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PubMed1988

[Parvoviruses as pathogenic agents in man].

Since 1981 an increasing number of human parvovirus infections have been reported. There is now clear evidence that parvovirus B19 is the causative agent of erythema infectiosum (fifth disease). Further clinical situations associated with this virus include aplastic crisis in patients with hemolytic anemia and acute and persistent arthropathies preferentially occurring in adult women. Transplacental infection during pregnancy may result in hydrops foetalis, intrauterine death and spontaneous abortion. Additional, thus far barely characterized parvoviruses have been isolated from individuals with enteritis or rheumatoid arthritis. The present review summarizes today's knowledge of the biological properties and relevance of human parvoviruses as pathogens. The potentialities and limitations of laboratory diagnosis in parvovirus infections are discussed.

Anemia, Hemolytic↗

PubMed1988

Nonimmunologic hydrops fetalis resulting from intrauterine human parvovirus B-19 infection: report of two cases.

Two cases of nonimmunologic hydrops fetalis associated with intrauterine human parvovirus B-19 infection are reported. In these cases, hydrops fetalis was diagnosed with ultrasound at 21 and 22 weeks' gestation after 10 or more days of maternal flu-like symptoms. The outcome was stillbirth in one case and neonatal death in the other. In both cases, intrauterine infection by human parvovirus B-19 was confirmed based on two findings: maternal serum positive for human parvovirus B-19 immunoglobulin M (IgM) antibody, and human parvovirus B-19 DNA detected in the fetal organs using Southern blotting and hybridization with a 32P-labeled probe. Laboratory tests on cord blood demonstrated a red blood cell count of 163 x 10(4)/microL, and nucleated red cells numbering 1267 per 50 white cells in the live-birth case. Histologic examinations of fetal tissues demonstrated leukoerythroblastic reaction in the liver and spleen, granular hemosiderin deposition in hepatocytes and Kupffer cells, and bilirubin deposition in the intercellular space in the liver. This evidence indicates that, in some fetuses with intrauterine human parvovirus B-19 infection, hydropic changes may be induced by the sudden decrease in oxygen-carrying capacity of the blood due to severe anemia caused by the infection.

Adult↗

PubMed1988

Human parvovirus infection in pregnancy.

During an outbreak of fifth disease in the Hartford, Connecticut area in the winter of 1986, nine pregnant women were exposed to the parvovirus. Five of these nine had serologic evidence of previous exposure and immunity; all five had uneventful pregnancies. Three of the four women who exhibited serologic evidence of recent exposure to the parvovirus had hydropic fetuses who died, one of whom was anencephalic. Histologic and DNA hybridization studies suggest parvovirus infection as a cause for nonimmune hydrops and fetal death. A review of the literature suggests that of 37 women who were exposed and infected by human B19 parvovirus during pregnancy, 14 (38%) had adverse outcomes, including spontaneous abortions, intrauterine fetal death, and congenital anomalies. Women at high risk for exposure (school teachers) should have screening for immunoglobulin G parvovirus-specific antibodies; if these are absent, they should avoid close contact with schoolchildren. Pregnant women with evidence of recent infection should have a level II ultrasound. Because no vaccine is currently available, routine screening cannot be recommended.

Adolescent↗

PubMed1982

Parvovirus enteritis in vaccinated juvenile bush dogs.

Parvovirus enteritis developed in 10 of 17 vaccinated juvenile bush dogs (Speothos venaticus) from 4 litters in a 5-month period. Nine dogs died. The first outbreak involved 6 of 9 bush dogs from 2 litters. Each had been vaccinated with a killed feline-origin parvovirus vaccine at 11 and 14 weeks of age. The 6 affected dogs became ill at 29 weeks of age and died. The second outbreak involved a litter of 6 bush dogs. Each had been vaccinated every 2 weeks starting at 5 weeks of age. Two were isolated from the colony at 16 weeks of age for treatment of foot sores. Three of the 4 nonisolated dogs developed parvovirus enteritis at 20 weeks of age; 2 died at 6 and 8 days, respectively, after onset of signs. The 3rd outbreak involved a litter of 2 bush dogs. Both had been vaccinated every 2 to 3 weeks, starting at 6 weeks of age. One of these dogs became ill at 17 weeks and died 13 days later. A litter of 6 maned wolves (Chrysocyon brachyurus) and a litter of 3 bush dogs were isolated from their parent colonies at 13 and 15 weeks of age, respectively. Each animal had been vaccinated weekly, beginning at 8 weeks of age, using an inactivated canine-origin parvovirus vaccine. None of the isolated animals developed the disease. Serologic testing during isolation did not reveal protective titers (greater than or equal to 1:80) against canine parvovirus in the bush dogs until they were 23 weeks old, whereas protective titers developed in the maned wolves when they were 14 to 18 weeks old. One hand-raised bush dog was vaccinated weekly, beginning at 8 weeks of age, and a protective titer developed by 21 weeks of age. It was concluded that the juvenile bush dogs went through a period during which maternal antibodies interfered with immunization, yet did not protect against the disease. When the pups were isolated from the colony during this period, then vaccinated repeatedly until protective titers developed, the disease was prevented.

