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PubMed1995

An epidemic of aplastic crisis caused by human parvovirus B19.

Human parvovirus B19 has been associated with several diseases. Aplastic crisis in patients with chronic hemolytic anemia, erythema infectiosum, hydrops fetalis and arthritis are among the common diseases caused by this virus infection. In the period between July, 1991, and March, 1992, 48 patients with aplastic crises were hospitalized at Saudi Aramco-Dhahran Health Center, Dhahran, Saudi Arabia. Forty-six patients had homozygous sickle cell disease, one had hemoglobin H disease and one had hereditary elliptocytosis. Evidence of recent human parvovirus infection was present in 91% of the cases. Leukopenia was present in 21%, neutropenia in 27% and thrombocytopenia in 42%. This differs from previous reports in which red blood cell aplasia causing anemia was the only hematologic finding reported in most patients. There were no cases of erythema infectiosum in either the patients or the community during the epidemic and the reason for this phenomenon is not obvious. The almost limited occurrence of aplastic crisis in patients with sickle cell disease in a population with a high incidence of other types of chronic hemolytic anemias is of interest.

Adolescent↗
PubMed1996

B19 parvovirus infection and transient aplastic crisis in a child with sickle cell anemia.

Transient aplastic crisis is reported in a young child with sickle cell anemia with acute B19 parvovirus infection. She also developed acute chest syndrome and bone marrow/bone infarction involving the right ilium. The clinically unsuspected bone marrow infarction in this patient may have contributed to acute chest syndrome secondary to pulmonary fat embolism. Transient cessation of erythropoiesis as a result of B19 parvovirus infection, and not the localized bone marrow infarction, was the probable cause of reticulocytopenia and worsening of anemia in this child.

Acute Disease↗
PubMed2005

Persistent parvovirus-associated chronic fatigue treated with high dose intravenous immunoglobulin.

We report a 16-year-old boy with no evidence of immunodeficiency who had a 2-year history of chronic fatigue, low grade fever and slapped-cheek rash associated with chronic parvovirus B19 viremia. Prolonged intravenous immunoglobulin therapy resulted in resolution of his symptoms and viremia. Intravenous immunoglobulin may be useful in the resolution of parvovirus viremia regardless of immune status.

Adolescent↗
PubMed2003

Detection of parvovirus B19 capsid proteins in lymphocytic cells in synovial tissue of autoimmune chronic arthritis.

The pathogenic influence of viral agents in chronic inflammatory joint diseases like rheumatoid arthritis has been discussed for many years. More recently, DNA of several viruses, among them parvovirus B19 (B19), was traceable by PCR analysis in synovial fluid and synovial tissue. To investigate the potential role of parvovirus B19 in rheumatoid arthritis, we analyzed the expression of B19 VP1/VP2 proteins by immunohistochemistry in paraffin sections of 63 synovial specimens in rheumatoid arthritis (RA; n = 29), psoriatic arthritis (PSA; n = 6), nonspecific arthritis or synovitis (n = 26), and normal synovia (n = 2). Thereby we could demonstrate replicative virus infection in a variable number of cells in about 90% of rheumatoid specimens and in four of six (66%) cases of psoriatic arthritis, but only in 38% of cases with chronic reactive inflammation and one case of normal synovia. In virus-positive rheumatoid specimens, moreover, the average number of affected cells was significantly higher than in virus-expressing synovia of nonspecific reactive inflammation. These findings support the importance of B19-viral infection in the pathogenesis of chronic arthritis. B19-positive cells in the synovia could be ascribed to CD20- or CD3-positive B- or T-lymphocytes by double immunostaining. Based on these results, B19 infection of lymphocytic cells also seems possible.

Arthritis↗
PubMed2001

Lymphocyte recognition of human parvovirus B19 non-structural (NS1) protein: associations with occurrence of acute and chronic arthropathy?

Immune recognition of recombinant parvovirus B19 non-structural (rNS1) protein was studied by immunoblot and lymphoproliferative assays in blood from the following B19 seropositive groups: B19 infected (n = 14), B19 exposed but non-infected (n = 16), other illness with rash (n = 3), chronic arthropathy of unknown aetiology (n = 4) and healthy controls (n = 7). Sera from 11 B19 seronegative subjects were also studied. Sera collected at initial diagnosis or at the time of accidental B19 exposure in pregnancy were tested for NS1 antibody and evidence of B19 DNA by nested PCR. Follow-up specimens were obtained 3-12 months later for serological, PCR and proliferation studies. B19 DNA was detected sporadically in early specimens and in one follow-up specimen from a subject who developed chronic arthropathy after B19 infection. There was no correlation with development of arthropathy. NS1-specific IgG was detected in early sera from B19-infected and exposed subjects but to a lesser degree in follow-up specimens, and in only one healthy control serum. No correlation with the presence of NS1-specific antibodies was found with development of acute or chronic arthropathy. Although lymphocyte proliferation in response to stimulation with rNS1 in vitro occurred at a higher frequency in patients who developed acute and chronic joint manifestations after B19 infection, suggesting an association with this outcome, NS1-reactive lymphocytes were also found in three B19 seronegative patients, two of whom had recently been exposed to B19 but had no illness. Hence, immune recognition of NS1 may be more indicative of recent infection with, or exposure to, parvovirus B19 than associated with development of arthropathy as previously reported.

