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At least 541 records · Page 30Linked to original sources
PubMed1984

An outbreak of erythema infectiosum associated with human parvovirus infection.

Erythema infectiosum (EI) or fifth disease is a mild, acute exanthematous disease, occurring mainly among children, for which a causative virus has long been sought. In May 1983 an outbreak of exanthematous illness was reported in a primary school in North London. Children attending the school were investigated by questionnaire and 162 (43.9%) reported an illness with the features of EI. In each of 36 cases investigated virologically the illness was associated with parvovirus infection. Moreover, pre-existing antibody to parvovirus was correlated with protection from EI in 16 of 17 close family contacts of cases. We propose therefore that EI is the common manifestation of infection with the human parvovirus.

Adult↗
PubMed1982

The development and use of an antibody capture radioimmunoassay for specific IgM to a human parvovirus-like agent.

An IgM-antibody capture radioimmunoassay (MACRIA) was developed for the detection of IgM antibody specific for the human parvovirus-like agent B19. Diagnosis of infection with this agent by either antigen detection or antibody seroconversion had been made by counter-current immunoelectrophoresis (CIE) in 18 cases of aplastic crisis occurring in children with homozygous sickle-cell disease. The MACRIA described here gave positive results in 17 of these 18 cases; in the remaining case only an acute specimen taken from the patient during viraemia and late convalescent specimens taken 184 and 247 days after onset of illness were available. The test was used to investigate 20 further cases of aplastic crisis in which neither viral antigen nor antibody seroconversion could be detected by CIE. Detection of virus-specific IgM permitted diagnosis of infection with this parvovirus-like agent in 17 of these cases. In the remaining three cases only single serum specimens taken late in convalescence, 82 days or more after the onset of symptoms, were available. In addition to these 34 cases of aplastic crisis in which primary infection with this agent was diagnosed by MACRIA, seven cases of apparent 'silent' infection detected by CIE were investigated. The test permitted the discrimination between primary infection and re-exposure to the virus in six of these patients. The use of this assay has added a considerable weight of evidence implicating primary infection with this parvovirus-like agent as an important cause of aplastic crisis in children with sickle-cell disease. Furthermore, MACRIA permits diagnosis of infection when only single serum specimens taken up to ten weeks after infection are available. Thus the use of this test will significantly facilitate the investigation of other clinical syndromes of presumptive infectious aetiology.

Adult↗
PubMed2002

Pure red cell aplasia due to parvovirus following treatment with CHOP and rituximab for B-cell lymphoma.

A 26-year-old woman, diagnosed with diffuse large B-cell lymphoma, was treated with CHOP (cyclophosphamide, hydroxydaunomycin, oncovin, prednisone), rituximab and radiotherapy. She developed transfusion-dependant anaemia, which persisted following chemotherapy. Bone marrow aspirate and biopsy were consistent with pure red cell aplasia and parvovirus infection. Serology was negative for previous or acute infection but parvovirus DNA was detected by polymerase chain reaction. Administration of intravenous immunoglobulin (1 g/kg) resulted in reticulocytosis and recovery of her haemoglobin. We hypothesize that rituximab caused depletion of her normal B cells, resulting in an inability to mount a primary immune response to parvovirus infection.

Acute Disease↗
PubMed1997

Association of parvovirus infection with isolated fetal effusions.

The association of parvovirus B19 infection and hydrops fetalis is well known. However, the association of parvovirus and fetal pleural or pericardial effusions has not been reported. We present five cases of isolated pleural or pericardial effusion with documented maternal parvovirus infection in four of these pregnancies. In the absence of structural or karyotypic abnormalities, spontaneous resolution of the effusion portends for a successful pregnancy outcome.

Female↗
PubMed1987

[Association of non-immunologically-induced hydrops fetalis with Parvovirus B19 infection].

Five weeks after the onset of clinical symptoms of erythema infectiosum, a 24 year old pregnant woman, gravida I, para 0, suffered a hydrops fetalis which resulted in fetal loss. The maternal infection with the human parvovirus B19 could be confirmed serologically with ELISA and immunoblot by detecting specific IgM antibodies against B19. In an amniotic sample of the fetus Parvovirus B19 DNA could be detected by hybridisation. Fetal loss was obviously due to a parvovirus B19 infection of the mother and the fetus.

Adult↗
PubMed1989

A genetically engineered cell line that produces empty capsids of B19 (human) parvovirus.

