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PubMed1991

Self-assembled B19 parvovirus capsids, produced in a baculovirus system, are antigenically and immunogenically similar to native virions.

B19 parvovirus is pathogenic in humans, causing fifth disease, transient aplastic crisis, some cases of hydrops fetalis, and acquired pure red cell aplasia. Efforts to develop serologic assays and vaccine development have been hampered by the virus's extreme tropism for human bone marrow and the absence of a convenient culture system. We constructed recombinants containing either the major (VP2) or minor (VP1) structural proteins of B19 in a baculovirus-based plasmid, from which the polyhedrin gene had been deleted; these recombinant plasmids were used to generate recombinant infectious baculovirus. Subsequent infection of insect cells in vitro resulted in high-level expression of either B19VP1 or VP2. Parvovirus capsids were obtained by self-assembly in cell cultures coinfected with either VP1- and VP2-containing baculoviruses or, surprisingly, VP2-containing baculoviruses alone. Empty B19 capsids composed of VP1 and VP2 could replace serum virus as a source of antigen in a conventional immunoassay for detection of either IgG or IgM antiparvovirus antibodies in human serum. Immunization of rabbits with capsids composed of VP1 and VP2 resulted in production of antisera that recognized serum parvovirus on immunoblot and neutralized parvovirus infectivity for human erythroid progenitor cells. Baculovirus-derived parvovirus antigen can substitute for scarce viral antigen in immunoassays and should be suitable as a human vaccine.

Amino Acid Sequence↗

PubMed2006

Isolation and molecular characterization of a new Muscovy duck parvovirus from Muscovy ducks in the USA.

Between 1997 and 1999 several cases of a new disease in Muscovy ducks were reported in Pennsylvania, USA. The cases were characterized by locomotor dysfunction, weakness, recumbency, 40 to 60% morbidity and 10 to 40% mortality. The most characteristic microscopic lesions were moderate to severe degenerative rhabodomyopathy. In order to characterize the aetiological agent, virus isolation was attempted from the spleen, liver, heart, skeletal muscle and intestine by inoculation of 14-day-old Muscovy duck embryos with tissue homogenates. Deaths occurred on the second egg passage and parvoviruses were isolated by serial passage of allantoic fluid from dead embryos and then in Muscovy duck embryo fibroblast (MDEF) cultures. Parvovirus particles were observed in allantoic fluids and supernatants of MDEF cultures by transmission electron microscopy. Two genomic fragments, comprising 1108 nucleotides of the right open reading frame that codes for the structural viral proteins 1, 2 and 3, were amplified by polymerase chain reaction from one of the isolates, Muscovy duck parvovirus (MDPV)/PSU-31010. Comparison of this fragment with available sequences of other MDPV and related goose parvovirus (GPV) isolates showed that it had only 84.5% sequence identity with other MDPV isolates and 84.6% identity with the GPV isolates. This region shares over 99% identity among previously sequenced MDPV isolates and 95% identity among the related GPV isolates. This suggests that MDPV/PSU-31010 is divergent from all other sequenced MDPV and GPV isolates, and may represent a new group of avian parvoviruses.

Amino Acid Sequence↗

PubMed1988

Size and antigenic comparisons among the structural proteins of selected autonomous parvoviruses.

The size and antigenic relationships among structural proteins (VPs) of canine parvovirus (CPV), feline parvovirus (FPV), porcine parvovirus (PPV), minute virus of mice (MVM) and bovine parvovirus (BPV) were determined by SDS-PAGE of radiolabelled, purified virus and immunoprecipitated viral proteins. Mature virions of CPV, FPV, PPV and MVM were composed of three VPs designated VP1, VP2 and VP3. The corresponding proteins of each virus were similar in molecular weight [79,000 to 82,500 (VP1), 65,000 to 66,000 (VP2), 62,000 to 63,500 (VP3)]. Additional similarities among VPs were indicated by antigenic relationships which included precipitation of VPs of CPV, FPV and PPV by both homologous antisera and antisera raised to each of the other two viruses and by precipitation of VPs of MVM by cat anti-FPV sera. A non-structural protein identified in lysates of cells infected with FPV and CPV was precipitated by cat anti-FPV and dog anti-CPV sera only. Mature virions of BPV were composed of four VPs [74,500 (VP1), 67,000 (VP2), 60,000 (VP3), 57,500 (VP4)] which were antigenically unrelated to those of the other parvoviruses tested. However, the possibility that swine are sometimes infected with a virus which is antigenically related to BPV was suggested by the finding that sera from conventionally raised swine, irrespective of their serological status for PPV, precipitated VPs of BPV, whereas neither pre-exposure sera nor anti-PPV sera from gnotobiotic pigs did so.

