Parvovirus B19 transmitted by bone marrow

2000 ◽  
Vol 111 (2) ◽  
pp. 659-661 ◽  
Author(s):  
Erik D. Heegaard ◽  
Bodil Laub Petersen
Keyword(s):  
Bone Marrow ◽  
Parvovirus B19

Human parvovirus B19 infection in bone marrow transplantation patients

1993 ◽  
Vol 44 (3) ◽  
pp. 207-209 ◽  
Author(s):  
A. Azzi ◽  
R. Fanci ◽  
S. Ciappi ◽  
K. Zakrzewska ◽  
A. Bosi
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Marrow Transplantation ◽  
Parvovirus B19 ◽  
Human Parvovirus B19 ◽  
Parvovirus B19 Infection

scholarly journals Pure red cell aplasia caused by Parvo B19 virus in a kidney transplant recipient

2012 ◽  
Vol 52 (186) ◽  
Author(s):  
A Baral ◽  
B Poudel ◽  
R K Agrawal ◽  
R Hada ◽  
S Gurung
Keyword(s):  
Bone Marrow ◽  
Transplant Recipient ◽  
Intravenous Immunoglobulin ◽  
Kidney Transplant ◽  
Parvovirus B19 ◽  
Kidney Transplant Recipient ◽  
Pure Red Cell Aplasia ◽  
Red Cell ◽  
Erythroid Progenitor ◽  
Red Cell Aplasia

Parvo B19 is a single stranded DNA virus, which typically has affi nity for erythroid progenitor cells in the bone marrow and produces a severe form of anemia known as pure red cell aplasia. This condition is particularly worse in immunocompromised individuals. We herein report a young Nepali male who developed severe and persistent anaemia after kidney transplantation while being on immunosuppressive therapy. His bone marrow examination revealed morphological changes of pure red cell aplasia, caused by parvovirus B19. The IgM antibody against the virus was positive and the virus was detected by polymerase chain reaction in the blood. He was managed with intravenous immunoglobulin. He responded well to the treatment and has normal hemoglobin levels three months post treatment. To the best of our knowledge, this is the fi rst such case report from Nepal. Keywords: Intravenous immunoglobulin, kidney transplant recipient, Parvovirus B19, pure red cell aplasia.

Relevance of Specific Immunoglobulin M and Immunoglobulin G for Parvovirus B19 Diagnosis in Patients With Acute Lymphoblastic Leukemia Receiving Chemotherapy: Prospective Study

2007 ◽  
Vol 131 (11) ◽  
pp. 1697-1699
Author(s):  
Maysaa El Sayed Zaki
Keyword(s):  
Bone Marrow ◽  
Immune Response ◽  
Acute Lymphoblastic Leukemia ◽  
Parvovirus B19 ◽  
Lymphoblastic Leukemia ◽  
Healthy Children ◽  
Immunocompromised Patients ◽  
Humoral Immune ◽  
Specific Immunoglobulin

Abstract Context.—Immunocompromised patients suffer from prolonged viral infections often without detectable immune response. However, even if the immune response occurs, can it clear the virus completely? Objective.—To detect parvovirus B19 DNA and its antibodies in bone marrow cells and in serum by polymerase chain reaction (PCR) in children with acute lymphoblastic leukemia receiving chemotherapy to highlight the relation of humoral immune response to the presence of viremia. Also, to evaluate the optimal diagnostic test(s) for a correct diagnosis of parvovirus B19 disease in immunocompromised patients. Design.—Forty-eight children with acute lymphoblastic leukemia receiving maintenance chemotherapy were included in the study in addition to 20 healthy children with matched age and sex. Study for parvovirus B19 was performed by serologic determination of specific immunoglobulin (Ig) M and IgG, and viral DNA was determined by PCR in both serum and bone marrow aspiration. Results.—Parvovirus B19 DNA was detected in both serum and bone marrow in 20% of patients. Specific IgG was found in 40% and IgM in 26.7%. Two cases (10%) in the control group were positive for IgG. The agreement between IgG and positive results of PCR in the bone marrow was 33.3%, and the agreement for IgM and PCR in the serum was 33.3%. Conclusions.—Parvovirus B19 is considered a common viral infection in children with acute lymphoblastic leukemia receiving chemotherapy. We must use our full potential to exclude such infection, which can mimic the side effects of chemotherapy in these patients. In immunocompromised patients, there are immunologic discrepancies in humoral immune responses for both IgM and IgG between individuals with parvovirus B19 persistence and healthy individuals, findings that may reflect both failed immunity and antigenic exhaustion. The contemporaneous determination of parvovirus B19 DNA by PCR in both bone marrow and peripheral blood and specific serologic markers appears to be the most appropriate diagnostic protocol for the correct laboratory diagnosis of parvovirus B19 infection in these patients.