B19 parvovirus is pathogenic in humans, causing the common childhood exanthem fifth disease and bone-marrow failure, both acute (transient aplastic crisis of hemolysis) and chronic (pure erythrocyte aplasia in immunodeficiency). The virus is tropic for a human red cell progenitor cell, and failure to culture B19 in a cell line has limited its clinical study. We cotransfected the right half of the cloned B19 genome and a minigene derived from the human dihydrofolate reductase gene (DHFR) into dhfr--Chinese hamster ovary cells and screened selected clones by RNA analysis; after amplification in methotrexate, clones were tested for capsid protein expression. A cell line, designated 3-11-5, stably expressed nearly full-length transcripts for the two capsid proteins. These cells produced the major and minor structural protein species in natural proportions that self-assembled into virion capsids. Capsids from 3-11-5 cells could be separated from virions by sucrose gradient sedimentation and had the density on cesium chloride isopycnic sedimentation of empty parvovirus capsids. Capsid protein was present in both nuclei and cytoplasm on immunofluorescence study but fractionated with the cytosol on purification. Empty capsid production was equal to or greater than virion production by infected bone-marrow cells, 1000-2000 capsids per cell, but cell growth was not diminished by capsid production. This cell line will be useful in developing practical assays for B19 parvovirus antibody and a vaccine for the virus, as well as potentially serving as a packaging cell line for gene therapy.

Animals↗
PubMed1987

Failure of vaccine or virulent strains of canine parvovirus to induce immunosuppressive effects on the immune system of the dog.

It is generally believed that canine parvovirus (CPV) is immunosuppressive and that immunosuppression plays an important role in the pathogenesis of canine parvovirus disease. However, there is little experimental evidence to support this assertion. The effects of virulent and vaccine strains of CPV on natural effector (NE) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), chemiluminescence (CL) of neutrophils, lymphocyte response to mitogen, specific antibody response to CPV, and dermal reaction to phytohemagglutinin (PHA) were examined. Neither a virulent nor a vaccine strain of CPV significantly suppressed the immune system. The only potential effect noted was that dogs infected with the virulent strain of CPV developed a transient peripheral blood leukopenia. It was concluded that CPV does not cause immunosuppression and that immunosuppression does not play a significant role in the pathogenesis of canine parvovirus disease.

Animals↗
PubMedDate not supplied

Human parvovirus B19: historical and clinical review.

Human parvovirus B19 has been associated with disease only for the past few years. First isolated from sera obtained for studies on hepatitis B in 1975, it was not until 1981 that infection with this small, single-stranded DNA virus was related to aplastic crisis associated with hemolytic anemia. A nonspecific viral prodrome, the occurrence in family members, and epidemics of aplastic crisis suggested the infectious etiology. Human parvovirus infection has since been associated with arthritis, erythema infectiosum (fifth disease), fetal death, and hydrops fetalis. Through the use of recently developed serologic tests, epidemics of erythema infectiosum and parvoviral infection have been related not only to aplastic crisis but also to intrauterine infection and hydrops; DNA hybridization studies have allowed the detection of viral DNA in serum and tissue extracts. Studies have been hampered by the lack of an ability to culture the virus, but this is now possible utilizing bone marrow culture and erythropoietin. This article is a historical and clinical review of human parvovirus infection and disease and considers potential questions regarding their consequences.

Anemia, Hemolytic↗
PubMed1988

Aplastic crisis in sickle cell disorders: bone marrow necrosis and human parvovirus infection.

Aplastic crisis in patients with sickle cell disease who develop a parvovirus infection may be associated with extensive bone marrow necrosis as well as acute selective erythroblastopenia. This illness may be manifested by pyrexia, lymphadenopathy, bone tenderness and significant hypoxemia with minimal roentgenographic findings in the lungs. It is uncertain whether the hypoxemia is caused by the effects of the viral infection on the lungs or is secondary to sickling of red blood cells in the pulmonary vasculature or both. The hypoxia may be sufficiently severe to require treatment with both oxygen and transfusion. The physical damage to the bone marrow associated with bone marrow necrosis may be more important than selective acute erythroblastopenia in inducing aplastic crisis in patients with sickle cell disorders. Studies of bone marrow biopsy specimens collected during parvovirus-associated aplastic crisis in patients with nonsickle cell hemolytic disorders would be helpful in determining the pathophysiology of parvovirus-associated disorders.

Acute Disease↗
PubMed1993

Parvovirus B19 infection in pediatric transplant patients.

Evidence of recent parvovirus virus infection (as determined by the presence of a positive IgM antibody titer) without other identified causes of anemia was found in 5 of 26 pediatric solid-organ transplant recipients evaluated for moderate-to-severe anemia between June 1990 and July 1991. Anemia tended to be chronic (median duration of anemia at the time of diagnosis was 12 weeks) and was associated with normal red blood cell indices in the absence of reticulocytes. The median age of the children at the time of presentation with anemia due to parvovirus was 1.8 years at a median time of 8 months after transplantation. Four of the 5 children were treated with i.v. immunoglobulin because of persistence of anemia requiring blood transfusions. A response characterized by an increase in reticulocyte count and normalization of hemoglobin was seen in each of these patients 2-4 weeks after treatment. The remaining patient experienced a spontaneous recovery from her anemia. Parvovirus infection should be included in the differential diagnosis of solid-organ transplant recipients presenting with severe anemia associated with low or absent reticulocytes.