Antibodies, Viral↗

PubMed1992

Canine parvovirus empty capsids produced by expression in a baculovirus vector: use in analysis of viral properties and immunization of dogs.

The VP-2 genes of canine parvovirus (CPV) and a recombinant consisting of CPV and feline panleukopenia virus (FPV) sequences were cloned into baculovirus expression vectors, fused to the baculovirus polyhedrin promoter. Recombinant baculoviruses were prepared and the properties of the parvovirus proteins expressed in insect cells examined. The proteins produced were the same size as the authentic CPV VP-2 protein, and were produced late after infection; the quantity of proteins recovered from the insect cell cultures was similar to those produced in CPV infections. Parvovirus particles formed had the haemagglutination (HA), sedimentation and buoyant density properties of authentic CPV capsids. Both the CPV capsids and the CPV-FPV recombinant capsids from the baculovirus system expressed the same epitopes as those seen in the viable parvoviruses when tested with a panel of anti-parvovirus monoclonal antibodies. Lysates of recombinant baculovirus-infected cells were inoculated into dogs, giving rise to serum neutralizing and HA-inhibiting antibodies, and the immunized dogs were protected from clinical disease upon challenge with a virulent isolate of the most recent antigenic type of CPV.

Animals↗

PubMed1992

Clinical and histopathological features of parvovirus B19 infection in the human fetus.

OBJECTIVE: To provide a comprehensive description of the clinical and histopathological features associated with parvovirus B19 infection of the human fetus. SUBJECTS: All cases of parvovirus B19-related fetal death presenting to the John Radcliffe Hospital, Oxford, over a 16 year period. Diagnosis was confirmed retrospectively by non-isotopic in situ hybridization for parvovirus B19 DNA. RESULTS: The ten cases occurred in two clusters (1979-80 and 1988-89) and presented between 15 and 29 weeks gestation. In at least three cases maternal infection was asymptomatic. Nine fetuses were grossly hydropic at necropsy. Histological features common to all cases included the presence of typical intranuclear inclusions in erythroid precursor cells and evidence of vasculitis within placental villi. Inflammatory changes were also present in the myocardium of four cases, with evidence of subendocardial fibroelastosis in three. CONCLUSIONS: Histological features of fetal parvovirus B19 infection are similar across a range of gestational ages. The heart failure and hydropic state associated with fetal parvovirus infection may be of multifactorial aetiology, and not due to fetal anaemia alone.

Adult↗

PubMed1983

The pattern of endemic parvovirus infection in four pig herds.

Serological surveys were conducted on the gilts and adult sows in 4 herds endemically infected with porcine parvovirus. The study assessed the influence of the type of management of breeders on the spread of virus infection and the influence of endemic parvovirus infection on reproductive parameters of the herd. The practice of holding gilts and sows in groups did not reliably promote infection or maintain a 100% level of active immunity amongst adult sows in 2 of 3 group husbandry herds. In the 4 herds, the prevalence of adult sows (greater than 12 months) with active immune haemagglutination inhibition titres (greater than or equal to 256) ranged between 44% and 100%, while between 0% and 100% of gilts (6 to 12 months of age) had active immune titres. Fully susceptible gilts older than 9 months of age held in groups, failed to become infected by 12 months of age on farms endemically infected with PPV. In 2 herds a continued low infection rate of gilts resulted in increasing the potential of breeding animals becoming susceptible to parvovirus infection as infected sows were replaced by noninfected gilts. In both herds, epidemics of parvovirus infection followed, which were characterised by an increase in reproductive failure. Parvovirus infection during the first 70 days of pregnancy reduced the average number of piglets born alive per litter by 1.6 piglets (p less than 0.05). This was due to the combined effect of more piglets being born dead per litter and an overall reduction in litter size.

