Coxsackie Virus-Induced Acute Pancreatitis in a Long-term Dialysis Patient

Lal, Sunder M.; Fowler, Dale; Losasso, Carl J.; Berg, Gregg G.

doi:10.1016/s0272-6386(88)80058-1

Cited by 25 publications

(16 citation statements)

References 10 publications

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“…In a review of 2,000 pediatric autopsies, 16 cases of myocardial damage were closely associated with a variety of pancreatic complications [Nezelof and LeSec, 1979]. Pancreatitis that was associated with an increased antibody titer against CVB5 was also complicated by pericarditis [Ursing, 1973]; Lal et al [1988] reported acute pancreatitis apparently induced by a CVB infection in a long-term dialysis patient. Okada and colleagues found 929 cases of myocarditis in 634,440 autopsies between 1958-1984 and reported pancreatitis as one of several complicating factors [Okada et al, 1989].…”

Section: Discussionmentioning

confidence: 99%

Group B coxsackievirus myocarditis and pancreatitis: Connection between viral virulence phenotypes in mice

et al. 2000

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The group B coxsackieviruses (CVB) induce experimental pancreatitis and myocarditis in mice and are established agents of human myocarditis, especially in children. We tested the hypothesis that the development of CVB-induced myocarditis is linked to CVB-induced pancreatitis by studying the replication of different CVB strains in mice. Eight of nine genotypically different type 3 CVB (CVB3) strains induced acute pancreatitis in mice; of these, three viruses also induced acute myocarditis. One CVB3 strain was avirulent for both organs. Myocarditis was not observed in the absence of pancreatitis. The results obtained by inoculation of mice with strains of other CVB serotypes were consistent with these data. Infectious virus titers were measured in serum, pancreas, and heart as a function of time after inoculation of mice with three CVB3 strains. Each strain was representative of one of the three viral virulence phenotypes: avirulent, pancreovirulent only, and cardiovirulent. All strains replicated well and persisted in the pancreas through 8 days post-inoculation, but the cardiovirulent CVB3 strain tended to replicate to higher titer earlier and persist longer in sera, pancreatic, and cardiac tissues than the noncardiovirulent strains. Replication of the CVB3 strains were studied in two human pancreatic tumor lines and in primary human endothelial cell cultures derived from cardiac artery. Cardiovirulent strains, both individually and as a group, tended to replicate to titers as high as, or higher than, noncardiovirulent strains did in cell culture. The data are consistent with the possibility of an etiologic link between CVB-induced pancreatic and heart disease.

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Section: Discussionmentioning

confidence: 99%

Group B coxsackievirus myocarditis and pancreatitis: Connection between viral virulence phenotypes in mice

et al. 2000

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“…The CVB have been associated with diverse human diseases, among the more serious of which are myocarditis, pancreatitis, and aseptic meningitis. The CVB have been soundly implicated as causes of human myocarditis (1, 26, 42, 60-62, 73, 74, 108, 109) and pancreatitis (2,41,54,58,66,107) and, furthermore, cause these diseases readily in mice (9,40,43,85,86,105). Although CVB have been suggested as infectious triggers of human insulin-dependent (type 1) diabetes mellitus (T1D) (7,22,34,53,116), there is no consensus as to the etiologic role for CVB in T1D development (25,32,33,47,52,63,64,110).…”

mentioning

confidence: 99%

Toward Testing the Hypothesis that Group B Coxsackieviruses (CVB) Trigger Insulin-Dependent Diabetes: Inoculating Nonobese Diabetic Mice with CVB Markedly Lowers Diabetes Incidence

