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Results for “Parvovirus B19, Human”

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At least 19 recordsLinked to original sources
PubMed2001

Two family members with a syndrome of headache and rash caused by human parvovirus B19.

Human parvovirus B19 infection can cause erythema infectiosum (EI) and several other clinical presentations. Central nervous system (CNS) involvement is rare, and only a few reports of encephalitis and aseptic meningitis have been published. Here, we describe 2 cases of B19 infection in a family presenting different clinical features. A 30 year old female with a 7-day history of headache, malaise, myalgias, joint pains, and rash was seen. Physical examination revealed a maculopapular rash on the patient's body, and arthritis of the hands. She completely recovered in 1 week. Two days before, her 6 year old son had been admitted to a clinic with a 1-day history of fever, headache, abdominal pain and vomiting. On admission, he was alert, and physical examination revealed neck stiffness, Kerning and Brudzinski signs, and a petechial rash on his trunk and extremities. Cerebrospinal fluid analysis was normal. He completely recovered in 5 days. Acute and convalescent sera of both patients were positive for specific IgM antibody to B19. Human parvovirus B19 should be considered in the differential diagnosis of aseptic meningitis, particularly during outbreaks of erythema infectiosum. The disease may mimic meningococcemia and bacterial meningitis.

Adult↗
PubMed2004

The structure of human parvovirus B19.

Human parvovirus B19 is the only parvovirus known to be a human pathogen. The structure of recombinant B19-like particles has been determined to approximately 3.5-A resolution by x-ray crystallography and, to our knowledge, represents the first near-atomic structure of an Erythrovirus. The polypeptide fold of the major capsid protein VP2 is a "jelly roll" with a beta-barrel motif similar to that found in many icosahedral viruses. The large loops connecting the strands of the beta-barrel form surface features that differentiate B19 from other parvoviruses. Although B19 VP2 has only 26% sequence identity to VP3 of adeno-associated virus, 72% of the C(alpha) atoms can be aligned structurally with a rms deviation of 1.8 A. Both viruses require an integrin as a coreceptor, and conserved surface features suggest a common receptor-binding region.

Capsid Proteins↗
PubMed1995

[Studies on the relationship between anaphylactoid purpura and human parvovirus B19].

Human parvovirus B19 (B19) has been shown to be the cause of erthema infectiousum (EI). Recently the various clinical manifestations with B19 infection are coming to light. The relationship between B19 and anaphylactoid purpura (Schölein-Henoch purpura: SHP) was investigated in a retrospective study. There were sixteen patients (male 9, female 7, average age 6.0 +/- 1.7) who were diagnosed as SHP. Serum specimens were used in the present study. Specific IgM and IgG were assayed by enzyme immunoassay, B19 DNA was assayed by polymerase chain reaction (PCR). Five of the sixteen patients were positive for B19 DNA assayed by PCR, three were positive for B19 IgM in the acute phase. Kidney involvement appeared in one case with B19 infection and in two cases without infection. Abdominal involvement appeared in one case with infection and in three cases without. In this study, five of the sixteen patients had evidence of recent B19 infection by the existence of antibodies and PCR method. In conclusion, it is necessary to investigate the B19 infection with or without EI in the cases of SHP.

Child↗
PubMed2002

A transgenic mouse model for non-immune hydrops fetalis induced by the NS1 gene of human parvovirus B19.

Human parvovirus B19 (B19) infection during pregnancy is associated with the adverse foetal outcome known as non-immune hydrops fetalis (NIHF). Although B19 is known to infect erythroid-lineage cells in vivo as well as in vitro, the mechanism leading to the occurrence of NIHF is not clear. To investigate the possible involvement of the B19 non-structural protein NS1 in NIHF, three independent lines of transgenic mice were generated that expressed NS1 under the control of the Cre-loxP system and the GATA1 promoter. Two of the three lines expressed NS1 in erythroid-lineage cells. Most of the transgenic mice died at the embryonic stage, some of which developed hydropic changes caused by severe anaemia at embryonic day 15.5 (E15.5). Histological examination of embryos at E15.5 showed significantly fewer erythropoietic islands in the liver parenchyma, whereas their hearts showed no abnormal signs, such as cardiomegaly and apoptotic cells. The NS1-transgenic mouse lines established here provide an animal model for human NIHF and suggest that NS1 plays a crucial role in the adverse outcome associated with intrauterine B19 infection in humans.

Animals↗
PubMed2004

Construction and sequencing of an infectious clone of the human parvovirus B19.