Animals↗

PubMed1974

Porcine parvovirus: natural and experimental infections of the porcine fetus and prevalence in mature swine.

Antibodies against porcine parvovirus were detected in 17 of 116 prenursing pig sera. Antibodies against transmissible gastroenteritis or ECPO-6 (an enterovirus) were not detected in prenursing sera of the pigs tested. Seventy-seven percent of 129 serum samples from 23 Ohio farms and 82% of 96 samples from slaughter plants in Ohio were serologically positive for porcine parvovirus. Mummies or other abnormalities were not observed in newly born pigs exposed to porcine parvovirus by the transuterine route 101 days after gestation. Indirect evidence suggested that the virus had not spread to other fet uses following exposure after 101 days at least not in a sufficient amount of time to stimulate detectable antibody. Direct intrafetal exposure to porcine parvovirus (i.m. injection, transutero) after 62 days of gestation resulted in dealth and mummification of the two fetuses, and apparently in the subsequent spread of the virus, as five of nine live pigs born were serologically positive for porcine parvovirus and these five pigs had not been injected with the virus. Immunoglobulin G was detected in all newborn pigs irregardless of known antigenic stimulation or the presence of specific antibody. In general, the presence of immunoglobulin M or immunoglobulin A in fetal serum was correlated with a history of antigenic stimulation or the presence of detectable antibody.

Animals↗

PubMed1984

Aphidicolin inhibition of the production of replicative-form DNA during bovine parvovirus infection.

Since parvoviruses apparently do not possess a DNA polymerase activity, one or more of the host cell DNA polymerases must be responsible for replicating the single-stranded DNA genome. We have focused on determining which polymerase, alpha, beta, or gamma (pol alpha, pol beta, or pol gamma, respectively), is responsible for the first step in bovine parvoviral DNA replication: conversion of the single-stranded DNA genome to a parental replicative form (RF). In this study, we used aphidicolin, a specific inhibitor of DNA pol alpha, to assay for the requirement of pol alpha activity in parental RF formation in vivo. Synchronized cell cultures were infected with bovine parvovirus with or without aphidicolin, and the products of viral replication were separated on agarose gels and identified by Southern blot analysis. We found that complete inhibition of viral DNA synthesis resulted when 20 microM aphidicolin was present throughout the infection. In addition, viral DNA synthesis was inhibited by as little as 1 microM aphidicolin, whereas lower concentrations (0.1 and 0.01 microM) resulted in partial inhibition of the replication process. Using 32P-labeled bovine parvovirus as the input virus we differentiated parental RF from daughter RF and progeny DNA synthesis. We conclude that DNA pol alpha is required for the production of RF during bovine parvovirus replication in vivo and that this requirement is most likely for the conversion of bovine parvovirus input single-stranded DNA to parental RF. These results do not rule out a possible role for DNA pol gamma in the first step, nor do they rule out a role for pol alpha or pol gamma in later stages of the replication cycle.

Animals↗

PubMed1986

Nucleotide sequence and genome organization of human parvovirus B19 isolated from the serum of a child during aplastic crisis.

The nucleotide sequence of an almost-full-length clone of human parvovirus B19 was determined. Whereas the extreme left and right ends of this genomic clone are incomplete, the sequence clearly indicates that the two ends of viral DNA are related by inverted terminal repeats similar to those of the Dependovirus genus. The coding regions are complete in the cloned DNA, and the two large open reading frames which span almost the entire genome are restricted to one strand, as has been found for all other parvoviruses characterized to date. From the DNA sequence we conclude that the organization of the B19 transcription units is similar although not identical to those of other parvoviruses. In particular, we predict that the B19 genome may utilize a fourth promoter to transcribe mRNA encoding the major structural polypeptide, VP2. Analysis of the putative polypeptides confirms that B19 is only distantly related to the other parvoviruses but reveals that there is a small region in the gene probably encoding the major nonstructural protein of B19, which is closely conserved between all of the parvovirus genomes for which sequence information is currently available.

