diabetes EBV DNA was detected the most frequently (25.4%), followed by HPV-19.1%, HSV-10.4% and CMV-5.2%. A higher percentage of EBV+HPV co-infection was found among men (30.8%). EBV DNA was statistically more often detected in patients living in rural areas (53.7%), while HPV (91.5%) and EBV+HPV co-infection (22.2%) prevailed among patients from urban areas. In patients with a DM2 history longer than 10 years viral infection was detected more frequently. The prevalence of EBV, HPV and the EBV+HPV co-infection was significantly higher in diabetic patients than in individuals without diabetes. The frequency of these infections depended on the duration of the disease (DM2).
Clinical and Experimental Immunology, 2012
OTHER THEMES PUBLISHED IN THIS IMMUNOLOGY IN THE CLINIC REVIEW SERIESMetabolic diseases, host responses, cancer, autoinflammatory diseases, allergy.Type 1 diabetes results from an interaction between genetic and environmental factors. Coxsackieviruses B (CV-B) are major environmental candidates, as suggested by epidemiological and experimental studies. The mechanisms leading to the disease involve interactions between the virus, host target tissue (pancreas) and the immune system. The infection of target cells with viruses can be prevented by antibodies. Conversely, the infection can be enhanced by antibodies. The antibody-dependent enhancement (ADE) of infection has been described with various viruses, especially Picornaviruses. In mice infected with CV-B3 this phenomenon resulted in an extended inflammatory reaction and myocarditis. In the human system non-neutralizing antibodies can increase the infection of monocytes with CV-B4 and stimulate the production of interferon (IFN)-α by these cells in vitro. CV-B4/immunoglobulin (Ig)G immune complexes interacted with a specific viral receptor [Coxsackievirus and adenovirus receptor (CAR)] and with IgG Fc fraction receptors (FcγRII and FcγRIII) at the surface of monocytes. The virus–antibody complexes are internalized (CAR) and receptors for the Fc of IgG (FcγRII and FcγRIII). Such antibodies have been detected in patients with type 1 diabetes and they could be responsible for the presence of enteroviral RNA and IFN-α in peripheral blood mononuclear cells (PBMC) of these individuals. The target of enhancing antibodies has been identified as the VP4 protein, which allowed the detection of these antibodies by enzyme-linked immunosorbent assay (ELISA). It cannot be excluded that antibodies enhancing the infection with CV-B may play a role in the pathogenesis of type 1 diabetes, induced or aggravated by these viruses. They can cause a viral escape from the immune response and may participate in the spreading of viruses to β cells. Whether enhancing antibodies raised against VP4 can play a role in iterative homologous and/or heterologous CV-B infections and in the persistence of viruses within the host deserves further study.
Cytomegalovirus (CMV) and Coxsackievirus (CV) are included in the environmental factors potentially relevant to the pathogenesis of type 1 diabetes (T1D). Thus, this study aimed to detect the prevalence of both anti-IgG for each of CV and CMV in diabetic children with (EV +) or without (EV-) enteroviruses infection. The current study revealed that the T1D-EV + and T1D-EV-groups had marked elevations in hemoglobin A1c (HbA1c), C-reactive protein (CRP) and glutamic acid decarboxylase autoantibodies (GADA) as compared to non-diabetic control. Moreover, anti-IgG for the CV and CMV groups were detected in three groups; diabetic infected (T1D-EV +), diabetic non-infected (T1D-EV-) and control group. Detection of anti-CV IgG achieved 22.7%, 6.7% and 64% in control, T1D-EV-and T1D-EV + , respectively. However, detection of anti-CMV IgG revealed 23.4%, 50% and 40% in control, T1D-EV-and T1D-EV + , respectively. In conclusion, the prevalence of the antibodies of CV-IgG and CMV-IgG in the sera of diabetic children more than that in healthy control children may give a role of these viruses in the etiology and progression of T1D.
Journal of Diabetes Research, 2018
Objective. Viruses trigger and promote islet cell destruction and cause type 1 diabetes mellitus (T1DM). However, the existence of a cause-and-effect relationship is under debate. The aim of this study is to investigate the sero-epidemiological and molecular evidence on enteroviruses and respiratory viruses in patients with newly diagnosed T1DM during the cold season. Design. Forty children newly diagnosed with T1DM and 30 healthy children who presented to the clinic over the course of a year were included in the study. The IgM antibodies against enteroviruses and respiratory viruses were studied using the indirect immunofluorescence assay (IFA) test, and no CBV4-specific RNA was detected in the children. The onset times of T1DM were classified into fall-winter and spring-summer seasons and separated into cold, moderate, or warm months in terms of temperature. Results. The percentages of viral IgM antibodies against most common viruses were detected in the patients as follows: influ...