Adult↗
PubMed1992

In vitro culture for the detection of infectious human parvovirus B19 and B19-specific antibodies using foetal haematopoietic precursor cells.

The inability to culture human parvovirus B19 in standard cell lines has rendered investigation of clinical samples for the presence of infectious virus problematic. Using haematopoietic precursors derived from first trimester foetal liver as targets for infection, and non-isotopic in situ hybridization to detect intracellular viral DNA, we have assessed infectivity in stored serum samples taken from nine volunteers at different stages following intranasal inoculation with parvovirus B19. Infectious virus was detected as early as 3 days after inoculation, the cessation of infectivity correlating with the rise in specific IgM. In all but two samples, infectivity correlated with the detection of B19 DNA by dot-blot hybridization, although in vitro culture was 10-fold more sensitive than dot-blot hybridization. B19 DNA was detected by the polymerase chain reaction in serum from one volunteer up to 36 days after inoculation, although samples containing specific antibody were non-infectious. Infection of erythroid precursors was completely inhibited by preincubation of virus with serum containing high titre B19-specific IgM and IgG. Unexpectedly, this was associated with a strong B19 DNA hybridization signal within the cytoplasm of phagocytic macrophages. This culture and detection system is a rapid and sensitive means of detecting infectious virus in serum samples, and of assessing the neutralizing ability of B19-specific antibodies.

Antibodies, Viral↗
PubMed1992

Non-permissiveness of synovial membrane cells to human parvovirus B19 in vitro.

The ability of cultured human synovial cells derived from synovial membrane and cartilage to support the replication of human parvovirus B19 was assessed. No viral DNA synthesis nor viral antigens were detected suggesting that B19 virus is not capable of replicating in synovial cells. The significance of this finding in relationship to the pathogenesis of parvovirus arthritis is discussed.

Bone Marrow↗
PubMed1992

Haemagglutination by parvovirus B19.

Human parvovirus B19 is a member of the autonomous parvoviridae but in contrast to other members of the genus has not been shown to agglutinate red blood cells. We now report that the virus agglutinates red cells of primate origin, though with plasma-derived virus this activity is masked by the presence of an IgM-like inhibitor. This observation is consistent with the presence on the erythroid precursor target cell of a specific receptor for parvovirus B19.

Animals↗
PubMed1994

Differential transcription, without replication, of non-structural and structural genes of human parvovirus B19 in the UT7/EPO cell as demonstrated by in situ hybridization.

Erythroid progenitor cells are the main target for B19 parvovirus infection. The UT7 cell line demonstrates a marked erythroid differentiation on induction by erythropoietin (EPO) (UT7/EPO cells) and therefore appears to be a potential target for B19 parvovirus. We aimed to evaluate the presence and localization of B19 nucleic acids in UT7/EPO cells by in situ hybridization. Three digoxigenin-labelled probes were used: two recognized specifically the non-structural region of the B19 genome and one probe was structural region-specific. In our experiment UT7/EPO cells were not permissive to B19 infection. Transcription led to nonstructural and structural gene transcripts without DNA replication or capsid protein synthesis.

Base Sequence↗
PubMed1995

Immunogenicity of poliovirus B and T cell epitopes presented by hybrid porcine parvovirus particles.

We have analysed the potential capacity of hybrid porcine parvovirus (PPV) capsids to present foreign epitopes to the immune system. Foreign sequences were introduced into the N and C termini of PPV VP2, which was previously shown to assemble spontaneously into parvovirus-like particles. The integrity of the C terminus was shown to be essential for preserving the structure of the capsid and therefore could not be used for epitope fusion. In contrast, insertion of sequences corresponding to T and B cell poliovirus epitopes in the N terminus did not alter the formation of particles. Moreover, the chimeric capsids containing the C3:T epitope were able to induce a T cell response in vivo. However, hybrid particles containing the C3:B epitope fused to the N terminus did not induce any peptide-specific antibody response, suggesting that the inserted B cell epitope was not exposed at the surface of the particles. These results show that the N terminus in PPV empty capsids is not an adequate site for insertion of B cell epitopes, but may be useful for T cell epitope presentation and suggest that the N terminus is located in an internal position.