Human parvovirus B19 has a nonenveloped, icosahedral capsid packaging a linear single-stranded DNA genome of 5.6 kb with long inverted terminal repeats (ITR) at both the 5' and 3' end. Previous attempts to construct a full-length B19 clone were unsuccessful due to deletions in the ITR sequences. We cloned the complete parvovirus B19 genome with intact ITRs from an aplastic crisis patient. Sequence analysis of the complete viral genome indicated that both 5' and 3' ITRs have two sequence configurations and several base changes within the ITRs compared to previous published sequences. After transfection of the plasmid into permissive cells, spliced and non-spliced viral transcripts and viral capsid proteins could be detected. Southern blot analysis of the DNA purified from the plasmid-transfected cells confirmed parvovirus B19 DNA replication. Production of infectious virus by the B19 plasmid was shown by inoculation of cell lysate derived from transfected cells into fresh cells. Together, these results indicate the first successful production of an infectious clone for parvovirus B19 virus.

3' Untranslated Regions↗
PubMed1995

An epidemic of aplastic crisis caused by human parvovirus B19.

Human parvovirus B19 has been associated with several diseases. Aplastic crisis in patients with chronic hemolytic anemia, erythema infectiosum, hydrops fetalis and arthritis are among the common diseases caused by this virus infection. In the period between July, 1991, and March, 1992, 48 patients with aplastic crises were hospitalized at Saudi Aramco-Dhahran Health Center, Dhahran, Saudi Arabia. Forty-six patients had homozygous sickle cell disease, one had hemoglobin H disease and one had hereditary elliptocytosis. Evidence of recent human parvovirus infection was present in 91% of the cases. Leukopenia was present in 21%, neutropenia in 27% and thrombocytopenia in 42%. This differs from previous reports in which red blood cell aplasia causing anemia was the only hematologic finding reported in most patients. There were no cases of erythema infectiosum in either the patients or the community during the epidemic and the reason for this phenomenon is not obvious. The almost limited occurrence of aplastic crisis in patients with sickle cell disease in a population with a high incidence of other types of chronic hemolytic anemias is of interest.

Adolescent↗
PubMed2005

Ku80 autoantigen as a cellular coreceptor for human parvovirus B19 infection.

Human parvovirus B19 (B19) infects human erythroid cells expressing P antigen. However, some cell lines that were positive for P antigen failed to bind B19, whereas some cell lines had an ability to bind B19 despite undetectable expression of P antigen. We here demonstrate that B19 specifically binds with Ku80 autoantigen on the cell surface. Furthermore, transfection of HeLa cells with the gene of Ku80 enabled the binding of B19 and allowed its entry into cells. Moreover, reduction of cell-surface expression of Ku80 in KU812Ep6 cells, which was a high-sensitive cell line for B19 infection, by short interfering RNA for Ku80 resulted in the marked inhibition of B19 binding in KU812Ep6 cells. Although Ku80 originally has been described as a nuclear protein, human bone marrow erythroid cells with glycophorin A or CD36, B cells with CD20, or T cells with CD3 were all positive for cell-surface expression of Ku80. B19 infection of KU812Ep6 cells and bone marrow cells was inhibited in the presence of anti-Ku80 antibody. Our data suggest that Ku80 functions as a novel coreceptor for B19 infection, and this finding may provide an explanation for the pathologic immunity associated with B19 infection.

Antibodies↗
PubMed1999

Possible interactions between the NS-1 protein and tumor necrosis factor alpha pathways in erythroid cell apoptosis induced by human parvovirus B19.

Human erythroid progenitor cells are the main target cells of the human parvovirus B19 (B19), and B19 infection induces a transient erythroid aplastic crisis. Several authors have reported that the nonstructural protein 1 (NS-1) encoded by this virus has a cytotoxic effect, but the underlying mechanism of NS-1-induced primary erythroid cell death is still not clear. In human erythroid progenitor cells, we investigated the molecular mechanisms leading to apoptosis after natural infection of these cells by the B19 virus. The cytotoxicity of NS-1 was concomitantly evaluated in transfected erythroid cells. B19 infection and NS-1 expression induced DNA fragmentation characteristic of apoptosis, and the commitment of erythroid cells to undergo apoptosis was combined with their accumulation in the G(2) phase of the cell cycle. Since B19- and NS-1-induced apoptosis was inhibited by caspase 3, 6, and 8 inhibitors, and substantial caspase 3, 6, and 8 activities were induced by NS-1 expression, there may have been interactions between NS-1 and the apoptotic pathways of the death receptors tumor necrosis factor receptor 1 and Fas. Our results suggest that Fas-FasL interaction was not involved in NS-1- or B19-induced apoptosis in erythroid cells. In contrast, these cells were sensitized to tumor necrosis factor alpha (TNF-alpha)-induced apoptosis. Moreover, the ceramide level was enhanced by B19 infection and NS-1 expression. Therefore, our results suggest that there may be a connection between the respective apoptotic pathways activated by TNF-alpha and NS-1 in human erythroid cells.

