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PubMedDate not supplied

[Auto-immune hemolytic anemia revealed by erythroblastopenia linked to a parvovirus infection].

In a 12 year-old boy presenting with auto-immune hemolytic anemia of the IgG type, human parvovirus infection was responsible for acute erythroblastopenia. Aplastic crisis quickly and spontaneously recovered but auto-hemolysis was durable. Human parvovirus induced erythroblastopenia has only been reported in patients with constitutional hemolytic anemia. On the other hand, in this case, human parvovirus infection revealed the auto-immune hemolytic anemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1987

On the pathogenesis of spontaneous parvovirus infection.

The internal organs of 21 beagles spontaneously infected with parvovirus were examined histologically and in 10 of the dogs immunofluorescence examination was also performed. The study showed that the pathological process had started in the small intestine and from there the viral agent had spread through the regional lymph nodes into the other lymphatic and the haemopoietic organs causing there depletion predominantly of lymphocytes and arrest of haemopoiesis. Four dogs displayed conspicuous oedema of the media of the arterioli in the liver. In the cytoplasm of probably Kupffer's cells specific fluorescence was present in all the 10 dogs examined. On the other hand neither viral antigen nor histological changes were found in kidneys. Our observations suggest that spontaneous infection of dogs with parvovirus takes place per os. Parvovirus is not eliminated from the organism with urine.

Animals↗
PubMed1986

[Acute parvovirus B 19-induced erythroblastopenia and hereditary spherocytosis. Apropos of 1 pediatric case and review of the literature].

Authors report a new case of acute erythroblastopenia linked to a parvovirus B 19 infection by a 10 years old boy suffering from an hereditary spherocytosis. Aurillac antigen or parvovirus B 19 is one of the smallest virus to be known. It has been well demonstrated in vitro that the virus inhibits especially erythropoiesis but mechanism remains unclear. Systematic vaccination of all children at risk with congenital or acquired chronic haemolytic anaemia should be in the near future the best prophylaxis of parvovirus B 19 infections.

Acute Disease↗
PubMed1978

Demonstration of parvovirus in Canadian swine and antigenic relationships with isolates from other countries.

A Canadian isolate of porcine parvovirus, isolated from cultured pig thyroid cells, was shown to be antigenically indistinguishable from a British (59e/63) and a German (G10/1) strain when treated by the modified direct complement-fixation, the hemagglutination-inhibition and the fluorescent antibody tests. These tests also revealed that antibodies to parvoviruses were detectable in a large proportion of the conventionally raised pigs in the provinces of Quebec and Ontario. Cell cultures, prepared from tissues collected in a slaughterhouse, were often found to be infected with parvovirus. In cell cultures the infection was demonstrated more effectively by immunofluorescence than by the hemagglutination test.

Animals↗
PubMed1979

Prenatal infection following maternal exposure to porcine parvovirus on either the seventh or fourteenth day of gestation.

Intranasal and oral exposure of two gilts to porcine parvovirus on either the seventh or 14th day of gestation resulted in prenatal infection. Normal appearing fetuses and necrotic remnants of what were believed embryos and extraembryonic membranes were found when the gilts were necropsied seven weeks after exposure. The presence of masses of porcine parvovirus antigen throughout necrotic tissues of six of seven embryos, but not in any of the nine normal appearing fetuses suggested that embryonic death was due to porcine parvovirus.

Animals↗
PubMed1984

Aplastic crisis and other effects of the human parvovirus infection.

Human parvovirus infections are common, provoke aplastic crises in patients with congenital haemolytic anaemia and cause fifth disease. An unknown proportion of the infections are subclinical. Parvoviraemia occurs in the early acute stage of infection and specific IgM can be detected during recovery. Most patients commencing an aplastic crisis are viraemic, but fifth disease arises after the viraemia. Serological tests for HPV, available at a small but increasing number of laboratories, will soon be complemented by tests for HPV DNA sequences present in blood, marrow and at other sites. Human parvovirus infection is occasionally fatal in patients with severe forms of congenital haemolytic anaemias and further study may reveal other unusual serious consequences of this ubiquitous infection. Short-term protection of vulnerable patients may be achievable with normal immunoglobulin, but there are still considerable obstacles to the preparation and use of a human parvovirus vaccine.