Anemia↗
PubMed1987

Bovine parvovirus DNA-binding proteins: identification by a combined DNA hybridization and immunodetection assay.

We have investigated the interaction between bovine parvovirus (BPV) capsid and non-capsid proteins and restriction fragments of the BPV genome by a combined DNA hybridization and immunodetection assay. 32P-labelled DNA was bound to nitrocellulose membranes bearing lysates of mock-infected and virus-infected cells whose proteins had been separated by SDS-polyacrylamide gel electrophoresis. The position of bound DNA was determined by autoradiography. The proteins on the membrane were still accessible to specific antibodies, allowing confirmation of the DNA-binding species by an immunodetection reaction. In 0.2 M-NaCl, BPV capsid proteins VP2 (72,000 daltons) and VP3 (62,000 daltons) bound the 0 to 16 map unit EcoRI fragment of BPV DNA which contained label in either the minus or plus strand. At higher salt concentration (0.5 M), only VP2 still bound DNA. Within this fragment, the capsid protein binding was restricted to those nucleotides between map units 0 and 4. No binding to capsid proteins was seen with the fragment spanning the middle of the genome and minor binding to VP3 was seen with the 5' end. Binding to the BPV non-capsid protein NP-1 was observed with the 0 to 16 map unit fragment when label was in the virion strand and to other possibly BPV-coded proteins when label was in the plus strand. The NP-1 binding was localized to map units 4 to 16. We did not detect binding to the BPV homologue(s) of the autonomous parvovirus non-capsid protein NS1, due in part to its low concentration in the cell lysates used. Points of the parvovirus replication cycle at which DNA-binding proteins may serve controlling functions are discussed.

Animals↗
PubMed1987

Structural and functional homology of parvovirus and papovavirus polypeptides.

We have compared the sequences of the putative polypeptides of the human pathogenic B19 parvovirus with protein sequences in the National Bethesda Research Foundation Library, and have discovered a significant homology between a B19 parvovirus non-structural (NS) protein and the T antigens of polyomaviruses and simian virus 40 (SV40) and the putative E1 proteins of papillomaviruses. The region of highest homology with the papovavirus proteins corresponds to the region that is most highly conserved in the NS1 proteins of several other parvoviruses. Studies with the T antigen of both polyomaviruses and SV40 have implicated this region as having an ATPase activity and nucleotide-binding function.

Amino Acid Sequence↗
PubMed1992

Cooperation of oncogenes in cell transformation and sensitization to killing by the parvovirus minute virus of mice.

The established line of normal Fisher rat fibroblasts (FR3T3) is naturally resistant to the parvovirus minute virus of mice (MVM), and was used as a model system to study the influence of stepwise transformation on the susceptibility of cells to this virus. When transformed with genes encoding the class I nuclear oncoproteins large T antigen of polyomavirus (PyLT) or v-myc, cells retained a normal appearance, but acquired some ability to form colonies in soft agar. On the other hand, the class II transforming oncogenes encoding the middle T antigen of polyomavirus (PyMT) and c-Ha-ras-1 induced both morphological alterations and a high capacity for anchorage-independent growth in transfected cells. The concomitant expression of oncogenes from both classes (PyLT-(+)PyMT; v-myc+c-Ha-ras-1) induced a supertransformed phenotype characterized by the piling-up of cells into poorly adherent foci, even in low density cultures. The progressive transformation of this cellular system was found to coincide with a gradual increase in its susceptibility to MVMp (MVM prototype strain) infection. Compared to parental cells, class I, class II and double transformants proved to be sensitized to killing by MVMp to a low, moderate and large extent, respectively. Thus, oncogenes from different functional classes appeared to cooperate in the responsiveness of cells to parvovirus attack. Interestingly, this cooperation exacerbated both the killing of infected cells and their capacity to produce viral non-structural (NS) proteins, in agreement with the reported cytotoxic activity of NS polypeptides. Therefore, in this system, parameters of the parvovirus life cycle may serve as indications of the overall progression of the transformation process.

Animals↗
PubMed1991

Congenital spherocytosis, B19 parvovirus infection and inherited interstitial deletion of the short arm of chromosome 8.