Apoptosis↗
PubMed2002

Persistence of human parvovirus B19 in human tissues.

Human parvovirus B19 infection causes various clinical symptoms, such as rash, arthropathy, anemias and fetal death, but it can also remain asymptomatic. The arthropathies and anemias can become chronic for several years, not infrequently resembling autoimmune syndromes. B19 replicates only in red blood cell precursors of bone marrow or fetal liver, resulting in high-titred short-lived viremia, but viral DNA is detectable also in cells of several other types. Recently B19 DNA has been found, by very sensitive amplification tests, in certain tissues not only of symptomatic but also of healthy individuals for several years or decades after B19 infection. The mere presence of B19 DNA in these tissues of a symptomatic patient (e.g. joints in chronic arthritis or skin in dermatomyositis) thereby does not prove that the present disease is caused by B19. The diagnosis has to be verified by other innovative means. How and why viral DNA persists in the tissues of healthy individuals is under investigation.

Autoimmune Diseases↗
PubMed2026

Tracing the evolution and diversity of human parvovirus B19 across human history.

Human parvovirus B19 (B19V) is an ubiquitously spread, exclusively human pathogen, mainly posing risks to children, as well as pregnant and immunocompromised individuals. Despite evidence of B19V infection of human populations as far back as 7,000 years, the evolutionary history of B19V remains poorly understood. In this study, we present B19V genomic data from the remains of 53 globally distributed individuals spanning more than 8,000 years, including 7 children. Our findings suggest that the most recent common ancestor of all present B19V lineages existed around 12,000 years ago, at the end of the last Ice Age. Additionally, we identified an extinct Eurasian clade that participated in the recombination event that led to the emergence of B19V genotype 2 (GT-2). We date this event to ∼3,200-1,800 BP, potentially in the greater Mediterranean area. Our study shows aspects of how ancient parvovirus variants arose, disseminated, and impacted human health through time.

ancient DNA↗
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↗
PubMed1993

Multiple primer pairs for polymerase chain reaction (PCR) amplification of human parvovirus B19 DNA.

Human parvovirus B19 is the etiologic agent of erythema infectiosum and transient aplastic crisis in patients with hemolytic anemias and has been associated with fetal death, arthritis, and chronic anemia. Acute B19 infection is best diagnosed by detection of IgM antibodies, whereas the diagnosis of chronic infection often requires the sensitivity of PCR to demonstrate presence of virus over time. To improve our ability to detect B19 DNA by polymerase chain reaction (PCR), we evaluated 19 primers combined into 16 different primer pairs for their ability to detect temporally and geographically diverse B19 isolates. All 16 pairs reacted with all isolates tested but with different sensitivity. Sequence analysis showed few nucleotide changes compared with published sequences. These changes did not explain observed differences in sensitivity between primer pairs. The most sensitive primer pairs detected 350 to 3500 DNA copies after 35 cycles. A second amplification cycle with nested primers improved the sensitivity 100-fold. These 16 primer pairs provide the diagnostic virologist with multiple options for B19 PCR assays.

Acute Disease↗
PubMed2000

[A case of Guillain-Barré syndrome (GBS) following human parvovirus B19 infection].

Human parvovirus B19 (HPV-B19) infection is recently known to produce variable clinical manifestations, but neurological disorder associated with this infection is uncommon. We reported a case of GBS associated with transient lupus-like status following HPV-B19 infection. This is the first report describing an adult case of GBS following HPV-B19 infection. A healthy female, aged 33, developed erythema infectiosum simultaneously with her 5-year-old daughter. On the same day, she noticed leg fatigue, which worsened in the following days. On the day 11th, she became unable to walk. Mild pancytopenia, liver injury, proteinuria, hypocomplementemia, and increased anti-nuclear antibody (ANA) were revealed at a hospital. Polymerase chain reaction detected HPV-B19 DNA in the serum. On the day 17th, she was admitted to our hospital because of moderate generalized weakness and mild sensory disturbance, which were symmetrical and distal-dominant. The deep tendon reflexes were absent. Analysis of cerebrospinal fluid showed albuminocytologic dissociation. Other laboratory data were normal except positive ANA. Enzyme-linked immunosorbent assay (ELISA) showed high titer of the serum IgM antibody to GM1 and GD1b. Serum anti HPV-B19 IgM and IgG tested by ELISA were also positive. She improved gradually after 2 courses of double filtrated plasma pheresis.