Tracy

Drescher

Chapman

et al. 2002

J Virol

144

163

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Insulin-dependent (type 1) diabetes mellitus (T1D) onset is mediated by individual human genetics as well as undefined environmental influences such as viral infections. The group B coxsackieviruses (CVB) are commonly named as putative T1D-inducing agents. We studied CVB replication in nonobese diabetic (NOD) mice to assess how infection by diverse CVB strains affected T1D incidence in a model of human T1D. Inoculation of 4-or 8-week-old NOD mice with any of nine different CVB strains significantly reduced the incidence of T1D by 2-to 10-fold over a 10-month period relative to T1D incidences in mock-infected control mice. Greater protection was conferred by more-pathogenic CVB strains relative to less-virulent or avirulent strains. Two CVB3 strains were employed to further explore the relationship of CVB virulence phenotypes to T1D onset and incidence: a pathogenic strain (CVB3/M) and a nonvirulent strain (CVB3/GA). CVB3/M replicated to four-to fivefold-higher titers than CVB3/GA in the pancreas and induced widespread pancreatitis, whereas CVB3/GA induced no pancreatitis. Apoptotic nuclei were detected by TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay in CVB3/M-infected pancreata but not in CVB3/GA-infected pancreata. In situ hybridization detected CVB3 RNA in acinar tissue but not in pancreatic islets. Although islets demonstrated inflammatory infiltrates in CVB3-protected mice, insulin remained detectable by immunohistochemistry in these islets but not in those from diabetic mice. Enzyme-linked immunosorbent assay-based examination of murine sera for immunoglobulin G1 (IgG1) and IgG2a immunoreactivity against diabetic autoantigens insulin and HSP60 revealed no statistically significant relationship between CVB3-protected mice or diabetic mice and specific autoimmunity. However, when pooled sera from CVB3/M-protected mice were used to probe a Western blot of pancreatic proteins, numerous proteins were detected, whereas only one band was detected by sera from CVB3/GA-protected mice. No proteins were detected by sera from diabetic or normal mice. Cumulatively, these data do not support the hypothesis that CVB are causative agents of T1D. To the contrary, CVB infections provide significant protection from T1D onset in NOD mice. Possible mechanisms by which this virus-induced protection may occur are discussed.The group B coxsackieviruses (CVB; family Picornaviridae, genus Enterovirus, species group B coxsackievirus; six serotypes, CVB1 to -6) are among the best studied of human enteroviruses (102). The CVB genome is a single strand of positive sense RNA 7,400 nucleotides in length that encodes 11 proteins in a single open reading frame (89). The CVB have been associated with diverse human diseases, among the more serious of which are myocarditis, pancreatitis, and aseptic meningitis. The CVB have been soundly implicated as causes of human myocarditis (1, 26, 42, 60-62, 73, 74, 108, 109) and pancreatitis (2,41,54,58,66,107) and, furthermore, cause these diseases readily i...

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“…The CVBs have been soundly implicated as causes of human myocarditis [2], pancreatitis [3] and respiratory diseases [4] and furthermore cause these diseases readily in mice [5,6]. In addition to other typical clinical syndromes, CVB has become an important cause of bronchial pneumonia [7].…”

Section: Introductionmentioning

confidence: 99%

Differential expression of coxsackievirus and adenovirus receptor on alveolar epithelial cells between fetal and adult mice determines their different susceptibility to coxsackievirus B infection

Sun

Li²,

Jia³

et al. 2012

Arch Virol

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Coxsackie Virus-Induced Acute Pancreatitis in a Long-term Dialysis Patient

Cited by 25 publications

References 10 publications

Group B coxsackievirus myocarditis and pancreatitis: Connection between viral virulence phenotypes in mice

Group B coxsackievirus myocarditis and pancreatitis: Connection between viral virulence phenotypes in mice

Toward Testing the Hypothesis that Group B Coxsackieviruses (CVB) Trigger Insulin-Dependent Diabetes: Inoculating Nonobese Diabetic Mice with CVB Markedly Lowers Diabetes Incidence

Differential expression of coxsackievirus and adenovirus receptor on alveolar epithelial cells between fetal and adult mice determines their different susceptibility to coxsackievirus B infection

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