Animals↗
PubMed1996

Differential expression in human cells from the p6 promoter of human parvovirus B19 following plasmid transfection and recombinant adeno-associated virus 2 (AAV) infection: human megakaryocytic leukaemia cells are non-permissive for AAV infection.

Expression from the human parvovirus B19p6 promoter fused to the firefly luciferase ('Luc') reporter gene was evaluated in a non-erythroid human nasopharyngeal carcinoma cell line, KB, and a human megakaryocytic leukaemia cell line, MB-02, known to become permissive for B19 replication following erythroid-differentiation. The B19p6-Luc construct was introduced into KB and MB-02 cells, both in undifferentiated and differentiated states, either via DNA-mediated transfection, or via infection with recombinant adeno-associated virus 2 (AAV), a non-pathogenic human parvovirus known to possess a broad host-range. Although Luc activity was readily detected in KB cells following transfection of the B19p6-Luc plasmid DNA, no expression from the B19p6 promoter was observed following infection with recombinant virus. In addition, transfection of the reporter plasmid resulted in high-level expression of Luc in differentiated but not in undifferentiated MB-02 cells. However, no Luc activity was detected, even in differentiated MB-02 cells, following infection with recombinant virus. Further studies with an additional recombinant as well as wild-type (wt) AAV revealed that MB-02 cells were non-permissive for AAV infection. A second human megakaryocytic leukaemia cell line, M07e, was likewise resistant to infection by recombinant as well as wt AAV. Taken together, these studies identify the first human cell type that cannot be infected by AAV. They indicate that expression from the B19p6 promoter, in the context of an AAV genome, is restricted to primary human haematopoietic cells, perhaps because parvoviral DNA replication and transcription are intrinsically coupled.

Cell Differentiation↗
PubMed1996

Sequence variability among different parvovirus B19 isolates.

Parvovirus B19 is the causative agent of a variety of clinical manifestations, ranging from asymptomatic to severe infection. The basis for this complex pattern of B19-associated diseases is as yet poorly understood. In general there are two different possibilities: firstly, the infected individuals may have a genetic or acquired predisposition, which renders them susceptible for a certain course of infection; secondly, differences in the B19 genome may result in different outcomes of infection. In order to investigate this second possibility we have partially sequenced the genomes of 20 different B19 isolates derived from serum samples from patients with various B19-associated diseases. Four distinct regions, which cover nearly half of the genome and include parts of the coding regions of all three major B19 proteins-NS1, VP1 and VP2, were selected for sequencing. Comparisons between the different extracted virus isolates at the DNA and protein levels revealed that isolates from patients with persistent parvovirus B19 infection show a tendency towards higher genome variability with respect to isolates derived from persons with acute infection.

Base Sequence↗
PubMed1997

Tropic determinant for canine parvovirus and feline panleukopenia virus functions through the capsid protein VP2.

Canine parvovirus (CPV) can productively infect canine and feline cell lines whereas feline panleukopenia virus (FPV) is restricted to the latter. The major determinants of tropism are two amino acids in the sequence shared by the capsid proteins, VP1 and VP2. We have shown that a rodent parvovirus-derived transducing genome, containing the luciferase reporter, can be packaged by VP1 and VP2 from separate helper sources. Canine A72 cells and feline CFK cells were transduced with recombinant virions generated using VP1 and VP2 combinations from CPV and FPV. Both VP1 and VP2 were necessary for production of transducing virions. Efficient transduction of A72 cells required VP2 of CPV. Therefore, the capsid determinants of tropism for CPV and FPV are in VP2, although a source of VP1 is also necessary to produce infectious particles. The results extend similar observations on the tropic determinants of different strains of minute virus of mice.

Animals↗
PubMed1998

No evidence for a role of modified live virus vaccines in the emergence of canine parvovirus.

In this study the early evolution and potential origins of canine parvovirus (CPV) were examined. We cloned and sequenced the VP2 capsid protein genes of three German CPV strains isolated in 1979-1980, as well as two feline panleukopenia virus (FPV) vaccine viruses that were previously shown to have some restriction enzyme cleavage sites in common with CPV. Other partial VP2 gene sequences were obtained by amplifying CPV DNA from paraffin-embedded tissues of dogs which were early parvovirus disease cases in Germany in 1978-1979. Sequences were analysed with respect to their evolutionary relationships to other CPV and FPV isolates. Those analyses did not support the hypothesis that CPV emerged as a variant of an FPV vaccine virus. Neither did they reveal ancestral sequences among the very early CPV isolates examined. Other possible sources for the origin of CPV are examined, including the involvement of viruses from wild carnivores.

Animals↗
PubMed1998

Binding of bovine parvovirus to erythrocyte membrane sialylglycoproteins.

