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PubMed2001

Human parvovirus B19 infection in patients with systemic lupus erythematosus.

OBJECTIVE: The clinical significance of the presence of B19 DNA in patients with SLE was studied. METHODS: Sera from 72 patients with systemic lupus erythematosus (SLE), 23 patients with rheumatoid arthritis (RA), 18 patients with Sjögren's syndrome (SS), eight patients with Raynaud's phenomenon (RP), five patients with primary biliary cirrhosis (PBC), five patients with polymyositis (PM), four patients with erythema infectiosum (EI) and 22 normal controls were examined for parvovirus B19 (B19) infection by serological assays, nested PCR and Southern blotting. RESULTS: Parvovirus B19 DNA was detected in 17 of 72 patients with SLE and in three of four patients with EI, but not in patients with other systemic rheumatic diseases. Of the 17 patients with B19 DNA, only one had IgG anti-B19 antibody and two had IgM anti-B19 antibodies, whereas IgG and IgM anti-B19 antibodies were detected in 27 (49.1%) and 21 (38.2%) of 55 SLE patients without B19 DNA respectively. All sera from the patients with EI contained both IgG and IgM anti-B19 antibodies. B19 DNA was found more commonly in sera from SLE patients without anti-B19 antibodies than in those with anti-B19 antibodies (P<0.05). CONCLUSIONS: B19 infection in patients with SLE may be due to lack of anti-B19 antibodies because of either the immunocompromised nature of the host or the use of immunosuppressive drugs. There was a higher prevalence of hypocomplementaemia and RP in patients with parvovirus B19 viraemia than in those without parvovirus B19 viraemia.

Adult↗

PubMed2002

No evidence of parvovirus B19, Chlamydia pneumoniae or human herpes virus infection in temporal artery biopsies in patients with giant cell arteritis.

OBJECTIVES: Recent studies have suggested that infective agents may be involved in the pathogenesis of giant cell arteritis (GCA), in particular Chlamydia pneumoniae and parvovirus B19. We investigated temporal arteries from patients with GCA for these infections as well as human herpes viruses using the polymerase chain reaction (PCR). METHODS: Thirty temporal artery biopsies from 30 patients suspected of having GCA within a period of 1 yr were examined. Thirteen patients had classical GCA, two had biopsy-negative GCA, 10 patients had polymyalgia rheumatica and five patients had other conditions. DNA was extracted from frozen biopsies and PCR was used to amplify genes from Chlamydia pneumoniae, parvovirus B19 and each of the eight human herpes viruses: herpes simplex viruses HSV-1 and 2, Epstein-Barr virus, cytomegalovirus, varicella zoster virus and human herpes viruses HHV-6, -7 and -8. RESULTS: In all 30 biopsies, PCR was negative for DNAs of parvovirus B19, each of the eight human herpes viruses and C. pneumoniae. CONCLUSIONS: We found no evidence of DNA from parvovirus B19, human herpes virus or C. pneumoniae in any of the temporal arteries. These agents do not seem to play a unique or dominant role in the pathogenesis of GCA.

Biopsy↗

PubMed2003

Lack of evidence for a direct involvement of muscle infection by parvovirus B19 in the pathogenesis of inflammatory myopathies: a follow-up study.

OBJECTIVE: To clarify the association between parvovirus B19 and myositis. METHODS: Biopsy samples of muscle from eight patients with inflammatory myopathies were studied for the presence of B19 DNA by polymerase chain reaction. Expression of VP1 and VP2 capsid proteins was evaluated by immunohistochemistry. Interleukin 6 (IL-6) production was measured in the supernatant of myoblasts following incubation with parvovirus B19. RESULTS: In seven samples, detection of B19 DNA was negative. The expression of VP1 and VP2 capsid proteins was not observed by immunohistochemistry. In one patient, detection was transiently positive but became negative despite a flare-up of muscle disease. In vitro, parvovirus B19 was not able to induce IL-6 production by myoblasts. CONCLUSION: Our results do not support the direct implication of parvovirus B19 in the pathogenesis of myositis.