Animals↗

PubMed1994

[Parvovirus B19-induced aplastic crisis in a patient with iron deficiency anemia].

A 38-year-old female was referred to Takaoka City Hospital for treatment of common-cold-like symptom and an episode of transient unconsciousness. Physical examination on admission revealed severe anemia and an ejection heart murmur. Complete blood count revealed microcytic hypochromic anemia (Hb 4.1 g/dl), leukocytopenia (2.600/microliters), thrombocytopenia (7.1 x 10(4)/microliters) and reticulocytopenia (17,000/microliters). The bone marrow cellularity was within normal limits. Cells in the erythroid series were decreased to 5% of total bone marrow nucleated cells with maturation arrest at the level of proerythroblasts. Giant proerythroblasts were observed in 0.2% of marrow nucleated cells. No stainable iron was seen. Both anti-parvovirus B19 IgM antibody and IgG antibody were positive in the serum and parvovirus B19 DNA was detected in the bone marrow cells by polymerase chain reaction. From these results, iron deficiency anemia complicated with pure red cell aplasia secondary to parvovirus B19-induced infection was diagnosed. The anemia gradually improved with administration of sodium ferrous citrate one month after admission. Parvovirus B19 has been reported to cause an aplastic crisis in the patients who has a rapid red cell turn over such as hemolytic anemia or acute blood loss. This report suggested that severe aplastic crisis is also induced in patients with iron deficiency anemia by parvovirus B19-induced infection and warns that careful observation is necessary for the follow up of patients with iron deficiency anemia.

Adult↗

PubMed1996

Human parvovirus infection: rheumatic manifestations, angioedema, C1 esterase inhibitor deficiency, ANA positivity, and possible onset of systemic lupus erythematosus.

OBJECTIVE: To investigate the clinical and serological characteristics of parvovirus infection. METHODS CASE SERIES: during 1993-4, 9 adult patients presented with polyarthralgias/polyarthritis. Clinical evaluation and serological studies of antinuclear antibodies, rheumatoid factor (RF), IgM and IgG antibodies to human parvovirus were done in all patients. Other serologies including anti-DNA, serum complement, and C1 esterase inhibitor levels were obtained in some patients. RESULTS: All 9 patients had polyarthralgias/polyarthritis, serological evidence of parvovirus B19 IgM and IgG antibodies, and normal sedimentation rate. All patients were seronegative for RF. Four women had positive ANA titers. In 2 of them the ANA positivity was transient. One developed systemic lupus erythematosus (SLE). Three women had angioedema of the face and tongue; one had transient C1 esterase inhibitor deficiency and another a transient decrease in C4 levels. CONCLUSION: Parvovirus may be implicated in the development of SLE as well as other chronic arthropathies. This is the first reported case of angioedema and decreased C1 esterase inhibitor levels associated with parvovirus infection.

Adult↗

PubMed1996

Parvovirus B19 infection and rheumatic diseases.

We reviewed the literature on relationships between human parvovirus B19 infection and rheumatic diseases. Parvovirus B19 causes erythema infectiosum in childhood, transient anemia in immunocompetent individuals, and potentially severe infections in fetuses; laboratory evidence that the virus is directly responsible for these disorders has been obtained. Acute arthropathy meeting American College of Rheumatology criteria for rheumatoid arthritis and disorders meeting some of the classification criteria for systemic lupus erythematosus are the most striking rheumatic manifestations of parvovirus B19 infection. Purpuric lesions have also been reported. Parvovirus B19 infection may be capable of inducing a number of manifestations that have not yet been described in the literature. Although the relationship between human parvovirus B19 infection and rheumatic diseases has been the focus of many studies, compelling evidence that the virus is directly involved in the pathogenesis of rheumatic diseases has not yet been obtained.

Humans↗

PubMed1998

[Seroprevalence versus Parvovirus B19 in blood donors].