Adolescent↗
PubMed1981

[Removal of polio- and parvovirus in sewage-sludge by lime-treatment (author's transl)].

Lime (CaO) applied as conditioner for dewatering municipal sewage sludge in filter-presses is suitable to disinfect sewage sludge with respect to virus. A pH-rise to more than 12 followed by release of ammonia inactivates Polio- and Bovine Parvovirus. Addition of 3 kg CaO and more per m3 of raw sludge inactivates Poliovirus within 30 minutes. 7.5 kg CaO per m3 of anaerobically digested sludge are required to inactivate Polio-virus within 5 days and Bovine Parvovirus within 24 hours. Parvovirus seems to be more sensitive against free ammonia than Poliovirus, but less sensitive against high pH-values.

Calcium↗
PubMed1982

Field evaluation of a canine parvovirus vaccination program, using feline origin modified live virus vaccine.

Antibody titers measured by hemagglutination inhibition testing were determined in previously vaccinated dogs at the time of booster vaccination and 2 weeks later. All vaccines consisted of modified live panleukopenia virus. The booster injection was administered approximately 6 months after the initial parvovirus vaccination series was given. Fecal and serum specimens were collected immediately before and 2 weeks after administration of the booster vaccine for hemagglutination and hemagglutination inhibition testing, respectively. All dogs were privately owned and were from the Columbus, Ohio, area but were from environments with various exposure potentials to canine parvovirus. Results of hemagglutination (HA) testing on feces were negative in all dogs before and after booster vaccination. Therefore, these vaccinations did not interfere with interpretation of HA testing of feces. Results of serum hemagglutination inhibition (HI) testing indicated that 50% of the dogs had serum titers less than 1:80 prior to vaccination and that, of these dogs, 65.2% still had serum titers less than 1:80 2 weeks after the booster vaccination. Only 10.9% of all dogs had a marked increase in serum HI titer after the booster vaccination, indicating that overall serologic response to vaccination was poor. High HI titers (greater than or equal to 1:640) were associated with exposure to other dogs and cats in the neighborhood or to dogs suspected of having had parvovirus infection.

Animals↗
PubMed1982

Development of a modified live, canine origin parvovirus vaccine.

A modified live, canine origin parvovirus vaccine was tested for safety, efficacy, and clinical performance. The vaccine protected dogs from challenge of immunity with canine parvovirus (CPV) that caused clinical illness in all nonvaccinated dogs. Vaccinates all developed CPV serum neutralization antibody titers, with a mean value of 1,664. Challenge virus was not isolated from vaccinates, but feces from nonvaccinated dogs were CPV-positive for up to 4 days following challenge. In a pathogenicity test, dogs inoculated orally with 10 times the label dose remained clinically normal. In a reversion-to-virulence test, the vaccine strain remained nonpathogenic through 6 passages in seronegative test dogs. An immunologic interference test demonstrated that test dogs developed antibodies for all antigens in a combined canine distemper virus-adenovirus 2-parainfluenza virus-parvovirus vaccine and a Leptospira interrogans serovars canicola and icterohaemorrhagiae bacterin. A total of 1,796 doses of the multivalent preparation was administered in a field study, with veterinary practitioners reporting 36 local and 5 generalized reactions.

Animals↗
PubMed1981

Characterization of a parvovirus strain isolated from human adenovirus type 12.

A parvovirus strain was isolated from type 12 human adenovirus. The parvovirus multiplied without helper virus in HEp-2 cell cultures, while its multiplication was enhanced by type 12 and type 18 adenoviruses. Haemagglutinating infective virions as well as soluble haemagglutinins were demonstrated by ultracentrifugation and gel filtration. Virus haemagglutination inhibiting antibodies were found in the sera of healthy rats, whereas sera of healthy persons did not contain antibodies. The parvovirus failed to cause illness in laboratory animals (hamster, mouse, guinea pig).