Ku80 autoantigen as a cellular coreceptor for human parvovirus B19 infection

Blood ◽  
2005 ◽  
Vol 106 (10) ◽  
pp. 3449-3456 ◽  
Author(s):  
Yasuhiko Munakata ◽  
Takako Saito-Ito ◽  
Keiko Kumura-Ishii ◽  
Jie Huang ◽  
Takao Kodera ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Surface ◽  
Cell Lines ◽  
Bone Marrow Cells ◽  
Parvovirus B19 ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Human Parvovirus B19 ◽  
Erythroid Cells ◽  
Interfering Rna

AbstractHuman parvovirus B19 (B19) infects human erythroid cells expressing P antigen. However, some cell lines that were positive for P antigen failed to bind B19, whereas some cell lines had an ability to bind B19 despite undetectable expression of P antigen. We here demonstrate that B19 specifically binds with Ku80 autoantigen on the cell surface. Furthermore, transfection of HeLa cells with the gene of Ku80 enabled the binding of B19 and allowed its entry into cells. Moreover, reduction of cell-surface expression of Ku80 in KU812Ep6 cells, which was a high-sensitive cell line for B19 infection, by short interfering RNA for Ku80 resulted in the marked inhibition of B19 binding in KU812Ep6 cells. Although Ku80 originally has been described as a nuclear protein, human bone marrow erythroid cells with glycophorin A or CD36, B cells with CD20, or T cells with CD3 were all positive for cell-surface expression of Ku80. B19 infection of KU812Ep6 cells and bone marrow cells was inhibited in the presence of anti-Ku80 antibody. Our data suggest that Ku80 functions as a novel coreceptor for B19 infection, and this finding may provide an explanation for the pathologic immunity associated with B19 infection.

Parvovirus B19 and Aplastic Anemia: Case Control Study: Preliminary Report from the ITESM Hematology Study Group.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3765-3765
Author(s):  
Jose R. Borbolla Escoboza ◽  
Marcos E. Garza-Madrid ◽  
Luis Villela ◽  
Manuel A. Lopez-Hernandez ◽  
Jorge Vela-Ojeda
Keyword(s):  
Bone Marrow ◽  
Aplastic Anemia ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Parvovirus B19 ◽  
Bone Marrow Failure ◽  
Control Group ◽  
Number Of Patients ◽  
Two Samples ◽  
Sense Primer

