scholarly journals Preservative Monitoring of a Greek Woman with Hydrops Fetalis due to Parvovirus B19 Infection

2017 ◽  
Vol 2017 ◽  
pp. 1-3
Author(s):  
Zacharias Fasoulakis ◽  
Panagiotis Antsaklis ◽  
Emmanuel N. Kontomanolis
Keyword(s):  
Parvovirus B19 ◽  
Hydrops Fetalis ◽  
Erythroid Progenitor ◽  
Fetal Demise ◽  
Erythroid Progenitor Cells ◽  
The Family ◽  
History Of ◽  
Greek Woman ◽  
B19 Parvovirus ◽  
Parvovirus B19 Infection

Primate erythroparvovirus 1 (parvovirus B19) is a member of theErythrovirusgenus of the Parvoviridae family and it is one of the few members of the family known to be pathogenic in human. B19 infection is common and widespread with the virus being associated with numerous rheumatologic and haematologic manifestations. More specifically, maternal infection with parvovirus B19 during pregnancy can cause severe anemia which may lead to nonimmune hydrops or fetal demise, as a result of fetal erythroid progenitor cells infection with shortened half-life of erythrocytes. We present a rare case reported in the Greek population, of subclinical transient reticulocytopenia due to B19 parvovirus infection, in an asymptomatic pregnant woman, without medical history of hemoglobinopathy, and with the presence of hydrops fetalis during the third trimester of her pregnancy.

scholarly journals A Case of Fetal Parvovirus B19 Myocarditis That Caused Terminal Heart Failure

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Atsuko Hichijo ◽  
Mikio Morine
Keyword(s):  
Heart Failure ◽  
Parvovirus B19 ◽  
Viral Myocarditis ◽  
Intrauterine Death ◽  
Fetal Anemia ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells ◽  
Terminal Heart Failure ◽  
Parvovirus B19 Infection ◽  
Postmortem Examinations

Parvovirus B19 is a well-established cause of fetal anemia and nonimmune fetal hydrops in pregnancy. Fetal parvovirus infection can cause severe destruction of erythroid progenitor cells, resulting in fetal anemia, hydrops, and intrauterine death. However, viral myocarditis with subsequent heart failure is another possible mechanism for hydrops formation as viral infection of fetal myocardial cells has been reported in postmortem examinations. We herein report a case of fetal cardiomegaly and massive pericardial effusion secondary to myocarditis as a result of parvovirus B19 infection. The case developed hydrops as consequence of severe anemia and experienced terminal heart failure, which led to the fetus dying an intrauterine death at 22 weeks of gestation. This case demonstrates that there may be an association between myocarditis caused by intrauterine parvovirus B19 infection and a poor outcome. The presence of viral myocarditis may be the determining prognostic factor in that situation.

scholarly journals Parvovirus B19: recent insights and implications for pathogenesis, diagnosis and therapy

2017 ◽  
Vol 32 (3) ◽  
Author(s):  
Giorgio Gallinella
Keyword(s):  
Parvovirus B19 ◽  
Immunological Methods ◽  
Erythroid Progenitor ◽  
Ongoing Research ◽  
Erythroid Progenitor Cells ◽  
Pathogenic Virus ◽  
The Family ◽  
Inflammatory Processes ◽  
Atypical Presentations ◽  
Differentiation And Proliferation

Parvovirus B19 is a human pathogenic virus, a ssDNA member of the family Parvoviridae, characterized by a selective tropism for erythroid progenitor cells (EPCs) in the bone marrow and an ample pathogenetic potential. The selective tropism for EPCs can be explained both in terms of receptor-mediated tropism and of an intracellular permissive environment conditioned by the cell differentiation and proliferation stage. Infection of EPCs is productive, induces apoptosis and leads to a temporary arrest of erythropoiesis, which can usually be manifest in cases of underlying erythropoietic disorders or immune system deficiencies. Endothelial cells constitute an additional diffuse target, whose infection is mediated by ADE phenomenon, but is normally nonproductive and mainly leading to inflammatory processes. The relevance of parvovirus as a cardiotropic virus is recently emerging, while its capability of intrauterine transmission and consequences on the fetus is known and should not be overlooked. To the purpose of diagnosis, a combination of molecular and immunological methods offers the best discrimination of active infectious processes, and an application of these methods especially in cases of atypical presentations should be encouraged. Ongoing research is directed towards the development of a vaccine and the discovery of antiviral drugs that may be useful in the prevention and treatment of parvovirus B19 infections.

History of parvovirus B19 infection is associated with silent cerebral infarcts

2017 ◽  
Vol 65 (1) ◽  
pp. e26767 ◽  
Author(s):  
Foluso J. Ogunsile ◽  
Kelli L. Currie ◽  
Mark Rodeghier ◽  
Adetola Kassim ◽  
Michael R. DeBaun ◽  
...  
Keyword(s):  
Parvovirus B19 ◽  
Cerebral Infarcts ◽  
History Of ◽  
Parvovirus B19 Infection

scholarly journals Ex Vivo-Generated CD36+ Erythroid Progenitors Are Highly Permissive to Human Parvovirus B19 Replication

2007 ◽  
Vol 82 (5) ◽  
pp. 2470-2476 ◽  
Author(s):  
Susan Wong ◽  
Ning Zhi ◽  
Claudia Filippone ◽  
Keyvan Keyvanfar ◽  
Sachiko Kajigaya ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Real Time ◽  
Cell Lines ◽  
Ex Vivo ◽  
Parvovirus B19 ◽  
Erythroid Progenitor ◽  
Hematopoietic Stem ◽  
Human Virus ◽  
Erythroid Progenitor Cells ◽  
Large Numbers