BACKGROUND: The aim of the study was to describe the seroprevalence against Parvovirus B19 in a random sample of blood donors in the Hospital Universitario de Salamanca. METHODS: We studied the presence of IgG and IgM antibodies against Parvovirus B19 in 136 sera from asymptomatic blood donors by enzyme immunoassay methods. RESULTS: From 136 samples tested, 88 (64.7%) had positive absorbance values for IgG. Forty eight samples (35.5%) were negative. IgM was negative in all cases. We did not find indeterminate results. DISCUSSION: Parvovirus primoinfection usually happens in the childhood. Thus, we can expect a high percentage of general population to have antibodies against Parvovirus B19. Anti-Parvovirus B19 antibodies prevalence in blood donors was 64.7%. This failure is similar to data reported before (65%). Clinical importance of these viruses in currently related with hemathopoyesis diseases and with the possible role in theratogenesis. The presence of IgG seems to give protection except in some chronic infections recently described.

Antibodies, Viral↗

PubMed1998

Development of antibodies to the nonstructural protein NS1 of parvovirus B19 during acute symptomatic and subclinical infection in pregnancy: implications for pathogenesis doubtful.

At present little is known about the mechanisms influencing the course and severity of parvovirus B19 infection. Antibodies to the parvovirus nonstructural protein NS1 were reported in patients with parvovirus-associated arthritis and those with persisting infection but not in those without complications, suggesting a potential involvement of NS1 or anti-NS1 antibodies in pathogenesis. The immune response to NS1 was examined retrospectively in 33 pregnant women with acute parvovirus B19 infection, 14 of whom experienced symptomatic infection and 19 in whom the infection was subclinical. Antibodies to NS1 were found in 15 (45%) of the women, seven with symptomatic and eight with subclinical infection. No association was found between the development of anti-NS1 antibodies and the occurrence of fetal complications. Of the seven cases in which fetal complications were observed, anti-NS1 antibodies were detected in only three. The finding that an immune response to NS1 can also be demonstrated in patients with asymptomatic infection suggests that anti-NS1 antibodies do not appear to represent a marker for an altered or severe course of infection in pregnant women or to contribute significantly to pathogenesis. Since anti-NS1 antibodies first become detectable at least six weeks postinfection, their presence can be used to exclude acute infection in patients with unclear serology or be used to aid differential diagnosis of rashlike illnesses.

Acute Disease↗

PubMed2003

Frequent infection with a viral pathogen, parvovirus B19, in rheumatic diseases of childhood.

OBJECTIVE: To find further evidence of the association of parvovirus B19 infection with juvenile rheumatic diseases, and to get new insights into the immunopathogenesis of these diseases. METHODS: Paired serum and synovial fluid samples from 74 children with rheumatic disease were analyzed with respect to their content of viral DNA and antibodies directed against the B19 viral proteins VP1, VP2, and NS1. Control sera from 124 children with noninflammatory bone diseases or growth retardation were also analyzed. The sequence of the viral DNA, amplified by polymerase chain reaction (PCR), was determined. IgG-complexed virus was isolated from sera and synovial fluid by adsorption to protein A beads. The amount of free virus versus immunocomplexed virus particles was determined by quantification of the viral genomes by quantitative PCR. RESULTS: Twenty-six of the 74 patients (35%) had detectable amounts of parvovirus B19 DNA in the serum (n = 22 [30%]) and/or the synovial fluid (n = 16 [22%]), whereas only 9 of the 124 control sera (7%) were positive for the viral DNA (P < 0.0001). Forty-six patients (62%) had serum IgG against the structural proteins, indicating past infection with B19. NS1-specific antibodies were detected in sera from 29 patients (39%) and 27 controls (22%) (P < 0.001). In addition, 3 patients (4%) showed VP2-specific IgM. In 15 patients, viral DNA could be repeatedly detected in followup samples of serum and synovial fluid. Sequencing revealed low-degree nucleotide variations that are in the range of genotype 1 of parvovirus B19. Immunocomplexed virus was present in varying amounts, both in the sera and in the synovial fluid samples. CONCLUSION: Parvovirus B19 is frequently found in serum or synovial fluid of children with rheumatism. The rate of persistent B19 infection in these patients is significantly higher than in age-matched controls.

Adolescent↗

PubMed1995

Absence of parvovirus B19 infection in chronic fatigue syndrome.

