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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human parvovirus B19 is a recently recognized cause of hydrops fetalis. It is a small, single-stranded DNA virus, which preferentially infects late erythroid precursors and produces red blood cell (RBC) aplasia, fetal anemia, and cardiac failure. Infection is accompanied by characteristic intranuclear inclusions in fixed and circulating RBC precursors. These inclusions have been shown to contain virus particles by electron microscopy and in situ hybridization. Infection of the fetus, mother, and newborn infant can be diagnosed by serological and molecular methods selected to match the stage of the infection. Recent work has shown that parvovirus B19 can infect cells other than erythroid precursors, and that additional mechanisms such as myocarditis may contribute to hydrops fetalis in some cases. Infected fetuses are not always hydropic. Maternal infection results in increased abortion and stillbirth even in the absence of transplacental transmission, which occurs in approximately one third of infected mothers. The overall risk of fetal loss following maternal exposure is much less than previously thought, and may be less than 3% in the first 20 weeks of gestation or approximately 10% if the mother is actually infected. Although parvoviruses are teratogenic in animals, there is no evidence that B19 is a significant teratogen in man. The long-term outlook of survivors of intrauterine infection, including those successfully treated by intrauterine blood transfusion, appears to be good, but requires further study.
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PMID:Parvovirus infection of the human fetus and newborn. 156 88

B19 virus infection is common in the population and is frequently asymptomatic. However, a viraemia and prompt antibody response occurs in normal individuals and this is associated with mild, non-specific respiratory tract symptoms at the time of the viraemia and/or a rash-illness a week or ten days later. Infection of red cell precursors is a regular occurrence and this leads to aplastic crisis if B19 virus infection occurs in an individual with chronic heamolytic anaemia. Fetal infection sometimes takes place if infection occurs during pregnancy and some fetuses fail to clear the infection, develop anaemia leading to heart failure and hydrops fetalis. Some immunocompromised patients also fail to clear the viraemia and this results in a persistent or relapsing anaemia.
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PMID:The pathogenesis of diseases associated with B19 virus. 217 86

The review of 15 cases of cardiac involvement demonstrate the cardiac tropism of the human parvovirus B19. Ten of these cases were collected from fetuses during second trimester of maternal-fetal infections. In situ hybridisation detects viral DNA sequences in the nucleus of infected myoblasts. Myocarditis is the most frequent histological damage. Cardiac failure, secondary to myocarditis, may occur in the absence of fetal anaemia. When the fetus is deeply anaemic, like usually in cases of hydrops, damages of the cardiac tissues might hamper the reactional increase of cardiac output; therefore, they might account for the poor prognosis of parvovirus B19 fetal hydrops in the second trimester of pregnancy, despite transfusional therapy attempts in the third trimester.
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PMID:[Cardiac involvement in fetal parvovirus B19 infection]. 853 80

A report is presented of a patient with neonatal erythema infectiosum who developed petechiae, transient thrombocytopenia and transient cardiac failure due to transplacental transmission of human parvovirus B19 (HPV B19) infection. It is suggested that the thrombocytopenia was caused by platelet-associated IgG produced by the patient, and that the cardiac failure may have been caused by direct entry of HPV B19 into the cardiac tissue.
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PMID:Neonatal erythema infectiosum. 958 10

Intrauterine human parvovirus B19 infection is related to non-immune hydrops fetalis and fetal death. First, we performed epidemiological studies to determine the critical period during which maternal infection led to hydrops fetalis. The studies showed that the hepatic period of hematopoietic activity was correlated with the critical period of maternal infection, which suggested that B19 might have affinity for erythroid lineage cells at the stage of hematopoiesis. We next established an in vitro infection experimental system of B19 using erythroid lineage cells derived from fetal liver cells. We demonstrated that the erythroid lineage cells proved to be appropriate targets for B19 virus and that B19 infection could induce apoptosis of infected cells. The massive destruction of erythroid lineage cells through apoptosis seems to cause severe anemia and to result in heart failure of the fetus. To analyze the cytotoxic mechanism in more detail, we established a stringent regulatory expression system of the NS1 protein encoded by the B19 genome and indicated that the apoptosis induced by B19 was directly caused by the NS1 protein. Experiments using mutations engineered in the ATP-binding domain of NS1 indicated that this domain played a critical role for the apoptosis induction. The present studies may contribute to a better understanding of the pathogenesis of hydrops fetalis associated with B19 infection during pregnancy.
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PMID:Pathogenesis of nonimmune hydrops fetalis caused by intrauterine B19 infection. 1077 Jun 16

