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PubMed1998

Presence and significance of human parvovirus B19 DNA in synovial membranes and bone marrow from patients with arthritis of unknown origin.

Acute rheumatologic symptoms are frequently associated with human parvovirus B19 (B19) infections. A nested PCR (nPCR) assay was used to test for the presence of parvovirus B19 DNA in synovial fluid and/or synovial membrane specimens obtained from a total of 90 patients with arthritis of unknown origin. Whereas only one out of 73 synovial fluid samples were found positive, 15 (16.7%) out of 90 patients had parvovirus B19 DNA in the synovium. B19 virus DNA was detected in nine bone marrow aspirates subsequently obtained from these 15 patients (60%). Whereas each one of the 15 corresponding blood samples contained anti-B19 IgG antibody, none contained anti-B19 IgM antibody and only one was positive for B19 virus DNA. The blood and synovial fluid samples that contained B19 virus DNA were obtained from the same patient, who also had B19 DNA in synovium and bone marrow. For one patient, two distinct synovial membrane specimens collected 10 months apart tested positive for B19 virus DNA. Parvovirus B19 DNA was also detected in synovial tissue of one out of nine nonarthritic patients serving as control group, who also had anti-B19 IgG circulating antibody. These data illustrate that human parvovirus B19 may persist in bone marrow and synovial tissues of patients with arthritis of unknown origin. In contrast, persistence of B19 virus DNA in synovial fluid is rare. The significance of parvovirus B19 DNA in synovium of healthy patients has to be established.

Adult↗

PubMed1997

The Simian Parvoviruses.

Autonomous parvoviruses with tropism for erythroid cells have recently been reclassified in a new genus, erythrovirus. Although B19 is the type member, and presently the only internationally accepted member of the erythrovirus genus, we have identified three new simian viruses, all of which have the molecular features of parvoviruses, and are highly tropic for erythroid progenitor cells. This review describes the identification of these new animal parvoviruses and summarises current knowledge of their molecular, clinical and epidemiological features. Most studies have been performed with the first virus discovered, simian parvovirus (SPV), which was isolated from anaemic cynomolgus monkeys. SPV is currently under investigation as an animal model for B19 parvovirus infection. Clinical similarities and molecular homology to parvovirus B19 justify the inclusion of these novel viruses as new members of the erythrovirus genus. Copyright 1997 by John Wiley & Sons, Ltd.

Journal Article↗

PubMed1986

Human parvovirus and aplastic crisis in chronic hemolytic anemias: a study of 24 observations.

From March 1984 through November 1985, 24 children and adults with aplastic crises were admitted in several Parisian hospitals. Twelve patients had known hemolytic anemia. Aplastic crisis revealed hemolytic anemia in the remaining patients. The detection of human parvovirus antigen was performed by counter-immunoelectrophoresis, and specific IgM antibodies were detected by IgM-antibody-capture-radioimmunoassay, in order to establish the incidence of human parvovirus infection in the genesis of the aplastic crisis. Twenty-one patients had acute infection with human parvovirus. In the three remaining patients, no marker of human parvovirus infection was found. The features of the human parvovirus linked aplastic crisis are described. We consider that human parvovirus infection, and unknown hemolytic anemia, must be systematically researched in any case of unexplained acute aplastic anemia.

Acute Disease↗

PubMed1996

Parvovirus B19 infection infrequently involved in children and adults with myelodysplastic syndrome.

Parvovirus B19 infection has occasionally been reported to mimic myelodysplastic syndrome (MDS) or to cause worsening of anemia in MDS. We examined the presence of parvovirus DNA in a series of children (n=19) and adults (n=39) with a diagnosis of MDS. The series of adults included only refractory anemia (RA) and RA with ring sideroblasts (RARS). Investigation for parvovirus B19 DNA in bone marrow cells was performed employing the nested form of the polymerase chain reaction (PCR). Only a 51-year-old male with RA tested positive for parvovirus DNA. Serial examinations demonstrated the disappearance of parvovirus DNA from the bone marrow. We conclude that parvovirus infection may only rarely mimic MDS or be a superimposed infection in childhood MDS or in RA and RARS in adults.