ABSTRACT The pathogenic parvovirus B19 (B19V) has an extreme tropism for human erythroid progenitor cells. In vitro, only a few erythroid leukemic cell lines (JK-1 and KU812Ep6) or megakaryoblastoid cell lines (UT7/Epo and UT7/Epo-S1) with erythroid characteristics support B19V replication, but these cells are only semipermissive. By using recent advances in generating large numbers of human erythroid progenitor cells (EPCs) ex vivo from hematopoietic stem cells (HSCs), we produced a pure population of CD36+ EPCs expanded and differentiated from CD34+ HSCs and assessed the CD36+ EPCs for their permissiveness to B19V infection. Over more than 3 weeks, cells grown in serum-free medium expanded more than 800,000-fold, and 87 to 96% of the CD36+ EPCs were positive for globoside, the cellular receptor for B19V. Immunofluorescence (IF) staining showed that about 77% of the CD36+ EPCs were positive for B19V infection, while about 9% of UT7/Epo-S1 cells were B19V positive. Viral DNA detected by real-time PCR increased by more than 3 logs in CD36+ EPCs; the increase was 1 log in UT7/Epo-S1 cells. Due to the extensive permissivity of CD36+ EPCs, we significantly improved the sensitivity of detection of infectious B19V by real-time reverse transcription-PCR and IF staining 100- and 1,000-fold, respectively, which is greater than the sensitivity of UT7/Epo-S1 cell-based methods. This is the first description of an ex vivo method to produce large numbers of EPCs that are highly permissive to B19V infection and replication, offering a cellular system that mimics in vivo infection with this pathogenic human virus.

scholarly journals History of parvovirus B19 infection is associated with a DNA methylation signature in childhood acute lymphoblastic leukemia

Epigenetics ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. 1436-1443 ◽  
Author(s):  
Gisele M. Vasconcelos ◽  
Brock C. Christensen ◽  
E. Andrés Houseman ◽  
Jianqiao Xiao ◽  
Carmen J. Marsit ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Acute Lymphoblastic Leukemia ◽  
Parvovirus B19 ◽  
Lymphoblastic Leukemia ◽  
Childhood Acute Lymphoblastic Leukemia ◽  
History Of ◽  
Parvovirus B19 Infection

scholarly journals Antibody-Mediated Enhancement of Parvovirus B19 Uptake into Endothelial Cells Mediated by a Receptor for Complement Factor C1q

2014 ◽  
Vol 88 (14) ◽  
pp. 8102-8115 ◽  
Author(s):  
Kristina von Kietzell ◽  
Tanja Pozzuto ◽  
Regine Heilbronn ◽  
Tobias Grössl ◽  
Henry Fechner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Parvovirus B19 ◽  
Cell Types ◽  
Complement Factor ◽  
Human Parvovirus B19 ◽  
Erythroid Progenitor ◽  
Antibody Dependent Enhancement ◽  
Erythroid Progenitor Cells ◽  
Additional Cell

ABSTRACTDespite its strong host tropism for erythroid progenitor cells, human parvovirus B19 (B19V) can also infect a variety of additional cell types. Acute and chronic inflammatory cardiomyopathies have been associated with a high prevalence of B19V DNA in endothelial cells of the myocardium. To elucidate the mechanisms of B19V uptake into endothelium, we first analyzed the surface expression of the well-characterized primary B19V receptor P antigen and the putative coreceptors α5β1integrins and Ku80 antigen on primary and permanent endothelial cells. The receptor expression pattern and also the primary attachment levels were similar to those in the UT7/Epo-S1 cell line regarded as functional for B19V entry, but internalization of the virus was strongly reduced. As an alternative B19V uptake mechanism in endothelial cells, we demonstrated antibody-dependent enhancement (ADE), with up to a 4,000-fold increase in B19V uptake in the presence of B19V-specific human antibodies. ADE was mediated almost exclusively at the level of virus internalization, with efficient B19V translocation to the nucleus. In contrast to monocytes, where ADE of B19V has been described previously, enhancement does not rely on interaction of the virus-antibody complexes with Fc receptors (FcRs), but rather, involves an alternative mechanism mediated by the heat-sensitive complement factor C1q and its receptor, CD93. Our results suggest that ADE represents the predominant mechanism of endothelial B19V infection, and it is tempting to speculate that it may play a role in the pathogenicity of cardiac B19V infection.IMPORTANCEBoth efficient entry and productive infection of human parvovirus B19 (B19V) seem to be limited to erythroid progenitor cells. However,in vivo, the viral DNA can also be detected in additional cell types, such as endothelial cells of the myocardium, where its presence has been associated with acute and chronic inflammatory cardiomyopathies. In this study, we demonstrated that uptake of B19V into endothelial cells most probably does not rely on the classical receptor-mediated route via the primary B19V receptor P antigen and coreceptors, such as α5β1integrins, but rather on antibody-dependent mechanisms. Since the strong antibody-dependent enhancement (ADE) of B19V entry requires the CD93 surface protein, it very likely involves bridging of the B19V-antibody complexes to this receptor by the complement factor C1q, leading to enhanced endocytosis of the virus.

Parvovirus Infects Cardiac Myocytes in Hydrops Fetalis

2003 ◽  
Vol 6 (5) ◽  
pp. 414-420 ◽  
Author(s):  
Aiveen O'Malley ◽  
Carole Barry-Kinsella ◽  
Caroline Hughes ◽  
Peter Kelehan ◽  
Deirdre Devaney ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Cardiac Myocytes ◽  
Cardiac Tissue ◽  
Parvovirus B19 ◽  
Negative Control ◽  
Hydrops Fetalis ◽  
Immunogold Electron Microscopy ◽  
Erythroid Precursor ◽  
Transmission Electron ◽  
Parvovirus B19 Infection

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, immunogold 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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