Adolescent↗

PubMed1997

Infection by parvovirus B 19 during pregnancy: a review.

Fetal infection by Parvovirus B 19 is a common cause of fetal anemia and nonimmune hydrops fetalis and may result in fetal death. Recent improvements in diagnosing parvovirus infections by sensitive molecular biology techniques now allow for a new insight into its pathogenic rule, immunology, and the varied clinical manifestations. The estimated overall risk of fetal loss after maternal exposure is about 6.5 percent, which is much less than previously thought. Inasmuch as complete spontaneous reversal of fetal hydrops has been commonly described, controversy exists regarding the management of the fetus with clinical signs of infection by Parvovirus B 19. According to the experience that has accumulated, it seems that only cases with severe fetal anemia or signs of fetal compromise should be managed by intrauterine transfusion. This procedure, however, is not without risk. Although an association between fetal viral infection and structural abnormalities has been described, it has not been proved yet. However, infection by Parvovirus B 19 has been recently proposed as a causative factor for congenital red blood cell aplasia.

Female↗

PubMed1996

Mouse parvovirus infection potentiates rejection of tumor allografts and modulates T cell effector functions.

Lymphocytotropic mouse parvoviruses can perturb immune responses. For example the recently identified mouse parvovirus designated MPV-1 persistently infects lymphoid tissues and interferes with the ability of cloned T cells to proliferate. As a consequence of these findings the present studies were undertaken to characterize further the immunomodulatory effects of MPV-1 on T cell-mediated immune responses in vivo and in vitro. To evaluate the effect of MPV-1 on CD8+ T cell-mediated responses sarcoma I (SaI) cells, devoid of class II major histocompatibility (MHC) antigens, were administered to MPV-1-infected adult BALB/c mice. MPV-1 infection accelerated tumor allograft rejection. Immunofluorescence staining and in situ hybridization studies of tumors suggested that direct infection of the tumor cells was not responsible for accelerated rejection. Furthermore, compared with uninfected mice, T cells from infected mice that had rejected SaI tumors had a diminished cytolytic capacity. Taken together these results suggest that MPV-1 may induce "bystander help." To examine the in vivo effect of MPV-1 on CD4+ T cell mediated responses adult mice were primed with ovalbumin (OVA) and infected with MPV-1. Spleen and popliteal lymph node cells from OVA-primed mice 3 or 7 days after MPV-1 inoculation had reduced proliferation responses, whereas the proliferative capacity of mesenteric lymph node cells from these mice was increased. Similarly, MPV-1 reduced cytokine-induced proliferation of allospecific CD8+ cloned L3 T cells and OVA-reactive CD4+ T cells without effecting cell viability. Since parvoviruses are widespread among laboratory rodents, these findings emphasize the importance of identifying and excluding parvovirus infections in mice used for transplantation studies and in cultures of mouse T lymphocytes.

Animals↗

PubMed2000

Human parvovirus B19 infection presenting as persistent anemia in renal transplant recipients.

BACKGROUND: Immunosuppression cannot be achieved without immunosuppressive effects. Human Parvovirus infection is known to occur after organ transplantation. We present our experience with Parvovirus infection in two cases. METHODS AND RESULTS: Two kidney transplant recipients developed symptomatic anemia requiring blood transfusions. Common causes of anemia, such as gastrointestinal bleeding, iron/vitamin deficiencies, hemolysis, and drug toxicities, were ruled out. A peripheral smear revealed low reticulocyte count. Bone marrow examination showed hypoplastic bone marrow with intranuclear inclusions suggestive of human Parvovirus. This was confirmed by immunohistochemical analysis. Treatment with i.v. immunoglobulin G resulted in a dramatic sustained response. Transplant kidney function remained stable. CONCLUSION: Human Parvovirus infections should be considered in immunosuppressed individuals with anemia with poor bone marrow response. Bone marrow examination can reveal viral inclusions and can be confirmed by immunohistochemical analysis. Intravenous immunoglobulin G results in resolution of anemia.

