An Immunofluorescent Study of Generalized Coxsackie Virus B3 Infection in a Newborn Infant

Iwasaki, Takuya; Monma, Nobuhiro; Satodate, Ryoichi; Kawana, Rinji; Kueata, Takeshi

doi:10.1111/j.1440-1827.1985.tb00615.x

Cited by 23 publications

(24 citation statements)

References 7 publications

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“…Regardless, there are numerous publications that suggest a large amount of damage is inflicted by the virus itself, in the murine model, early post-infection, that is correlated with the number of myocarditic lesions spatially coincident with positivity by in situ hybridization for CVB3 genome (Cheung et al, 2008;Chow et al, 1992;Marchant et al, 2009a;McManus et al, 1993). These observations are supported by findings in autopsy cases, particularly in infants (Iwasaki et al, 1985a;Iwasaki et al, 1985b).…”

Section: Viral Replication As the Central Regulator Of Viral Myocarditissupporting

confidence: 72%

Cellular and Immunological Regulation of Viral Myocarditis

Marchant¹,

Garmaroudi²,

McManus³

2011

Myocarditis

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Section: Viral Replication As the Central Regulator Of Viral Myocarditissupporting

confidence: 72%

Cellular and Immunological Regulation of Viral Myocarditis

Marchant¹,

Garmaroudi²,

McManus³

2011

Myocarditis

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“…A predisposing, multigenic component has been described but accounts for fewer than 50% of cases (7,35,45); environmental factors (e.g., viral infections) have therefore been proposed to explain the remaining cases of T1D (3,6,32,57,58) that cannot be ascribed solely to host-driven pathogenic autoimmunity. Human enterovirus (HEV) infections have long been suspected as environmental triggers of human T1D (12,22,27); infections by common HEVs, such as the group B coxsackieviruses (CVB 1 to 6) and diverse echoviruses, have been implicated as triggers of T1D onset at the time of or shortly after infection (8,9,13,19,28,37,39,40,42,52,60). Nonetheless, it remains unclear whether HEV initiates T1D in humans (18,21,24,26); evidence supporting an etiologic connection between HEV infection and T1D onset is not as well-established as the links between, for example, specific HEV infections and poliomyelitis, aseptic meningitis, or myocarditis (43).…”

mentioning

confidence: 99%

Group B Coxsackievirus Diabetogenic Phenotype Correlates with Replication Efficiency

Kanno

Kim

Kono

et al. 2006

J Virol

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Group B coxsackieviruses can initiate rapid onset type 1 diabetes (T1D) in old nonobese diabetic (NOD) mice. Inoculating high doses of poorly pathogenic CVB3/GA per mouse initiated rapid onset T1D. Viral protein was detectable in islets shortly after inoculation in association with beta cells as well as other primary islet cell types. The virulent strain CVB3/28 replicated to higher titers more rapidly than CVB3/GA in the pancreas and in established beta cell cultures. Exchange of 5-nontranslated regions between the two CVB3 strains demonstrated a variable impact on replication in beta cell cultures and suppression of in vivo replication for both strains. While any CVB strain may be able to induce T1D in prediabetic NOD mice, T1D onset is linked both to the viral replication rate and infectious dose.Insulin-dependent (type 1) diabetes mellitus (T1D) is an autoimmune, largely T-cell-mediated disease typically diagnosed before the end of the teen years (5, 6). A predisposing, multigenic component has been described but accounts for fewer than 50% of cases (7,35,45); environmental factors (e.g., viral infections) have therefore been proposed to explain the remaining cases of T1D (3,6,32,57,58) that cannot be ascribed solely to host-driven pathogenic autoimmunity. Human enterovirus (HEV) infections have long been suspected as environmental triggers of human T1D (12,22,27); infections by common HEVs, such as the group B coxsackieviruses (CVB 1 to 6) and diverse echoviruses, have been implicated as triggers of T1D onset at the time of or shortly after infection (8,9,13,19,28,37,39,40,42,52,60). Nonetheless, it remains unclear whether HEV initiates T1D in humans (18,21,24,26); evidence supporting an etiologic connection between HEV infection and T1D onset is not as well-established as the links between, for example, specific HEV infections and poliomyelitis, aseptic meningitis, or myocarditis (43).The nonobese diabetic (NOD) mouse is widely used as a model for the study of T1D. Previous work demonstrated that CVB inoculation protects young NOD mice significantly better from T1D as they age than no treatment (mock infected) (55). Unlike all other treatments that protect NOD mice from T1D (reviewed in references 4 and 46), the CVB are widely thought to be instigators of T1D onset with no protective effect. The extent of protection from T1D onset correlates directly with replication efficiency of the specific CVB strain that is employed: CVB strains that replicate to higher titers protect more mice than do CVB strains which replicate to lower titers. As NOD mice age, naturally occurring, pathogenic autoimmune insulitis develops rapidly (4) with widespread islet inflammation (insulitis) present by week 12 to 15 of age, when T1D also begins to occur. T1D rapidly ensues following inoculation of old (Ͼ12 weeks of age) NOD mice with virulent CVB (14), a model that recapitulates observations of sudden T1D onset in humans reported to occur during or shortly after an infection (37, 52). Initiation of rapid T1D onset in older mice...