Adenoviruses, Human↗
PubMed1980

Parvovirus infection in translocated raccoons.

Severe enteritis attributed to parvovirus infection was diagnosed in raccoons (Procyon lotor) purchased from a commercial animal dealer for interstate translocation. Intestinal lesions included edema, hyperemia, and focal mucosal necrosis. Microscopically, intestinal villi were reduced markedly, and there was necrosis of the glandular crypts. Intranuclear inclusions were seen in many crypt cells. A parvovirus that was infective for Crandell feline kidney cells and primary canine kidney cells was isolated from the spleen of a sick raccoon. The raccoon virus was distinguished from feline panleukopenia virus by the former's ability to hemagglutinate swine erythrocytes at a pH of 7.2. Serum neutralization testing of infected raccoons indicated that the raccoon isolate differed from feline panleukopenia virus and may have been canine parvovirus.

Animals↗
PubMed1995

[Rheumatic manifestations of parvovirus B19 infection].

Parvoviruses are small single-strand DNA viruses. Human parvovirus (PV B19) was isolated in the 1970s and recognized as a pathogen in the 80s. Its role was first demonstrated in acute erythroblastopenia in patients with chronic haemolytic anaemia, then in epidemic megalerythema. More recently PVB19 has been shown to be the aetiologic agent in fetal loss and chronic infection in immunodepressed patients. Further attention has focused on rheumatologic manifestations, particularly in prolonged joint diseases raising the problem of differential diagnosis and a possible pathogenic relationship with rheumatoid arthritis and systemic lupus erythematosus. Clinically, subjects with parvovirus B19 infection have flu-like manifestations of joint pain and myalgia lasting for about 1 week. Generally, the joint pain is symmetrical, of inflammatory type usually involving proximal joints (phalangeal joints in two-thirds of the cases). Acute back pain or associated extra-articular signs are often absent. Signs regress spontaneously in 10 to 15 days although longer periods have been observed. Diagnosis can be confirmed by ELISA identification of specific IgM antibodies. Nonsteroid antiinflammatory drugs are generally effective.

Adult↗
PubMed1976

Antibody to porcine, feline and rat parvoviruses in various animal species.

Porcine, feline and rat parvoviruses were shown to be antigenically distinct. Specific antibody to feline and rat parvoviruses was shown in a high proportion of porcine sera, and to the porcine parvovirus in sera from cattle, sheep, cats, guinea-pigs, mice and rats, but not from horse, dog, rabbit, chicken or human.

Animals↗
PubMed2026

Estimating the impact of parvovirus B19 outbreaks on congenital anomalies and fetal outcomes in Wales.

OBJECTIVES: Parvovirus B19 (B19V) is a common infection that can cause complications in pregnancy. Outbreaks of B19V in Europe and the UK were recorded in 2024. We aimed to describe the epidemiology of maternal parvovirus in Wales and to investigate associated fetal outcomes widely and in 2024 specifically. STUDY DESIGN: A retrospective observational study. METHODS: All cases of maternal B19V reported to the Congenital Anomaly Register Information Service (CARIS) were analysed. Maternal risk factors included gestational age at the time of infection and maternal age. Spatio-temporal analysis was performed to look for clusters. Poisson regression was used to model incidence of maternal B19V over time. Fetal outcomes were tested for association with risk factors using linear regression and Fisher's exact test. Outcomes and congenital anomalies were descriptively analysed. RESULTS: Between 1998 and 2025, there were 79 cases of maternal B19V across 81 fetuses, mostly reported in South Wales (74/81, 91.3%). There were 24 (29.6%) cases of at least one confirmed congenital anomaly and 57 (70.3%) cases reporting no anomalies; 53 (93%) of these cases had a positive outcome. Congenital anomalies were associated with worse fetal outcomes. Excluding terminations, the overall fetal survival rate was 88%. No association between maternal risk factors and fetal outcome was identified. There was an increase in cases in 2024 with an increase in fetal losses. CONCLUSIONS: The 2024 European B19V outbreak led to an increase in maternal cases and negative fetal outcomes in Wales.