Adolescent↗

PubMed1988

Characterization of biological and antigenic properties of raccoon dog and blue fox parvoviruses: a monoclonal antibody study.

Parvovirus isolates from blue foxes and raccoon dogs were characterized by studying their haemagglutination properties, host range in vitro and antigenic structure. In all 3 characters, raccoon dog parvovirus resembled canine parvovirus (CPV), while blue fox parvovirus was similar to mink enteritis virus (MEV). Monoclonal antibodies (MAbs) were prepared against both viruses. Raccoon dog parvovirus, while resembling CPV, had a unique antigenic site which could be specified by MAbs. The pattern of MAbs prepared against blue fox parvovirus indicated that it is a member of Type 2 MEV.

Animals↗

PubMed1996

Parvovirus B19 outbreak in a rehabilitation hospital.

A nurse (index case) at a rehabilitation hospital was diagnosed with acute parvovirus B19 infection. A 2-year-old male patient was identified as the source patient. The epidemiological investigation focused on 15 individuals with symptomatic disease or risk factors for complications of parvovirus B19 infection. Serologic testing confirmed parvovirus B19 infection in the index case and source patient and identified a second health care worker who possibly contracted acute parvovirus B19 infection through nosocomial transmission. Parvovirus B19 infection can cause serious complications in pregnant women, persons with chronic hemolytic anemia, and persons with immunodeficiencies. Measures to control the transmission of parvovirus B19 infection should be part of the infection control plan at rehabilitation hospitals.

Adult↗

PubMed1983

Electron microscopic comparison of the sequences of single-stranded genomes of mammalian parvoviruses by heteroduplex mapping.

The sequence homologies among the linear single-stranded genomes of several mammalian parvoviruses have been studied by electron microscopic analysis of the heteroduplexes produced by reannealing the complementary strands of their DNAs. The genomes of Kilham rat virus, H-1, minute virus of mice and LuIII, which are antigenically distinct non-defective parvoviruses, have considerable homology: about 70% of their sequences are conserved. The homologous regions map at similar locations in the left halves (from the 3' ends) of the genomes. No sequence homology, however, is observed between the DNAs of these nondefective parvoviruses and that of bovine parvovirus, another non-defective virus, or that of defective adenoassociated virus, nor between the genomes of bovine parvovirus and adenoassociated virus. This suggests that only very short, if any, homologous regions are present. From our results, we predict an evolutionary relationship among Kilham rat virus, H-1, minute virus of mice and LuIII. It is interesting to note that, although LuIII was originally isolated from a human cell line and is specific for human cells in vitro, its genome has sequences in common only with the rodent viruses Kilham rat virus, minute virus of mice and H-1, and not with the other two mammalian parvoviruses tested.

Base Sequence↗

PubMed1986

The inactivation of a bovine enterovirus and a bovine parvovirus in cattle manure by anaerobic digestion, heat treatment, gamma irradiation, ensilage and composting.

A bovine enterovirus and a bovine parvovirus seeded into liquid cattle manure were rapidly inactivated by anaerobic digestion under thermophilic conditions (55 degrees C), but the same viruses survived for up to 13 and 8 days respectively under mesophilic conditions (35 degrees C). The enterovirus was inactivated in digested liquid manure heated to 70 degrees C for 30 min, but the parvovirus was not inactivated by this treatment. The enterovirus, seeded into single cell protein (the solids recovered by centrifugation of digested liquid manure), was inactivated by a gamma irradiation dose of 1.0 Mrad, but the parvovirus survived this dose. When single cell protein seeded with bovine enterovirus or bovine parvovirus was ensiled with cracked corn, the enterovirus was inactivated after a period of 30 days, while the parvovirus survived for 30 days in one of two experiments. Neither the enterovirus nor the parvovirus survived composting for 28 days in a thermophilic aerobic environment when seeded into the solid fraction of cattle manure. It was concluded that, of the procedures tested, only anaerobic digestion under thermophilic conditions appeared to be reliable method of viral inactivation to ensure the safety of single cell protein for refeeding to livestock. Composting appeared to be a suitable method for the disinfection of manure for use as a soil conditioner.

Anaerobiosis↗

PubMed1995

Parvovirus B19 infection in hospital workers: community or hospital acquisition?