OBJECTIVE: To evaluate the presence of infection with parvovirus B19 in patients with chronic fatigue syndrome (CFS) who also had rheumatologic symptoms and mild hematologic abnormalities. METHODS: Seven patients meeting the Centers for Disease Control and Prevention working case definition for CFS who also had mild leukopenia, thrombocytopenia, or anemia were studied. Bone marrow was aspirated from each patient, and examined for morphologic abnormalities, including features seen in marrow infections with parvovirus B19, as well as for parvoviral DNA, using polymerase chain reaction (PCR) amplification. Serum obtained at the time of marrow aspiration was also evaluated for parvoviral DNA, using the PCR method, and was examined for the presence of IgM and IgG antibodies to the virus. RESULTS: No evidence of marrow involvement with parvovirus B19 was found in any patient. One patient had antibody evidence of a transient parvoviral infection, during which time an underlying thrombocytopenia worsened. CONCLUSION: Despite examining a selected group of patients thought most likely to have parvoviral infection, based on clinical and hematologic measures, no evidence of clinically important parvoviral infection was noted. Thus, it seems unlikely that parvovirus B19 plays a role in CFS, even though it has been associated with fibromyalgia, a clinically similar syndrome.

Adult↗

PubMed1994

Human parvovirus B19 infection and unbalanced translocation in a case of hydrops fetalis.

In a case of hydrops fetalis, serological examination showed a recent maternal human parvovirus B19 infection. Amniocentesis revealed a unique unbalanced translocation between chromosomes 3 and 11 of the fetus. The mother proved to have a balanced reciprocal translocation between chromosomes 3 and 11. A grossly macerated hydropic male fetus was delivered with a flat nose and low implanted deformed ears. Histopathological examination revealed nuclear inclusion bodies in fetal erythroid cells, confirming human parvovirus B19 infection. Parvovirus B19 DNA was demonstrated by in situ hybridization in the nuclei of heart muscle cells. Our finding of two different disorders in one case illustrates the importance of a complete evaluation of every case of hydrops fetalis, especially concerning counselling on the outcome of future pregnancies. The human parvovirus B19 infection will not recur due to the acquired immunity of the mother, whereas the balanced reciprocal translocation will endanger future pregnancies.

Adult↗

PubMed1993

Early and late gene expression in UT-7 cells infected with B19 parvovirus.

UT-7, a human megakaryocytoblastoid cell line, can be persistently infected with B19 parvovirus. We performed detailed serial analysis of parvovirus DNA replication and RNA transcription of synchronized cells. RNA transcription appeared as an early event following infection, with viral RNA detected about 6 hr after infection. In contrast, dimer-replicative intermediate forms of parvovirus DNA did not appear until more than 16 hr after infection. Northern analysis of specific transcripts showed an earlier appearance of nonstructural protein RNA (6 hr) compared to capsid protein RNA (24 hr). The addition of an inhibitor of protein synthesis to block synthesis of nonstructural protein abolished capsid protein RNA transcription as well as DNA replication. Primer extension analysis confirmed the initiation of all transcription from the single P6 promoter. RNA transcription precedes DNA replication of B19 parvovirus in these cells, and RNA processing may have a major role in regulating gene expression.

Base Sequence↗

PubMed1994

Complete nucleotide sequence and genomic organization of the Aedes albopictus parvovirus (AaPV) pathogenic for Aedes aegypti larvae.

We have cloned the replicative form of the Aedes albopictus parvovirus (AaPV) genome and determined the complete sequence of the viral strand. The sequence is 4176 nucleotides (nt) in length. The first 134 nt at the 3' end and the terminal 182 nt at the 5' end of the viral (minus) strand can both generate by folding and annealing of complementary sequences a typical terminal T-shaped structure although they differ in their sequence. Three large open reading frames (ORFs), each one in a different frame, are present between map units (mu) 8.0 and 87.6 on the complementary (plus) strand. The left, mid (located within the left ORF), and right ORFs have potential coding capacities of 95, 41, and 40 kDa, respectively. Two potential promoters were found upstream from the left and right ORFs, at mu 7.2 and mu 60.0, respectively. Computer search for sequence homologies suggests that the left ORF very likely encodes the nonstructural NS-1 protein since it contains the highly conserved NTP-binding amino acid (aa) domain (GKRN sequence) of all parvoviruses. Comparison with other invertebrate and vertebrate parvoviruses revealed that the AaPV genome shares 77.3% nt sequence homology and between 73 and 78% aa sequence homologies with the Aedes aegypti densonucleosis virus (Aedes DNV). Organization of both genomes was similar except that no potential ORF was found on the minus strand of AaPV. The difference of 167 nt in length between AaPV and Aedes DNV (4009 nt) genomes is due to additional noncoding sequences located between the internal coding region and the terminal palindromes in the AaPV genome. No significant homology was found between AaPV and the two other insect parvoviruses sequenced so far, the Bombyx mori DNV (BmDNV) and the Junonia coenia DNV (JcDNV).