We report two siblings with congenital spherocytosis, multiple phenotypic abnormalities and an inherited interstitial deletion of the short arm of chromosome 8 (8p). The propositus came to our attention with acute bone marrow hypoplasia secondary to B19 parvovirus infection. The bone marrow trephine biopsy appearances of intranuclear eosinophilic degeneration in the erythroblasts may be pathognomonic of B19 parvovirus induced acute bone marrow aplasia. The presence of B19 parvovirus DNA was demonstrated in erythroblasts by in situ hybridization. Chromosome analysis of peripheral blood lymphocytes from both siblings showed an interstitial deletion of the short arm of chromosome 8, del (8) (p11p21). This abnormal chromosome was inherited from their mother, who showed this deletion as well as a small fragment representing the deleted 8p chromosome portion, del (8) (p11p21), +f. Centromeric material from chromosome 8 was detected in this chromosome fragment by in situ hybridization using an alpha satellite probe (pJM 128), but not by C banding. Chromosome analysis of skin fibroblasts from the mother and a third sibling with a similar karyotype showed the deleted fragment in over 80% of cells. Cells in which the fragment was absent exhibited the deleted 8p, suggesting there was no mosaicism. The mother and the third sibling were phenotypically normal without spherocytosis. A fourth sibling and the father were normal. The chromosome abnormality was not observed in five of the mother's siblings, suggesting that it arose de novo in the mother. Our findings strongly support a locus for congenital spherocytosis on the short arm of chromosome 8. The frequency of defects at this locus is unknown.

Adolescent↗
PubMed1992

Recurrent granulocytic aplasia as clinical presentation of a persistent parvovirus B19 infection.

We report a case of persistent infection with human parvovirus B19 (PVB19), manifesting clinically as recurrent agranulocytosis and in bone marrow biopsy as recurrent pure granulocytic aplasia. Persistence of parvovirus infection was documented by the presence of PVB19 DNA and anti-PVB19-IgM antibodies in the serum for a period of 19 months. Granulocytic aplasia occurred only when anti-PVB19-IgG antibodies were not detectable in the serum and granulopoiesis showed immediate recovery with high dose intravenous immunoglobulin treatment. This case report suggests that the erythroid precursor cell may not be the only target cell of PVB19 infection. We suggest testing for active parvovirus infection in cases of aplasia of any lineage of the haematopoietic system.

Aged↗
PubMed1995

Management of persistent B19 parvovirus infection in AIDS.

An HIV+ 26-year-old white man with a CD4 count of 0.06 x 10(9)/l was found to have red blood cell aplasia secondary to B19 parvovirus infection. Regular infusions of intravenous immunoglobulin (IVIG) were begun and resulted in marked reticulocytosis and correction of anaemia. The patient has been followed for over 4 years and has become anaemic and reticulocytopenic whenever IVIG was interrupted. Serial dot blot analysis of the patient's sera for B19 parvovirus DNA showed absence of DNA immediately following IVIG treatments but reappearance within 3-6 weeks. Regular IVIG was effective in controlling but not eradicating B19 parvovirus infection in this HIV+ patient.

AIDS-Related Opportunistic Infections↗
PubMed1986

Inhibition of erythropoiesis by human parvovirus-containing serum from a patient with hereditary spherocytosis in aplastic crisis.

Aplastic phase serum from a patient with aplastic crisis of hereditary spherocytosis, which was demonstrated to contain human parvovirus, inhibited in vitro erythroid colony formation almost completely. Human parvovirus was resistant to heating for 30 min at 56 degrees C. The suppressive effect of the serum was completely abrogated by adding convalescent phase serum from another patient with aplastic crisis of hereditary spherocytosis. Some normal sera had similar neutralizing ability. The results suggested that aplastic crisis of a patient with hereditary spherocytosis is caused by human parvovirus and that the neutralizing test could offer a tool for predicting the future occurrence of aplastic crisis in the patients with chronic hemolytic anemia.

Adolescent↗
PubMed1984

Association of parvoviruses with rheumatoid arthritis of humans.

A small virus resembling parvoviruses in its morphological and physicochemical properties was derived from synovial tissue of a patient with severe rheumatoid arthritis. This virus, designated RA-1, elicits a syndrome in neonatal mice that includes neurological disturbances, permanent crippling of limbs, dwarfism, alopecia, blepharitis, "masking," and a rigid curvature of the thoracic spine. Polyclonal antibodies against RA-1 display high virus neutralizing activity and in immunoassays detect reactive antigen in synovial cells from different rheumatoid arthritis patients but not persons with osteoarthritis. Putative parvoviruses isolated from several other rheumatoid arthritis patients are only weakly pathogenic for newborn mice but can generate RA-1 virus-specific antigens in tissues of these animals. It has not been established that RA-1 and existing parvoviruses of mammalian species are related.

Animals↗