Amino Acid Sequence↗

PubMed1986

Mink parvoviruses and interferons: in vitro studies.

Although interferons can inhibit the replication of a number of viruses, little is known about their ability to inhibit parvovirus replication. Therefore, in vitro experiments were done to determine if Aleutian disease virus and mink enteritis virus, two autonomously replicating mink parvoviruses, induced interferon, were sensitive to the effects of interferon, or inhibited the production of interferon. The results indicated that these parvoviruses neither induced nor were sensitive to the effects of interferon. Furthermore, preexisting parvovirus infections did not inhibit poly(I).poly(C)-induced interferon production. This independence from the interferon system may, therefore, be a general property of the autonomously replicating parvoviruses.

Animals↗

PubMed1988

Nucleotide sequence and genomic organization of Aleutian mink disease parvovirus (ADV): sequence comparisons between a nonpathogenic and a pathogenic strain of ADV.

A DNA sequence of 4,592 nucleotides (nt) was derived for the nonpathogenic ADV-G strain of Aleutian mink disease parvovirus (ADV). The 3'(left) end of the virion strand contained a 117-nt palindrome that could assume a Y-shaped configuration similar to, but less stable than, that of other parvoviruses. The sequence obtained for the 5' end was incomplete and did not contain the 5' (right) hairpin structure but ended just after a 25-nt A + T-rich direct repeat. Features of ADV genomic organization are (i) major left (622 amino acids) and right (702 amino acids) open reading frames (ORFs) in different translational frames of the plus-sense strand, (ii) two short mid-ORFs, (iii) eight potential promoter motifs (TATA boxes), including ones at 3 and 36 map units, and (iv) six potential polyadenylation sites, including three clustered near the termination of the right ORF. Although the overall homology to other parvoviruses is less than 50%, there are short conserved amino acid regions in both major ORFs. However, two regions in the right ORF allegedly conserved among the parvoviruses were not present in ADV. At the DNA level, ADV-G is 97.5% related to the pathogenic ADV-Utah 1. A total of 22 amino acid changes were found in the right ORF; changes were found in both hydrophilic and hydrophobic regions and generally did not affect the theoretical hydropathy. However, there is a short heterogeneous region at 64 to 65 map units in which 8 out of 11 residues have diverged; this hypervariable segment may be analogous to short amino acid regions in other parvoviruses that determine host range and pathogenicity. These findings suggested that this region may harbor some of the determinants responsible for the differences in pathogenicity of ADV-G and ADV-Utah 1.

Aleutian Mink Disease Virus↗

PubMed1990

Mutation of lysine 405 to serine in the parvovirus H-1 NS1 abolishes its functions for viral DNA replication, late promoter trans activation, and cytotoxicity.

A consensus sequence in parvovirus nonstructural protein NS1 has been predicted to be an ATP-binding domain associated with an ATPase and a DNA helicase activity. To investigate the function of NS1 in viral gene expression, a site-directed mutagenesis converting NS1 lysine 405 to serine in parvovirus H-1 was carried out by the polymerase chain reaction. As shown previously, a parvovirus genome containing a deleted NS1 gene was excised from a bacterial plasmid and replicated when a wild-type NS1 gene was provided in trans but failed to be excised and replicate when the mutant NS1 gene was supplied. Interestingly, the serine 405 mutation totally lost the activity of trans activation on the virus late promoter (P38) in a chloramphenicol acetyltransferase (CAT) assay and it lost evidence for cytotoxicity in two tumor cell lines (HeLa Gey and NB324K). The serine 405 NS1 protein was translocated normally to the nucleus. These results suggest that the NS1 lysine 405 of H-1 in its putative purine nucleotide-binding site is essential for viral DNA replication and that this domain may be involved in the regulation of the P38 promoter by an unknown mechanism. The loss of NS1 cytotoxicity on tumor cells suggests that NS1 expression is the major cause of cell killing by parvoviruses, which may facilitate further study of the mechanism of oncosuppression by parvoviruses.