Adult↗

PubMed1996

Acute transient hemolytic anemia with a positive Donath-Landsteiner test following parvovirus B19 infection.

PURPOSE: A case of childhood acute hemolytic anemia following parvovirus infection provided an hypothesis for the high frequency of Donath-Landsteiner antibodies and inappropriately low reticulocyte counts in this disease. PATIENTS AND METHODS: A 3-year-old boy with hematuria and jaundice was found to have autoimmune hemolytic anemia due to a biphasic IgG Donath-Landsteiner antibody. Despite profound anemia (hematocrit 14.5%), the reticulocyte count was low (1.0%) and examination of his normocellular bone marrow showed erythroid hypoplasia. RESULTS: A clinical diagnosis 2 weeks earlier of acute parvovirus B19 was serologically confirmed as the associated antecedent infection. Hemolytic anemia resolved with packed red cell transfusion, and intravenous immune globulin and steroid treatment. CONCLUSIONS: The high-frequency red cell P antigen is both the unusual specificity of Donath-Landsteiner antibody and the viral receptor for parvovirus infection of red cell precursors. We speculate that interaction of the virus with its receptor may change antigenicity such that anti-P autoantibody forms. Parvovirus B19 may be a primary cause of reticulocytopenic postinfectious hemolytic anemia in children.

Acute Disease↗

PubMedDate not supplied

Parvovirus B19 infection in a child with acute lymphoblastic leukemia during induction therapy.

Immunocompromised children, including those undergoing chemotherapy treatment of malignant disease, are at particular risk for infection with parvovirus B19. However, these patients' attenuated immune responses may obscure the serologic and clinical manifestations of the infection. The authors describe a patient undergoing induction therapy for acute lymphoblastic leukemia whose parvovirus B19 infection was identified by the incidental detection of giant pronormoblasts and absence of normal mature erythroid precursors, characteristic of parvovirus infection, on a routine bone marrow examination. Intravenous immunoglobulin was administered and the patient's aplastic anemia resolved completely within 3 weeks. This highlights the importance of alertness to the possibility of parvovirus infection in children with cancer.

Anemia, Aplastic↗

PubMed1995

Antibodies to parvovirus B19 NS-1 protein in infected individuals.

Human parvovirus B19 is the aetiological agent of the common childhood disease erythema infectiosum (fifth disease). The infection is usually benign and self-limiting, but in adults cases of severe arthritis which may persist for years have been reported. Neutralizing antibodies directed against the structural proteins are usually produced shortly after the infection. The immune response against the third major protein, the non-structural protein NS-1, of parvovirus B19 has not been characterized so far. We cloned and expressed the full-length NS-1 protein and fragments thereof in Escherichia coli. The purified recombinant proteins were used to investigate the presence of antibodies to the NS-1 protein in sera from patients with parvovirus B19 infection. Specific antibodies could be detected in sera from patients suffering from severe parvovirus B19-associated arthritis using Western blot analysis and an ELISA. Sera from patients with acute or past infection without complications did not contain detectable levels of immunoglobulin to NS-1. The use of subfragments of the NS-1 protein allowed localization of the antigenic domains in the carboxy-terminal region of the protein.

Antibodies, Viral↗

PubMed2006

Severe parvovirus B19 encephalitis after renal transplantation.

Human parvovirus B19 is a common cause of benign erythema infectiosum (fifth disease) in otherwise healthy children. Immunocompromized patients are at risk of developing chronic infections leading to chronic hyporegenerative anemia. We report the case of a nine-year-old boy who presented five days after renal transplantation with seizures and signs of encephalitis on MRI. The clinical course was characterized by anemia and seroconversion for parvovirus B19 accompanied by a high viral load (>10(9) copies per milliliter). A transfusion of red blood cells that the patient required after transplantation was found to be negative for parvovirus B19, leaving the donated organ as the most likely source of infection. Reduction of the immunosuppressive regimen led to complete recovery of the patient with a stable RBC count upon discharge. Parvovirus B19 infections should be considered in the differential diagnosis of seizures after solid organ transplantation.

