Acute parvovirus B19 infection associated with fulminant hepatitis of favourable prognosis in young children

Sokal, Étienne; Melchior, Marie; Cornù, C.; Vandenbroucke, Anne-Thérèse; Buts, Jean Paul; Cohen, B. J.; Burtonboy, Guy

doi:10.1016/s0140-6736(98)06165-0

Cited by 113 publications

(67 citation statements)

References 13 publications

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“…The results obtained for case 3 corroborate other data providing evidence that parvovirus B19 may be a cause of hepatic dysfunction by mechanisms that are not yet elucidated (3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Some authors suggest a direct effect of parvovirus B19 infection after interaction with its cellular receptors, the erythrocyte P antigens, which are present on erythroid and liver cells (29).…”

Section: Discussionsupporting

confidence: 85%

“…Liver dysfunctions associated with parvovirus B19 have been described by several authors, especially involving acute hepatitis cases (3)(4)(5)(6)(7)(8)(9)(10)(11)(12), and the transmission of parvovirus B19 to patients with liver diseases has possibly led to exacerbations of disease in patients with cirrhosis (13) and liver transplant (14).…”

Section: Introductionmentioning

confidence: 99%

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Detection of human parvovirus B19 in a patient with hepatitis

Pinho

Alves

Vieira

et al. 2001

Braz J Med Biol Res

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Parvovirus B19 has been associated by some investigators with cases of severe hepatitis. The aim of the present study was to determine the presence of active parvovirus B19 infection among 129 Brazilian patients with non-A-E hepatitis. The patients were assayed for antibodies against parvovirus B19, IgM class, by ELISA. In IgM-positive cases, parvovirus B19 DNA was assayed by PCR in serum and liver tissue and parvovirus VP1 antigen in liver tissue was assayed by immunohistochemistry. Antibodies against parvovirus B19, IgM class, were detected in 3 (2.3%) of 129 patients with non-A-E hepatitis. Previous surgery and blood transfusions were reported by these 3 patients. One patient was a 56-year-old female with severe hepatitis, with antimitochondrial antibody seropositivity and submassive necrosis at liver biopsy, who responded to corticosteroid therapy. Strong evidence for active parvovirus B19 infection was found in this patient, with parvovirus B19 DNA being detected by PCR in liver tissue. Furthermore, parvovirus VP1 antigen was also detected in liver tissue by immunohistochemistry. The other two IgM-positive patients were chronic hepatitis cases, but active infection was not proven, since neither viral DNA nor antigen were detected in their liver tissues. This and other reports suggest a possible relation between parvovirus B19 infection and some cases of hepatitis.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Detection of human parvovirus B19 in a patient with hepatitis

Pinho

Alves

Vieira

et al. 2001

Braz J Med Biol Res

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“…Interestingly, previous studies have indicated that that B19V can infect immortalized human microvascular endothelial cells and the human hepatocyte cell line HepG2 (18,45), which might play a role in B19V infection-caused myocarditis (4,6) and fulminant hepatitis (5,23,41,48), respectively. EpoR is detectable on endothelial cells (35) and on hepatocytes (44), which may explain the B19V permissiveness of these cells under certain conditions.…”

Section: Discussionmentioning

confidence: 99%

Role of Erythropoietin Receptor Signaling in Parvovirus B19 Replication in Human Erythroid Progenitor Cells