A suspected nosocomial outbreak of parvovirus B19 infection in a maternity ward was investigated in February 1994. Questionnaires were administered and sera collected from maternity ward staff (n = 91), other ward staff in the same hospital (n = 101), and maternity ward staff at a nearby hospital (n = 81). Blood donors (n = 265) were used as community controls. Recent infection (parvovirus B19 IgM positivity) in susceptible persons (parvovirus B19 IgG-negative or IgM-positive) was common among all 4 groups (23%-30%). This high rate of recent infection occurred during a large community outbreak of fifth disease. Environmental samples collected from a room where a stillborn parvovirus B19-infected fetus was delivered were positive for parvovirus B19 DNA. Thus, this suspected nosocomial outbreak actually reflected transmission outside the hospital, but contaminated environmental surfaces were identified as one potential source for transmission of parvovirus B19.

Antibodies, Viral↗

PubMed1989

Porcine parvovirus: DNA sequence and genome organization.

We have determined the nucleotide sequence of an almost full-length clone of porcine parvovirus (PPV). The sequence is 4973 nucleotides (nt) long. The 3' end of virion DNA shows a Y-shaped configuration homologous to rodent parvoviruses. The 5' end of virion DNA shows a repetition of 127 nt at the carboxy terminus of the capsid proteins. The overall organization of the PPV genome is similar to those of other autonomous parvoviruses. There are two large open reading frames (ORFs) that almost entirely cover the genome, both located in the same frame of the complementary strand. The left ORF encodes the non-structural protein NS1 and the right ORF encodes the capsid proteins (VP1, VP2 and VP3). Promoter analysis, location of splicing sites and putative amino acid sequences for the viral proteins show a high homology of PPV with feline panleukopenia virus and canine parvoviruses (FPV and CPV) and rodent parvovirus. Therefore we conclude that PPV is related to the Kilham rat virus (KRV) group of autonomous parvoviruses formed by KRV, minute virus of mice, Lu III, H-1, FPV and CPV.

Amino Acid Sequence↗

PubMed1993

Encapsidation of a recombinant LuIII parvovirus genome by H1 virus and the fibrotropic or lymphotropic strains of minute virus of mice.

We previously constructed a recombinant LuIII parvovirus genome lacking viral coding sequences and used it to generate luciferase-transducing virions, by cotransfection of cells with a helper plasmid expressing LuIII viral proteins. Here, we describe similar cotransfections using alternative, replication-defective helpers encoding the non-structural and capsid proteins of parvovirus H1, or of either the fibrotropic or lymphotropic parvovirus strain of minute virus of mice [MVM(p) or MVM(i)]. Each cotransfection generated transducing virus which directed luciferase expression after infection of HeLa cells. The transducing activity of virus produced using either LuIII or H1 helper plasmids could be specifically neutralized by antiserum raised against the corresponding infectious virus. When the recombinant LuIII parvovirus was pseudotyped with MVM(p) or MVM(i), the resulting virions efficiently expressed luciferase after infection in human or murine cells known to be permissive for both MVM strains. The MVM(p) pseudotyped virus also expressed this reporter efficiently when infected into the murine A9 fibroblast line. In contrast, the recombinant virus generated with an MVM(i) helper gave luciferase expression that was barely detectable after infection of A9 cells which are highly restrictive for MVM(i) productive infection. These results support the notion that the allotropic determinant of these MVM strains functions through their capsid proteins. Pseudotyping of recombinant parvovirus genomes should be useful in controlling their host range as vectors, and in studying mechanisms influencing the permissiveness of parvovirus infections.

Capsid↗

PubMed2004

A parvovirus isolated from royal python (Python regius) is a member of the genus Dependovirus.

Parvoviruses were isolated from Python regius and Boa constrictor snakes and propagated in viper heart (VH-2) and iguana heart (IgH-2) cells. The full-length genome of a snake parvovirus was cloned and both strands were sequenced. The organization of the 4432-nt-long genome was found to be typical of parvoviruses. This genome was flanked by inverted terminal repeats (ITRs) of 154 nt, containing 122 nt terminal hairpins and contained two large open reading frames, encoding the non-structural and structural proteins. Genes of this new parvovirus were most similar to those from waterfowl parvoviruses and from adeno-associated viruses (AAVs), albeit to a relatively low degree and with some organizational differences. The structure of its ITRs also closely resembled those of AAVs. Based on these data, we propose to classify this virus, the first serpentine parvovirus to be identified, as serpentine adeno-associated virus (SAAV) in the genus Dependovirus.