Capsid↗

PubMed2003

Long term follow up of serostatus after maternofetal parvovirus B19 infection.

BACKGROUND: Maternofetal parvovirus B19 infection may result in fetal hydrops or abortion. Chronic infection has been associated with long term complications (polyarthritis, persistent aplastic anaemia, hepatitis). In pregnancy maternal immunosuppression caused by a TH2 dominant response to viral antigens has been observed. There is little information on long term reactivity to intrauterine infection. AIMS: To assess the serological status in children and their mothers after maternofetal parvovirus B19 infection and development of fetal hydrops. METHODS: A total of 18 children and their mothers, and 54 age matched control infants were studied. Main outcome measures were parvovirus B19 DNA, specific IgM and IgG against the virus proteins VP1/VP2, and NS-1 in venous blood. RESULTS: Parvovirus B19 DNA and antiparvovirus B19 (IgM) were undetectable in all sera. A significant larger proportion of maternal sera compared to study children's sera contained IgG against the non-structural protein NS-1. Mean levels of VP1/VP2 IgG antibodies were significantly lower in the children than in their mothers (48 (36) v 197 (95) IU/ml). There was no history of chronic arthritis in mothers and children. Five women had subsequent acute but transient arthritis postpartum, which was not correlated with antibodies against NS-1. CONCLUSIONS: Serological evidence of persistent infection after maternofetal parvovirus B19 disease could not be detected. Increased maternal prevalence of anti NS-1 (IgG) and increased levels of antiparvovirus B19 (IgG) may reflect prolonged viraemia compared to fetal disease.

Antibodies, Viral↗

PubMed1988

Parvovirus as a cause of hydrops fetalis: detection by in situ DNA hybridisation.

Lung tissue from 13 cases of unexplained non-immunological hydrops fetalis was examined by in situ hybridisation to detect parvovirus. Four specimens contained parvovirus DNA in cells in the blood vessel lumina and alveoli. Twenty six control cases were negative for parvovirus DNA. As there was no known epidemic of parvovirus infection during the study period, this suggests that parvovirus is a relatively common cause of non-immunological hydrops fetalis. In situ hybridisation may have a role in clinical medicine, particularly for retrospective investigations.

DNA, Viral↗

PubMed1989

Characterization of a parvovirus isolated from the diarrheic feces of a pig.

A small DNA virus was isolated from the feces of a sow with diarrhea and identified as a parvovirus on the basis of its properties. The virus replicated preferentially in cell cultures of swine origin, including primary porcine thyroid gland and kidney cell cultures in which the cytopathic effect developed. The virus agglutinated erythrocytes of guinea pig, mouse and human group O but not these of chicken. The growth of the virus was inhibited by 5-iodo-2'-deoxyuridine. The virus was resistant to ether and heating at 56 degrees C for 30 min and stable at pH 3.0. The buoyant density of the infectious particles was 1.40 g/ml in CsCl density gradient, and the virions were 27 nm in diameter by electron microscopy. The viral protein seemed to be separated into four polypeptides with molecular weights of 81k, 70k, 66k and 62k daltons respectively. Cross serum neutralization test demonstrated that the virus was antigenically different from porcine parvovirus as well as bovine and canine parvoviruses. These findings and the survey on neutralizing antibody distribution indicated indirectly that another parvovirus which could be antigenically distinguished from well-known porcine parvovirus had been widespread among swine in Japan.

Animals↗

PubMed1990

Persistent B19 parvovirus infection in patients infected with human immunodeficiency virus type 1 (HIV-1): a treatable cause of anemia in AIDS.