Coxsackieviruses and adenoviruses are common agents of viral heart disease. In the majority of exposed individuals they do not cause myocardial disease, however, since they are not primarily cardiotropic. Until recently the molecular basis of their anomalous tropism in patients who develop viral heart disease was unknown. An important step towards clarification of the molecular basis of cardiotropic viral infections was achieved in 1997, when a common receptor for the two structurally unrelated viruses was cloned. This coxsackievirus-adenovirus receptor (CAR) is a key determinant for the cellular uptake of both viruses and for the molecular pathogenesis of coxsackievirus and adenovirus diseases. We have mapped the CAR expression in human hearts and observed highly variable expression patterns. Healthy donor hearts had low CAR expression levels, whereas explanted hearts of patients with dilated cardiomyopathy (DCM) displayed high CAR expression in the myocardium. Remarkably, however, heart failure per se was not associated with CAR induction, since in heart failure of non-DCM origin no induction was found. Additional studies on the molecular mechanisms of CAR induction in cardiomyocytes indicated the existence of a cell-cell contact-dependent molecular mechanism regulating CAR expression, whereas cellular virus uptake and low level replication had no effect. Recombinant expression of human CAR in cardiomyocytes strongly increased their virus uptake rate suggesting that CAR induction enhances cardiac vulnerability to viral disease, whereas healthy myocardium is rather resistant to CAR-dependent viruses. Receptor induction may significantly aggravate the clinical course of viral heart disease, so that the blockade of receptor expression or receptor-virus interactions opens new therapeutic perspectives. Elucidation of the molecular mechanism of CAR induction in DCM, but not in heart failure per se, may reveal a particular pathogenetic process in this disease. A broader analysis of the cardiovascular expression patterns of receptors for other potentially cardiotropic viruses (CMV, EBV, HIV, HHV-6, Parvo-B19, etc.) should lead to a better understanding of individual risk factors for viral heart diseases and of their highly variable clinical courses, and offer new therapeutic options.
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PMID:Highly variable expression of virus receptors in the human cardiovascular system. Implications for cardiotropic viral infections and gene therapy. 1249 Sep 88

A report is given on an 8-year-old boy who suddenly and unexpected died. Autopsy findings point to acute heart failure. Microscopic examination of the heart showed increased interstitial and perivasal fibrosis and myocarditis with macrophage infiltration. Polymerase chain reaction (PCR) analysis for parvovirus B19 was positive in heart samples and in the spleen. Immunostaining for parvoviral surface antigens was negative. Although the virus does not appear to have infected the cardiomyocytes, we speculate that myocarditis arose from immunological cross-reaction to epitopes shared between the virus and the myocardium.
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PMID:Fatal parvovirus B19 myocarditis in an 8-year-old boy. 1453 5

We report the case of a 34-year-old female patient who died 4 days after hospital admission of acute heart failure clinically mimicking ischemic heart disease. Microscopic examination of the heart showed severe myocarditis. Polymerase chain reaction (PCR), including quantitative real-time PCR, disclosed exclusively parvovirus B19 (PVB19), with a high viral load of 4.3x10(5) PVB19 viral genome equivalents per microg myocardial nucleic acid. Radioactive in situ hybridization detected viral genomes in endothelial cells (ECs) predominantly in the venular compartment and (to a lesser degree) in small arteries and arterioles of the heart, but not in cardiac myocytes or other tissue components. Concomitant with EC infection, marked expression of the adhesion molecule E-selectin was noted, accompanied by margination, adherence, penetration, and perivascular infiltration of T lymphocytes. We speculate that, due to the high viral load in cardiac ECs, PVB19 infection of endothelial cells was sufficient to induce impaired coronary microcirculation with secondary cardiac myocyte necrosis.
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PMID:Fatal parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: an endothelial cell-mediated disease. 1260 72

Endomyocardial biopsy (EMB) is often performed in patients presenting with sudden onset of heart failure to identify myocarditis. The introduction of immunohistochemical techniques for the detection and differentiation of infiltrating immune cells, specific adhesion molecules and MHC class I and II molecules increased the prognostic value of EMB in the diagnosis of myocarditis considerably. A major breakthrough in the understanding of pathogenetic mechanisms in myocarditis was achieved by diagnostic use of molecular biological methods. By application of in situ hybridization and PCR, enteroviruses, and more recently, parvovirus B19 (PVB19) have been identified as relevant agents of myocarditis. The different cell tropism of these viruses implicates distinct pathogenic principles, which, at present, are not completely understood. Whereas enteroviruses damage the heart primarily via direct lysis of infected myocytes, PVB19 does not infect myocytes, but endothelial cells of small intracardiac arterioles and venules, resulting in impairment of myocardial microcirculation with secondary myocyte necrosis during acute infection. Histological and immunohistological stainings combined with molecular biological approaches in EMB will help us to resolve the question of whether patients with myocarditis should be treated by specific antiviral agents or by immunosuppressive therapies.
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PMID:Molecular pathology of inflammatory cardiomyopathy. 1292 May 83

Parvovirus infection during pregnancy is an important cause of hydrops fetalis. It is attributed to anemia caused by viral-induced destruction of red blood cells. Infection of other organs has been reported including the heart, liver, and lungs. Few of these reports, however, convincingly demonstrate virions within the functional parenchyma of the tissue. This is of particular concern regarding myocardium in the context of hydrops fetalis which is, in part, due to cardiac failure. The problem in routine pathology practice is that most fetuses with the infection are macerated. This, in part, probably explains the paucity of published information on cardiac involvement. This study examined five cases of fatal hydrops fetalis with variable maceration with serologically proven parvovirus B19 infection. Transmission electron microscopy of cardiac tissue demonstrated intranuclear virions in both erythroid precursor cells and in cardiac myocytes in three of these cases. In each of these, immuno-gold electron microscopy provided confirmatory evidence of parvovirus infection. Virions were not identifiable where maceration had caused disintegration of nuclei in the myocytes. In addition, virions were absent in the three negative control cases where retroplacental hemorrhage was confirmed as the cause of death. This study suggests that parvovirus infection of cardiac myocytes may play a more important role in causing hydrops fetalis than previously realized. It also demonstrates that maceration should not discourage the use of electron microscopy.
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PMID:Parvovirus infects cardiac myocytes in hydrops fetalis. 1470 34


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