Clinical Immunology and Immunopathology, 1990
To investigate whether cytomegalovirus (CMV) infection may be related to islet cell antibodies (ICA) production and/or to insulin-dependent diabetes mellitus (IDDM) development, we have analyzed the prevalence of anti-CMV, IgM, and IgG antibodies and of ICA in 80 healthy siblings of IDDM patients (HSIDDP) and in 60 control subjects with negative familiar anamnesis of IDDM. HSIDDP and controls were also typed for HLA-A-B-C and DR antigens. IgM and IgG anti-CMV were detected by an ELISA method, whereas the ICA assay was performed by standard indirect immunofluorescence on 5-p,m unfixed sections of human pancreas. HLA-A-B and C antigens were studied by standard microlymphocytotoxicity; DR antigens were also studied by a standard microlymphocytotoxicity on a B-enriched lymphocyte population. Our results indicate a significant association (P < 0X401) between high titers of anti-CMV IgG antibodies and ICA in HSDIDDP, whereas no correlation was found between the presence of any HLA-A-B-C and DR antigens and the prevalence of anti-CMV IgM and IgG antibodies and/or ICA. Thus, these data may support the hypothesis that a chronic CMV infection may be associated with ICA production whereas other factors seem to be needed for the complete development of type 1 diabetes. Q 1990 Academic press, hc.
Clinical & Experimental Immunology, 2012
The hypothesis that under some circumstances enteroviral infections can lead to type 1 diabetes (T1D) was proposed several decades ago, based initially on evidence from animal studies and sero-epidemiology. Subsequently, enterovirus RNA has been detected more frequently in serum of patients than in control subjects, but such studies are susceptible to selection bias and reverse causality. Here, we review critically recent evidence from human studies, focusing on longitudinal studies with potential to demonstrate temporal association. Among seven longitudinal birth cohort studies, the evidence that enterovirus infections predict islet autoimmunity is quite inconsistent in our interpretation, due partially, perhaps, to heterogeneity in study design and a limited number of subjects studied. An association between enterovirus and rapid progression from autoimmunity to T1D was reported by one longitudinal study, but although consistent with evidence from animal models, this novel observation awaits replication. It is possible that a potential association with initiation and/or progression of islet autoimmunity can be ascribed to a subgroup of the many enterovirus serotypes, but this has still not been investigated properly. There is a need for larger studies with frequent sample intervals and collection of specimens of sufficient quality and quantity for detailed characterization of enterovirus. More research into the molecular epidemiology of enteroviruses and enterovirus immunity in human populations is also warranted. Ultimately, this knowledge may be used to devise strategies to reduce the risk of T1D in humans.
Association of Anti-Coxsackie Virus-B IgG with Autoantibodies Related to Type 1 Diabetes Mellitus
Association of Anti-Coxsackie Virus-B IgG with Autoantibodies Related to Type 1 Diabetes Mellitus, 2022
Background Coxsackievirus B is a virus may cause type 1 diabetes. There are links between Coxsackievirus B infections and type 1 diabetes. The presence of autoantibodies in pancreatic beta cells has been linked to the development of type 1 diabetes following Coxsackievirus B infection. Objective To detect autoantibodies in patients with type 1 diabetes. Also, to find if there is an association between pancreatic beta cell autoantibodies and Coxsackievirus-B IgG. Methods This study was done from January to March 2021, it included two groups of 75 children; their ages ranged from one month to fifteen years. Children with type 1 diabetes were admitted to the diabetic and endocrine glands center in Thi-Qar governorate, whereas children without diabetes (control group) were admitted to Bint Al-Huda Children's Hospital in Nasiriyah/Thi-Qar. Venous blood was taken from each person for estimation of random blood sugar, serum fructosamine, and HbA1c in the laboratory of the diabetic and endocrine glands center. Pancreatic beta cell autoantibodies and anti-Coxsackievirus-B IgG was detected by enzyme-linked immunosorbent assay. The statistical analyses were done using SPSS 25. The study population P-values below 0.05 to be statistically significant. The study was authorized by Al-Nahrain University's Institutional Review Board and parental consent was taken. Results The patients had significantly greater levels of random blood sugar, fructosamine, and HbA1c than healthy controls. Anti-islet antigen, anti-islet cell, anti-glutamic acid decarboxylase, and anti-Coxsackievirus-B IgG antibody titers were greater in patients than controls. The majority of autoantibodies tested correlated with Coxsackievirus-B IgG antibodies. Conclusion Anti-Coxsackievirus-B IgG antibody positivity was associated with autoantibodies related to type 1 diabetes mellitus.
Behring Institute Mitteilungen, 1984
The etiology of IDDM remains incompletely understood, with genetic predisposition, autoimmune destruction of the beta cells and viral infections interacting to produce disease. It appear that the underlying genetic defect is an alteration in cellular and/or humorally-mediated immunological responsiveness. There are at least two (and probably more) genetically determined defects identified by HLA B-8 (DR3) and B-15 (DR4). A number of viruses have been implicated in IDDM causation, including Coxsackie, mumps, rubella, Epstein-Barr, hepatitis and influenza viruses, but in only a few cases is viral etiology fully documented. Viral infections may trigger autoimmunity. Alterations in immunoglobulin concentration, particularly IgA deficiency, have been reported by several investigators. Collaborative prospective studies of individuals at high risk for the development of IDDM (siblings with HLA identical to the index case) are essential in the future study of IDDM etiology.