Amino Acid Sequence↗

PubMed1987

Novel transcription map for the B19 (human) pathogenic parvovirus.

The B19 parvovirus, a small single-stranded DNA virus of 5.4 kilobases, is pathogenic in humans. B19 has remarkable specificity for erythroid progenitor cells and has been propagated in vitro only with human erythroid bone marrow. Replication of viral DNA and the viral protein products of B19 appear similar to those of other animal parvoviruses. However, B19 transcription had unusual features in comparison with that in other animal parvoviruses. At least nine overlapping poly(A)+ transcripts were identified in infected cells; all but one contained large introns. B19 differed from other parvoviruses in the initiation of all transcripts at a strong left side promoter (p6) and the absence of a functional internal promoter; the presence of short 5' leader sequences of about 60 bases and very large introns for RNAs encoded by the right side of the genome; two separate transcription termination sites, in contrast to cotermination at the far right side of the genome for other parvoviruses; the probable utilization by three transcripts of a variant polyadenylation signal (ATTAAA or AATAAC) in the middle of the genome; and the abundance of two unique transcripts from the middle of the genome which did not code for capsid proteins. The unusual transcription map of B19 suggests that regulation of the relative abundance of transcripts occurs by splicing and termination-polyadenylation events rather than by promoter strength. In combination with the published nucleotide sequence, the novel transcription map separated the pathogenic B19 virus at a molecular level from other animal parvoviruses and human adeno-associated virus.

Bone Marrow↗

PubMed1988

Analysis of the termini of the DNA of bovine parvovirus: demonstration of sequence inversion at the left terminus and its implication for the replication model.

The distribution of terminal-sequence orientations in the viral DNA of bovine parvovirus (BPV), an autonomous parvovirus, was studied by end labeling and restriction enzyme digestion and also by cloning. The left (3') end of the minus strand of BPV was found in two alternative sequence orientations (designated as flip and flop, which are reverse complements of each other), with a 10-fold excess of flip. This is in contrast to the autonomous rodent parvoviruses which encapsidate minus-strand DNA with only the flip orientation at this end. The right (5') end of the minus strand of BPV contained both sequence orientations with equal frequencies, as in the rodent parvoviruses. Sequence inversions were also detected at both ends of the plus strand, which makes up about 10% of the encapsidated BPV DNA. Each terminus of BPV DNA had a characteristic ratio of flip to flop forms, and this ratio was restored in the progeny DNA resulting from transfection with genomic clones of different defined terminal conformations. Replicative-form DNA showed the same distribution of terminal-sequence orientations as the reannealed plus and minus virion DNAs, suggesting that the distribution of flip and flop forms observed in virion DNA is not due to selective encapsidation, but rather to the specific distribution of replicative forms. The current replication model for autonomous parvoviruses, which was based on the available data for the rodent parvoviruses, cannot account for the observed distribution of BPV DNA. An alternative model is suggested.

Animals↗

PubMed1990

Susceptibility of human cells to killing by the parvoviruses H-1 and minute virus of mice correlates with viral transcription.

Human fibroblasts and epithelial cells differing in their susceptibility to killing by the autonomous parvoviruses H-1 and minute virus of mice were compared for their capacity to express viral mRNAs and proteins. The transition from a parvovirus-resistant to a parvovirus-sensitive phenotype correlated with a proportional increase in the production of the three major viral transcripts and of structural and nonstructural proteins. In contrast, cell sensitization to parvovirus could not be correlated with detectable changes in virus uptake, intracellular localization of gene products, stability of viral mRNAs, or phosphorylation of viral nonstructural polypeptides. Moreover, the H-1 virus-sensitive keratinocyte line studied did not sustain a greater level of viral DNA amplification than its resistant derivative. Therefore, the differential susceptibility of the human cells tested to parvovirus infection appears to be mainly controlled at the level of transcription of the viral genome. Parvoviral gene expression could not be elevated by increasing the input multiplicity of infection in either of the cell systems analyzed. Together, these data suggest that a cellular factor(s) regulating parvoviral transcription may be modulated by oncogenic transformation or by differentiation, as both features have been shown to affect cell susceptibility to parvoviruses.