Abstract Aplastic anemia (AA) is a classic bone marrow failure syndrome simply defined as peripheral blood pancytopenia and a hypocelular bone marrow, yet the diagnosis must be made by excluding other causes of bone marrow failure. The incidence rate of AA reported by the International Aplastic Anemia and Agranulocytosis Study (IAAAS) in the 1980s was 2 cases per 1 million people. This disease is known to be caused by exposure to radiation, chemotherapy and some viral agents, yet most of the cases are idiopathic. Epstein Barr virus and non-A, non-B or non-C Hepatitis virus have classically been related to the development of some AA cases. Recently there have been some reports of AA following Parvovirus B19 (PvB19) infection. This virus, the only parvoviridae virus capable of infecting humans, attacks erythrocyte precursors attaching to the P antigen in their surface and requiring Beta1 integrin for viral entry. Although PvB19 seems to infect only erytroid precursors, it is widely recognized that the infection with this virus can cause not only anemia, but neutropenia and thrombocytopenia as well, producing aplastic crisis of varying intensity. A correlation has recently been found between PvB19 DNA in peripheral blood and AA in children. We pretend to corroborate this observation and include adult patients in order to improve our understanding of the relationship between PvB19 and AA. So far we have taken peripheral blood samples from 9 AA patients and 9 controls paired by age, sex and community; we plan to include 100 AA patients and their controls from several hospitals around Mexico. DNA was extracted using the PUREGENE DNA extraction kit (Gentra, Minneapolis MN). Nested PCR was performed using the sense primer (P1) 5-AATACACTGTGGTTTTATGGGCCG-3, antisense (P2) 5-CCATTGCTGGTTATAACCACAGGT-3 for the first round and the sense primer (P3) 5-AATGAAAACTTTCCATTTAATGATGTAG-3 and antisense primer (P4) 5-CTAAAATGGCTTTTGCAGCTTCTAC-3for the second round. A DNA sample from a patient with active infectious mononucleosis with positive IgG and IgM against PvB19 in serum was used as positive control. Two samples from the AA group (22%) and 1 from the control group (11%) have turned positive for PvB19 DNA. The reported incidence for the presence of this virusDNA in the peripheral blood of the population is 3%. We expect that, as the number of patients grows, the percentage of positive samples in the control group will decrease, while the percentage of positive samples in the AA group will rise or be sustained. Our partial results point towards a possible relationship between AA and the presence of PvB19 DNA in the peripheral blood cells. It is possible that this virus is one of many factors capable of precipitating the development of AA by limiting the bone marrows capacity to produce blood cells. We are in the process of gathering more samples to prove if a relationship really exists and, if so, future studies will likely shed light upon the mechanism by which PvB19 contributes to the development of AA and other marrow failure syndromes.

Changes in erythron peripheral component during chemotherapy in patients with malignant lymphomas and parvovirus B19 infection.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e20086-e20086
Author(s):  
Nailya K. Guskova ◽  
Tatiana A. Zykova ◽  
Irina B. Lysenko ◽  
Ekaterina A. Guskova ◽  
Anastasia S. Nozdricheva ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Viral Load ◽  
Parvovirus B19 ◽  
Microcytic Anemia ◽  
Malignant Lymphomas ◽  
Hypochromic Microcytic Anemia ◽  
Before And After ◽  
Parvovirus B19 Infection ◽  
Expected Increase ◽  
Timely Treatment