Bovine parvovirus (BPV), an autonomous parvovirus, haemagglutinates human type O erythrocytes and infects certain bovine cells in culture. Little is known about the receptor to which it attaches, either on nucleated host cells or on erythrocytes. Haemagglutination assays and radiolabelled virus-binding tests measuring the effects of trypsin, chymotrypsin, neuraminidase, phospholipase C and sodium periodate on attachment of BPV to receptors indicated that BPV interacted with N-acetylneuraminic acid-containing (sialyl) glycoproteins. SDS-polyacrylamide gel separation of erythrocyte ghost proteins and virus overlay protein-binding revealed BPV binding to glycophorin A. Confirmation testing showed BPV binding to purified glycophorin A on dot blots and on gels containing membrane glycophorin A and purified glycophorin A. Further, in competition assays, purified glycophorin A completely inhibited the BPV haemagglutination reaction. The results of this study indicate that BPV binds to sialated membrane glycoproteins, one of which is the major erythrocyte membrane glycoprotein, glycophorin A.

Animals↗
PubMed2001

The VP1-unique region of parvovirus B19: amino acid variability and antigenic stability.

The unique region of structural protein VP1 of parvovirus B19 (erythrovirus B19) is important for eliciting neutralizing antibodies that are responsible for eliminating the virus from the peripheral blood and for inducing lifelong immunity. Neutralizing human MAbs bind a conformationally defined epitope spanning VP1 residues 30-42. The DNA sequence encoding the VP1-unique region was determined in parvovirus B19 isolated from peripheral blood and amniotic fluid of nine acutely infected pregnant women, five arthritis patients and two chronically infected children. The amino acid sequences of the VP1-unique region exhibited higher variability in comparison with other B19-specific proteins. To analyse the influence of amino acid variations on antibody binding and protein conformation, two variants of the VP1-unique region were selected and expressed in E. coli as intein-fusion proteins. The selected variants displayed a number of amino acid exchanges in the VP1-unique region and had mutations in the determined epitope and adjacent regions. After purification via affinity chromatography, the dissociation constants K(D) of VP1-specific human MAbs interacting with the variant antigens and a viral prototype of the VP1-unique region were determined with a quartz crystal microbalance biosensor. A value of 5.4 x 10(-8) M was determined for the prototype isolate pJB; the affinity constants for the variant VP1-unique regions were similar. Comparable values were obtained for interaction of antibodies with non-infectious VP1/VP2 capsids produced by recombinant baculovirus and with B19 virions from amniotic fluid. It is concluded that the conformation of the epitope is unaffected by mutations or the environment of the VP1-unique region in virus capsids.

Amino Acid Sequence↗
PubMed2001

Analysis of canine parvovirus sequences from wolves and dogs isolated in Italy.

The VP2 genes of Italian canine parvovirus (CPV) type 2 strains isolated from dogs and wolves were sequenced and a three-dimensional model of the VP2 capsid protein was constructed. Two mutations were detected in the VP2 sequences of the Italian strains: one at residue 297 and one at residue 265. Variant 297 is the predominant CPV isolate in Europe, whereas variant 265 has never been detected before. The mutation at residue 265 causes a disruption in a G strand of the beta-barrel in the VP2 protein. Data on strains isolated from wolves demonstrated that the same strain of CPV can circulate among domestic and wild canids; therefore, this result leads us to exclude the possibility that a separate parvovirus pool exists in wild populations.

Amino Acid Sequence↗
PubMed2005

T helper cell-mediated interferon-gamma expression after human parvovirus B19 infection: persisting VP2-specific and transient VP1u-specific activity.

Human parvovirus B19 is a small non-enveloped DNA virus with an icosahedral capsid consisting of proteins of only two species, the major protein VP2 and the minor protein VP1. VP2 is contained within VP1, which has an additional unique portion (VP1u) of 227 amino acids. We determined the ability of eukaryotically expressed parvovirus B19 virus-like particles consisting of VP1 and VP2 in the ratio recommended for vaccine use, or of VP2 alone, to stimulate, in an HLA class II restricted manner, peripheral blood mononuclear cells (PBMC) to proliferate and to secrete interferon gamma (IFN-gamma) and interleukin (IL)-10 cytokines among recently and remotely B19 infected subjects. PBMC reactivity with VP1u was determined specifically with a prokaryotically expressed VP1u antigen. In general, B19-specific IFN-gamma responses were stronger than IL-10 responses in both recent and remote infection; however, IL-10 responses were readily detectable among both groups, with the exception of patients with relapsed or persisting symptoms who showed strikingly low IL-10 responses. Whereas VP1u-specific IFN-gamma responses were very strong among the recently infected subjects, the VP1u-specific IFN-gamma and IL-10 responses were virtually absent among the remotely infected subjects. The disappearance of VP1u-specific IFN-gamma expression is surprising, as B-cell immunity against VP1u is well maintained.

Adult↗