Humans↗
PubMed1992

Replication and cytopathology of human parvovirus B19 in human umbilical cord blood erythroid progenitor cells.

Human parvovirus B19 productively infected erythroid progenitor (EP) cells from umbilical cord blood, in vitro as shown by an increase of viral DNA in supernatant fluid assayed by dot blot hybridization and liquid scintillation counting. Progeny virus was released into the supernatant fluid of CD34+ EP cells which had been purified by immunomagnetic separation. This supernatant fluid was infectious for bone marrow cells. Erythroid bursts infected with virus showed characteristic cytopathic effect by electron microscopy consisting of cytoplasmic vacuolization, marginated chromatin, and nuclear inclusions of lattice or crystalline arrays. Cultures of umbilical cord blood EP cells may be useful for the propagation of parvovirus B19 serological testing reagents and the study of virus-host cell interactions.

Base Sequence↗
PubMed1995

Most of the VP1 unique region of B19 parvovirus is on the capsid surface.

B19 parvovirus is pathogenic in man and a vaccine is desirable. In convalescence after acute infection, the dominant humoral immune response is directed to the minor capsid protein called VP1, which differs from the major capsid protein by an additional NH2-terminal 227 amino acids. We have previously shown that this unique region contains multiple linear neutralizing epitopes. We produced seven recombinant B19 capsids that contained progressively truncated VP1 unique region sequences, each fused to a Flag peptide (AspTyrLysAspAspAspAspLys) at the NH2-terminus. Capsids containing normal VP2 and truncated Flag-VP1 proteins and, in some cases, only truncated Flag-VP1 chimeric proteins, were analyzed by ELISA, affinity chromatography, and electron microscopy using anti-Flag monoclonal antibody. All regions examined showed binding to anti-Flag antibody in multiple assays, indicating that most of the VP1 unique region is external to the capsid and accessible to antibody binding. These results have implications for the design of a B19 parvovirus vaccine and the use of empty capsids for presentation of heterologous protein antigens.

Amino Acid Sequence↗
PubMed1994

Biochemical and genomic characterization of muscovy duck parvovirus.

A duck parvovirus (DPV) isolated from muscovy ducks during the epizootic in France in 1989 was purified from inoculated allanto-amniotic fluids by CsCl density gradient centrifugation and characterized. Full and empty non-enveloped icosahedral viral particles were observed banding at densities of 1.39 to 1.42 and 1.38 respectively, with a diameter of 22 to 23 nm. Viral proteins were analyzed by SDS-PAGE and the estimated molecular weights of the 3 major proteins were 91, 78 and 58 kDa. The nucleic acid was shown to be a single-stranded DNA of about 5,300 bases with terminal palindromic hairpins. These results confirm the previous classification of the virus in the family Parvoviridae established by Jestin et al. [14] on morphological and serological bases. The DPV DNA was reannealed indicating that complementary DNA strands were encapsidated. A partial restriction endonuclease map was also established. This work constitutes the first biochemical and genomic description of a muscovy duck parvovirus.

Animals↗
PubMed1995

Extent of sequence variability in a genomic region coding for capsid proteins of B19 parvovirus.

Genomic variability in human parvovirus B19 was analysed by direct partial sequencing of different isolates collected in Italy between 1989 and 1994. DNA was purified from viremic serum samples and the region of viral genome coding for structural proteins was amplified by polymerase chain reaction and partially sequenced (nt. 2400-3400). Data were compared to reference isolates Wi (U.K., 1973) and Au (U.S.A., 1982). The average relative distance between isolates was estimated at the low level of 0.61%, comparable with the distance to reference isolates. Out of 22 nucleotide substitutions found, 9 resulted in amino acid changes. From our results, this region of human parvovirus B19 genome appears to be stably conserved.

Amino Acid Sequence↗