Adult↗
PubMed1993

Thrombocytopenia induced by human parvovirus B19 infections.

Human parvovirus B19 (B19) has a remarkable tissue-tropism for erythroid elements--from erythroid precursors (BFU-E, CFU-E) to erythroblasts. B19 is thought to be incapable of propagating in cells other than erythroid progenitors. Leukocytopenia and thrombocytopenia sometimes occur in addition to erythrocytopenia in patients with B19 infection. We retrospectively investigated the possible cause of thrombocytopenia by B19 infection in 23 patients with thrombocytopenia admitted to our hospital in the past 5 years. Two patients were found to be infected by B19. Mild thrombocytopenia in both cases was thought to be an early event in B19 infection.

Child↗
PubMed2006

A case of pure red cell aplasia and systemic lupus erythematosus caused by human parvovirus B19 infection.

Human parvovirus B19 (B19) rarely induces pure red cell aplasia (PRCA) in healthy hosts. Meanwhile B19 infection is often clinically similar to systemic lupus erythematosus (SLE), and several cases have been reported wherein B19 actually stimulated SLE exacerbation in an immunocompetent subject. An 82-year-old healthy woman was diagnosed to have complicated with B19 infection and PRCA. Four weeks later, she had high fever, polyarthritis, and oral ulcers, additionally diagnosed with SLE, and subsequently, 15 mg of prednisone was started. This is the first case wherein B19 infection caused both PRCA and SLE in a healthy patient as far as our investigations are concerned.

Aged, 80 and over↗
PubMed1994

Immunochemiluminescent Southern blot assay for polymerase chain reaction detection of human parvovirus B19 DNA.

Human parvovirus B19 is not only an acute self-limited infection causing erythema infectiosum, transient aplastic crisis, foetal hydrops and arthritis but can also be a chronic infection causing chronic anaemia and associated with chronic neuropathy and vasculitis. Serologic studies have proven to be the most sensitive way to detect acute infection in the immunologically normal patient while polymerase chain reaction (PCR) assays for B19 DNA are the most sensitive way to detect chronic infection. The ability to detect B19 in clinical specimens can be further increased with a second amplification step using nested primers. However, nested PCR is both time consuming and enhances the risk of false-positive results due to contaminating DNA. In this study, we developed a sensitive immunochemiluminescent Southern blot assay for detecting PCR amplified B19 DNA with a digoxigenin labelled primer. The sensitivity and specificity of this assay were comparable to nested PCR and at least 100-fold more sensitive than a single PCR amplification.

Blotting, Southern↗
PubMed1996

Human parvovirus B19 infection.

Human parvovirus B19 shows remarkable tropism for human erythroid progenitor cells. The pathogenesis of disease resulting from infection is a dynamic between the viral suppression of erythropoiesis and the host's ability to mount an effective immune response. Understanding this process has led to strategies for treating chronic anemia in persistently infected patients and may result in the development of a vaccine to prevent infection.

Anemia↗
PubMed1994

Application to immunoglobulin M capture hemadherence assays of hemagglutination of monkey erythrocytes by native and recombinant human parvovirus B19 antigens.

Human parvovirus B19 recently was shown to agglutinate baboon and human erythrocytes. We have now demonstrated that both recombinant and native B19 antigens agglutinate rhesus, cynomolgus, and Saimiri monkey erythrocytes. Using cynomolgus erythrocytes and the recombinant antigen, we developed an immunoglobulin M (IgM) antibody capture hemadherence test (MACHAT) for the detection of specific B19 IgM antibodies in human sera. The results obtained with MACHAT were compared with those obtained with an IgM capture enzyme immunoassay (MACEIA) employing the native antigen routinely used in our laboratory. For 229 patient serum samples, we found 96% agreement between the results of the two assays. There was some evidence that MACHAT was slightly more sensitive than MACEIA. Our results add to the range of erythrocytes that can be agglutinated by B19 virus and show that native as well as recombinant antigens may be used in MACHAT.

Animals↗