Aedes↗

PubMed1994

The structure of human parvovirus B19 at 8 A resolution.

Empty capsids of the human parvovirus B19, self-assembled in a baculovirus expression system, have been crystallized in a cubic space group P2(1)3 with a = 362 A. In spite of extensive purifications, the crystals diffract X-rays to only 8.0 A resolution. Diffraction data were collected using oscillation photography with synchrotron radiation. The orientations of the particles in the unit cell were determined with a self-rotation function and their positions were obtained with an R-factor search using the known homologous canine parvovirus (CPV) structure. The resultant phases were improved by electron density averaging and solvent flattening to include all the terms between 23.0 and 8.0 A resolution. The central eight-stranded antiparallel beta-barrel, common to many viruses, is situated similarly in B19 with respect to the icosahedral symmetry axes to that observed for feline panleukopenia virus (FPV) and CPV. However, the surface structure of B19 is significantly different from the other known parvoviruses. The most striking difference is that B19 lacks the prominent spikes on the threefold icosahedral axes observed in FPV and CPV. This spike region contains residues involved in host recognition and antigenicity for the latter viruses, showing that there are major differences between subgroups of autonomous parvoviruses.

Amino Acid Sequence↗

PubMed1995

Analysis of the complete nucleotide sequences of goose and muscovy duck parvoviruses indicates common ancestral origin with adeno-associated virus 2.

The complete nucleotide sequences of two parvoviruses isolated from goose and muscovy duck were determined. The two virus genomes share 81.9% nucleotide sequence identity, indicating that they are closely related. The coding regions are bracketed by inverted terminal repeats containing palindromes. This is similar to the genome organization of human parvoviruses, adeno-associated virus 2, and B19. Amino acid sequence comparison shows that the closest relative of the goose and muscovy duck parvoviruses is adeno-associated virus 2. This is surprising, because the goose and muscovy duck parvoviruses do not require any helper virus for productive replication, suggesting that adeno-associated virus 2 has been derived from a helper-independent ancestor.

Amino Acid Sequence↗

PubMed2002

Caspase activation is required for permissive replication of Aleutian mink disease parvovirus in vitro.

Aleutian mink disease parvovirus (ADV) is distinct among the parvoviruses as infection in vivo is persistent, restricted, and noncytopathic. In contrast, infections with other more prototypic parvoviruses, like mink enteritis virus (MEV), are acute, cytopathic, and characterized by permissive replication in vivo. Although apoptosis results in the death of cells acutely infected by parvoviruses, the role of apoptosis in ADV infections is unknown. Permissive infection of ADV resulted in apoptosis of Crandell feline kidney (CrFK) cells as indicated by TUNEL staining, Annexin-V staining, and characteristic changes in cell morphology. Pretreatment of infected cells with caspase 3 or broad-spectrum caspase inhibitors prevented apoptosis. In addition, treatment of infected cells with these inhibitors caused a 2 log(10) reduction in the yield of infectious virus compared to untreated cultures. This block in replication preceded substantial viral DNA amplification and gene expression. However, inhibitors of caspases 1, 6, and 8 did not have this effect. MEV also induced caspase-dependent apoptosis following infection of CrFK cells, although production of infectious progeny was not affected by inhibition of apoptosis. Thus, permissive replication of ADV in vitro depended upon activation of specific caspases. If ADV infection of cells in vivo fails to initiate caspase activation, the requirement of caspase activity for replication may not be met, thus providing a possible mechanism for persistent, restricted infection.

Aleutian Mink Disease↗

PubMed1996

Detection of parvovirus B19 in skin biopsy, serum, and bone marrow of a patient with fever, rash, and polyarthritis followed by pneumonia, pericardial effusion, and hepatitis.

A previously healthy 33-year-old male patient presented with fever, rash and polyarthritis. Subsequently, he developed pleuropneumonitis, pericardial effusion and hepatitis. The diagnosis of parvovirus B19 infection was based on the detection of parvovirus DNA by PCR in a skin biopsy, bone marrow cells and serum. The patient had high parvovirus IgG antibody titres but remained negative for IgM at a three month follow-up, suggesting persistence of the virus or reinfection. It is concluded that detection of viral DNA is needed to verify a parvovirus B19 infection even in an immunologically healthy host.

Adult↗