e20086 Background: The purpose of the study was to analyze changes in the erythron peripheral component during chemotherapy for malignant lymphomas in patients infected with parvovirus B19 (B19V). Methods: The study included 34 patients with lymphomas (48.7±4.3 years). B19V infection was determined by the presence of IgM/IgG antibodies to B19V in blood serum and DNA in blood plasma and bone marrow before chemotherapy (CT). Parameters of the erythron peripheral component - RBC, HGB, MCW, MCH, MCHC, RDW, PLT, RET (#), IRF, LFR, MFR, HFR (%), and myelogram were evaluated before and after CT (Sysmex XE 2100, Japan). Results: 82.5% of patients had IgG to B19V, including IgM in 11.8%. B19V DNA was detected in 23.4% of patients: in the bone marrow and blood in 11.7%, only in the bone marrow in 11.7%. The range of viral load in the bone marrow was 1435-79573 IU/ml, in the blood 2-349 IU/ml. RBC in all patients before CT was within the reference range, with a tendency to decrease in the group with B19V: 4.01±0.06×1012/L with B19V and 4.57±0.08×1012/L without B19V. Levels of HGB before CT were respectively 112±1.26 g/L and 116±1.26 g/L, decreasing after CT by 1.5 and 1.3 times (p < 0.05) depending on the viral load. MCV, MCH and MCHC varied: 78.6 – 84.8 fl, 24.9 – 28.0 pg and 314–330 g/L in the group with B19V, and 89.7–91.3 fl, 29.5–29.8 pg and 324–337 g/L, respectively, in the group without B19V, which indicates the development of hypochromic microcytic anemia. RET levels before CT in the group with B19V were 38.3±3.44×109/L, after CT – 10.6±2.7×109/L, being lower than in the group without B19V by 1.8 and 3.8 times (p < 0.001), respectively. IRF, MFR and HFR in patients with B19V before CT were 10.6±2.23%, 9.5±1.54% and 1.1±0.022%, being lower than in non-infected patients by 1.6, 1.3 and 3.6 times, respectively. After CT, the downward trend in the proportion of young fractions continued. The noted changes in the erythron peripheral unit indicated inhibition of erythropoiesis, more pronounced in patients with B19V, and were consistent with the myelogram data. Conclusions: The development of anemia without the expected increase in RET, and in particular immature forms - IRF, MFR, HFR - in patients with lymphomas and B19V infection indicates inhibition of erythropoiesis. Early manifestation of these changes allows for timely treatment correction.

Human parvovirus B19-associated disease in bone marrow transplantation

Infection ◽  
1999 ◽  
Vol 27 (2) ◽  
pp. 114-117 ◽  
Author(s):  
M. Schleuning ◽  
G. Jäger ◽  
E. Holler ◽  
W. Hill ◽  
C. Thomssen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Marrow Transplantation ◽  
Parvovirus B19 ◽  
Human Parvovirus B19

scholarly journals Parvovirus B19-induced perturbation of human megakaryocytopoiesis in vitro

Blood ◽  
1990 ◽  
Vol 76 (10) ◽  
pp. 1997-2004 ◽  
Author(s):  
A Srivastava ◽  
E Bruno ◽  
R Briddell ◽  
R Cooper ◽  
C Srivastava ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Replication ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Parvovirus B19 ◽  
Northern Analysis ◽  
Viral Dna ◽  
Viral Dna Replication ◽  
Marrow Cells

Abstract Parvovirus B19 infection leads to transient aplastic crises in individuals with chronic hemolytic anemias or immunodeficiency states. An additional unexplained sequela of B19 infection is thrombocytopenia. Because B19 is known to have a remarkable tropism for human erythropoietic elements, and is not known to replicate in nonerythroid cells, the etiology of this thrombocytopenia is uncertain. We sought to define the pathobiology of B19-associated thrombocytopenia by examining the role of B19 on in vitro megakaryocytopoiesis. B19 infection of normal human bone marrow cells significantly suppressed megakaryocyte (MK) colony formation compared with mock-infected cells. No such inhibition was observed with a nonpathogenic human parvovirus, the adeno-associated virus 2 (AAV). The B19-MK cell interaction was also studied at the molecular level. Whereas low-density bone marrow cells containing erythroid precursor cells supported B19 DNA replication, no viral DNA replication was observed in B19-infected MK-enriched fractions as determined by the presence of viral DNA replicative intermediates on Southern blots. However, analysis of total cytoplasmic RNA isolated from B19-infected MK fractions showed a low-level expression of the B19 genome as detected by quantitative RNA dot blots as well as by Northern analysis. Furthermore, a frame-shift mutation in a recombinant AAV-B19 hybrid genome segment that encodes the viral nonstructural (NS1) protein significantly reduced the observed inhibition of MK colony formation. These studies indicate tissue- tropism of B19 beyond the erythroid progenitor cell, and lend support to the hypothesis that B19 genome expression may be toxic to cell populations that are nonpermissive for viral DNA replication.

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