OBJECTIVE: To determine the role of B19 parvovirus in red cell aplasia of patients infected with human immunodeficiency virus type 1 (HIV-1). DESIGN: Uncontrolled clinical trial, with assay of serum, peripheral blood cells, and bone marrow for virus using DNA hybridization and immunocytochemistry techniques; these assays were then correlated with clinical findings, results of immunoassays for antivirus antibodies, and with immunoglobulin (Ig) therapy. SETTING: Government medical referral center, and university and private hospitals. PATIENTS: Seven patients with pure red cell aplasia and serologic evidence of infection with HIV-1. MEASUREMENTS AND MAIN RESULTS: All patients had giant pronormoblasts in the bone marrow (present in transient aplastic crisis caused by acute B19 parvovirus infection). High concentrations of B19 parvovirus were demonstrated in sera, in several cases in samples separated by weeks or months. Viral DNA and capsid protein were present in the bone marrow of three patients studied, and active viral replication was detected by southern analysis. There was no antivirus IgG in capture immunoassay and no or very low levels of antivirus IgM. The patients did not have symptoms of fifth disease, the illness caused by this virus in immunologically normal persons. Six patients were treated with a regimen of intravenous commercial immunoglobulin. In all cases, this therapy resulted in rapid reduction in serum virus concentrations and full recovery of erythropoiesis. Relapses in two cases were predicted by DNA hybridization studies, and these cases were successfully retreated. CONCLUSIONS: The B19 parvovirus is a remediable cause of severe chronic anemia in HIV-infected patients. Recognition of and therapy for parvovirus in this population will avoid erythrocyte transfusion and should prevent transmission of the virus to other persons, including immunosuppressed persons and women of child-bearing age.

Acquired Immunodeficiency Syndrome↗

PubMed2000

Parvovirus B19 infection in a human immunodeficiency virus-infected patient with anemia.

Anemia is generally attributed to zidovudine therapy in human immunodeficiency virus (HIV)-infected patients, although parvovirus B19 infection has been reported as a rare cause. We report on a 24-year-old homosexual man infected with HIV who presented with anemia. He had received aggressive daily antiretroviral therapy (zidovudine 600 mg, lamivudine 300 mg, and saquinavir 1,800 mg) for 2 years. At the time of admission, his CD4+ count was 10 x 10(6) cells/L. A bone marrow aspirate smear showed a marked decrease in erythropoiesis and immunocytochemical staining for parvovirus B19 was positive. Parvovirus B19 viral DNA was detected in the peripheral blood using a polymerase chain reaction-based assay. Serologic studies were positive for parvovirus B19 immunoglobulin (Ig)M antibodies, but negative for IgG antibodies. The patient was treated with packed red blood cell transfusion. Zidovudine was stopped and replaced with zalcitibine 2.25 mg daily after anemia occurred. He did not receive intravenous Ig therapy because of its cost. After discontinuation of zidovudine for 1 year, anemia persisted and the patient depended on regular blood transfusions to control the anemia. This case emphasizes that, in addition to drug-related causes, parvovirus B19 infection should be included in the differential diagnosis of chronic anemia in HIV-infected individuals.

Adult↗

PubMed1990

Molecular biology and pathogenicity of human and animal parvoviruses.

The so-called autonomous parvoviruses comprise a wide spectrum of viral agents with quite similar physicochemical and biological properties. Characteristically, they are small, naked, and extraordinarily stable particles made up of only 2-4 structural proteins and a genome of linear, single-stranded DNA consisting of 4500-5600 nts. For replication they depend on cellular helper functions which become available at distinct stages during cellular differentiation (developmentally-dependent functions) and transiently during the phase of DNA synthesis in the mitotic cycle (cell cycle-dependent function(s)) of a susceptible cell. Most of the clinical syndromes induced by parvoviruses therefore can be related to infection of mitotically active cells or tissues at different stages in the development and maturation of the host organism. This view of parvovirus pathogenicity holds true for all animal parvoviruses as well as for the human parvovirus B19.

Animals↗