Chen

Guan

Lou

et al. 2010

J Virol

123

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Parvovirus B19 (B19V) infection is highly restricted to human erythroid progenitor cells. Although previous studies have led to the theory that the basis of this tropism is receptor expression, this has been questioned by more recent observation. In the study reported here, we have investigated the basis of this tropism, and a potential role of erythropoietin (Epo) that EpoR signaling is absolutely required for B19V replication in ex vivo-expanded erythroid progenitor cells after initial virus entry and at least partly accounts for the remarkable tropism of B19V infection for human erythroid progenitors.Parvovirus B19 (B19V) is pathogenic to humans. It replicates autonomously and belongs to the genus Erythrovirus in the family Parvoviridae (14). Clinical manifestations of B19V infection vary among different health conditions. The most common manifestation is erythema infectiosum. However, B19V infection often results in bone marrow failure under the following conditions (9, 10, 62). In patients with increased destruction of erythrocytes and a high turnover of erythrocytes (e.g., sickle cell disease patients), acute B19V infection can cause transient aplastic crisis. In immunocompromised patients, persistent B19V infection may develop manifestations as pure red-cell aplasia, a chronic anemia. Moreover, B19V fetal infection can cause severe anemia in the fetus, resulting in nonimmune hydrops fetalis and fetal death (1,2,16,47,57).Erythropoiesis is the process whereby a fraction of primitive multipotent hematopoietic stem cells (CD34 ϩ ) commit to the erythroid lineage, forming burst-forming units-erythroid (BFU-E; earlier erythroid progenitor) cells, CFU-erythroid (CFU-E; later erythroid progenitor) cells, normoblasts, erythroblasts, reticulocytes, and ultimately, mature erythrocytes. B19V infection shows a remarkable tropism for BFU-E and CFU-E progenitors in human bone marrow and fetal livers. Notably, both cell types express the cell surface marker CD36 (30,39,50,60). The clinical manifestations of B19V infection seen in both aplastic crisis and pure red-cell aplasia are direct outcomes of cell death of the erythroid progenitors that are targets of B19V replication, and this cell death is due to direct cytotoxicity of the virus infection (9, 13). Progressive host cell apoptosis has been observed during B19V infection of erythroid progenitor cells (29,49,60), and this is likely induced during infection of the abundantly expressed 11-kDa nonstructural protein of the virus (12). Apoptosis of erythroid progenitor cells is also characteristic of B19V-induced hydrops fetalis (60).Polyadenylation at the proximal site [(pA)p], which is located in the center of the B19V genome, precludes the inclusion of the capsid-encoding open reading frame (ORF) in transcripts under some conditions (38,61). We have recently shown that replication of the B19V genome enhances readthrough of the (pA)p and, thereafter, the polyadenylation of B19V transcripts at the distal site. Therefore, replication of the B19V genome facilitates the p...

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“…Parvovirus B-19 infection leads to transient erythroid aplasia, induces severe AA, and only rarely causes hepatitis. 23,32,33 HIV infection is frequently associated with varying degrees of cytopenia and in rare cases hepatitis. The marrow is often cellular, but occasional cases of AA have been reported.…”

Section: Discussionmentioning

confidence: 99%

Lack of known hepatitis virus in hepatitis-associated aplastic anemia and outcome after bone marrow transplantation

Safadi

Ilan

et al. 2001

Bone Marrow Transplant

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Summary:Viral infection has been shown to induce aplastic anemia, unidentified types of hepatitis being the most common cause for aplastic anemia-associated viral hepatitis. The survival rate for this group of patients after bone marrow transplantation with stem cells from an HLAmatched sibling is not well known. The aim of this study was to determine the prevalence of hepatitis G virus (HGV) and transfusion transmitted virus (TTV) infection in non-A, non-B, non-C hepatitis associated-aplastic anemia (HAAA) patients, and to define the role of bone marrow transplantation (BMT) as a therapeutic modality for this disease.

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Acute parvovirus B19 infection associated with fulminant hepatitis of favourable prognosis in young children

Cited by 113 publications

References 13 publications

Detection of human parvovirus B19 in a patient with hepatitis

Detection of human parvovirus B19 in a patient with hepatitis

Role of Erythropoietin Receptor Signaling in Parvovirus B19 Replication in Human Erythroid Progenitor Cells

Lack of known hepatitis virus in hepatitis-associated aplastic anemia and outcome after bone marrow transplantation

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