Capsid↗

PubMed1999

Activation of promoter P4 of the autonomous parvovirus minute virus of mice at early S phase is required for productive infection.

Autonomous parvoviruses are tightly dependent on host cell factors for various steps of their life cycle. In particular, DNA replication and gene expression of the prototype strain of the minute virus of mice (MVMp) are closely linked to the onset of host cell DNA replication, pointing to the involvement of an S-phase-specific cellular factor(s) in parvovirus multiplication. The viral nonstructural protein NS-1 is absolutely required for parvovirus DNA replication and is able to transcriptionally regulate parvoviral and heterologous promoters. We previously showed that the promoter P4, which directs the transcription unit encoding the NS proteins, is activated at the onset of S phase. This activation is dependent on an E2F motif in the proximal region of promoter P4. An infectious MVM DNA clone was mutated in the E2F motif of P4. The wild type and the E2F mutant derivative were tested for their ability to produce progeny viruses after transfection of permissive cells. In the context of the whole MVMp genome, the E2F mutation abolished P4 induction in S phase and inactivated the infectious molecular clone, which failed to become amplified and generate progeny particles. The virus could be rescued when NS proteins were supplied in trans, showing that P4 hyperactivity in S is needed to reach a level of NS-1 expression that is sufficient to drive the viral replication cycle. These data show that E2F-mediated P4 activation at the early S phase is a limiting factor for parvovirus production. The primary barrier to parvovirus gene expression in G1 is thought to be promoter formation rather than activation, due to the poor conversion of the parental single-strand genome to a duplex form. The S dependence of P4 activation may therefore be a sign of the virus adaptation to life in the S-phase host cell. If the conversion block in G1 were to be leaky, the S induction of promoter P4 could be envisioned as a safeguard against the production of toxic NS proteins until cells reach the S phase and provide the full machinery for parvovirus replication.

Animals↗

PubMed1984

Detection of antibodies to human parvovirus in erythema infectiosum (fifth disease).

Two Japanese outbreaks of erythema infectiosum were investigated for evidence of human parvovirus infection by a solid phase antibody capture radioimmunoassay based on a monoclonal antibody to human parvovirus. Specific IgM and high concentrations of specific IgG were detected in 37 sera from 27 children with erythema infectiosum. No anti human parvovirus IgM was detected in a remaining case of erythema infectiosum, in five patients with Kawasaki disease, or in the 17 control children. Seven of the controls were also anti human parvovirus IgG negative, and the 10 who were seropositive had lower concentrations of anti human parvovirus IgG than the patients with erythema infectiosum. These data indicate that human parvovirus is a cause of erythema infectiosum.

Antibodies, Viral↗

PubMed1989

Immune response to B19 parvovirus and an antibody defect in persistent viral infection.

B19 parvovirus has been shown to persist in some immunocompromised patients, and treatment with specific antibodies can lead to decreased quantities of circulating virus and hematologic improvement. A defective immune response to B19 parvovirus in these patients was shown by comparison of results using a capture RIA and immunoblotting. In normal individuals, examination of paired sera showed that the dominant humoral immune response during early convalescence was to the virus major capsid protein (58 kD) and during late convalescence to the minor capsid species (83 kD). In patients with persistent parvovirus infection, variable titers against intact particles were detected by RIA, but the sera from these patients had minimal or no IgG to capsid proteins determined by Western analysis. Competition experiments suggested that this discrepancy was not explicable on the basis of immune complex formation alone and that these patients may have a qualitative abnormality in antibody binding to virus. In neutralization experiments, in which erythroid colony formation in vitro was used as an assay of parvovirus activity, sera from patients with poor reactivity on immunoblotting were also inadequate in inhibiting viral infectivity. A cellular response to purified B19 parvovirus could not be demonstrated using proliferation assays and PBMC from individuals with serologic evidence of exposure to virus. These results suggest that production of neutralizing antibody to capsid protein plays a major role in limiting parvovirus infection in man.

Acquired Immunodeficiency Syndrome↗