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“…Vertical transmission of CV-B associated with foetal thymus infection has been reported [Iwasaki et al, 1985;Lozovskaia et al, 1997]. In addition, it has been shown that enterovirus infections in utero may induce b-cell autoimmunity [Otonkoski et al, 2000], and that CV-B4 infection during pregnancy was a risk factor for childhood-onset type 1 diabetes [Dahlquist et al, 1995;Hyöty et al, 1995].…”

Section: Introductionmentioning

confidence: 97%

Coxsackievirus B4 infection of murine foetal thymus organ cultures

Brilot

Jaïdane

Geenen

et al. 2008

Journal of Medical Virology

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The infection of foetal thymus with coxsackievirus B4 (CV-B4) E2 has been studied ex vivo by using CD-1 mice on foetal day 14, as a ready source of organs for experimentation to investigate the hypothesis of the role of thymic viral infections in the pathogenesis of type 1 diabetes. The replication of CV-B4 E2 in murine foetal thymus organ cultures has been demonstrated by evaluating the levels of positive-and negativestranded viral RNA in cells by using a real-time quantitative RT-PCR method and by determining titres of infectious viral particles in culture supernatants for 7 days post-infection (p.i.). Staining of tissue sections with an anti-cytokeratin antibody and haematoxylin-eosin showed that CV-B4 infection had no visible effect on cell survival and organ integrity. Cell counts in mock-and virus-infected foetal thymus organ cultures increased from day 1 through day 7, and live cell numbers were comparable in both conditions as shown by Trypan blue exclusion test and 7-amino-actinomycin D staining of thymocytes. Compared with controls on day 7 p.i., cytofluorometric analyses on cells from CV-B4 E2-infected foetal thymus organ cultures displayed a marked increase in the percentage of the most immature CD3 À CD4 À CD8 À thymocytes, and a decrease in the percentage of immature CD3 À CD4 þ CD8 þ cells, together with an increase in the percentage of mature CD3 þ CD4 þ and CD3 þ CD8 þ cells. These data show that CV-B4 E2 disturbs T-cell maturation and differentiation processes in infected murine foetal thymus organ cultures and provide evidence of a suitable system to investigate the effect of viruses in T-cell differentiation.

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An Immunofluorescent Study of Generalized Coxsackie Virus B3 Infection in a Newborn Infant

Cited by 23 publications

References 7 publications

Cellular and Immunological Regulation of Viral Myocarditis

Cellular and Immunological Regulation of Viral Myocarditis

Group B Coxsackievirus Diabetogenic Phenotype Correlates with Replication Efficiency

Coxsackievirus B4 infection of murine foetal thymus organ cultures

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