Anemia↗

PubMed1997

Human parvovirus B19 infection associated with hydrops fetalis.

Human parvovirus B19 infection has been associated with fetal anaemia, hydrops and in some cases fetal demise. We report our experience with nonimmune hydrops fetalis due to human parvovirus B19 infection in 17 pregnancies which were identified sonographically over a period of 10 years. The only baby who survived received repeated intrauterine transfusions and was normal neurodevelopmentally at 2 years follow-up. Two other fetuses who also received intrauterine transfusion did not survive. All pregnancies complicated with nonimmune hydrops should be investigated by fetal blood sampling looking for the evidence of parvovirus infection. Intrauterine transfusion should be reserved for hydropic fetuses with a low haematocrit. A greater understanding of the natural history of human parvovirus infection is needed prior to deciding the optimum mode of therapy.

Adult↗

PubMed2005

Exposure of hematologic patients to parvovirus B19 as a contaminant of blood cell preparations and blood products.

BACKGROUND: Patients with hematologic malignancies often require blood products, and parvovirus B19 is known to be transmitted by this route. Primary infection with parvovirus B19 shows a wide variety of disease manifestation. In immunocompromised patients, symptoms are severe and viral clearance is delayed or missing. STUDY DESIGN AND METHODS: A total of 2123 blood products given to all patients of a hematologic ward over a period of 6 months were retrospectively examined for the presence of parvovirus B19 DNA by an in-house real-time polymerase chain reaction (PCR; TaqMan). Patients who had received B19 DNA-positive blood products were further investigated serologically and by PCR for the presence of parvovirus B19 antibodies and DNA. RESULTS: Twenty-one (1%) of 2123 blood products tested positive for the presence of B19 DNA (2% of pooled products, 0.7% of single-donor products, and 17.6% of allogeneic peripheral blood progenitor cells), the median viral load was 700 genome equivalents per mL. During the study period, 114 patients were treated on the ward, and 14 (12%) of them received B19 DNA-positive blood components. None of them developed symptoms of an acute B19 infection, although one had a short low-level viremia. CONCLUSIONS: Although B19 DNA was detected in 1 percent of blood products given to hematologic patients, the exposure of 12 percent of patients did not result in symptomatic infections.

Adult↗

PubMed2005

Autologous peripheral blood progenitor cells are a potential source of parvovirus B19 infection.

BACKGROUND: Parvovirus B19 is a cause of delayed red blood cell (RBC) engraftment after marrow transplantation (BMT). The diagnosis of parvovirus infection requires serologic and DNA testing in the context of clinical disease and characteristic marrow morphologic findings; however, the source of infection is often difficult to determine. STUDY DESIGN AND METHODS: Investigation of a case of delayed RBC engraftment and pure RBC aplasia (PRCA) occurring 3 months after autologous peripheral blood progenitor cell (PBPC) transplantation in a patient with high-risk diffuse large B-cell lymphoma. DNA testing of serum and of a sample of cryopreserved PBPCs was performed. RESULTS: Marrow morphology showed a maturational arrest of erythroid cells with giant proerythroblasts. Polymerase chain reaction and nucleic acid hybridization confirmed the presence of parvovirus DNA in the serum and in a sample of sequestered PBPCs saved at the time of PBPC harvest. PRCA resolved after the administration of intravenous immune globulin. CONCLUSION: Autologous PBPCs are a potential source of parvovirus infection, which may cause significant disease after autologous BMT.

DNA, Viral↗

PubMed1995

[Responsiveness of a new parvovirus B19 antigen produced in baculovirus expression system to B19-specific IgG and IgM antibodies in every epidemic, 1968, 1980, 1987 and 1992 in Japan].

A new recombinant parvovirus B19 antigen was tested whether it was responsive to human serum antibodies in every epidemic year of erythema infectiosum for 25 years, because wild strains of B19 parvovirus were changeable genetically. The antigen was empty particles of both B19-VP1 and VP2 produced in baculovirus expression system. Specimens were 21 sera in 1968, 19 in 1980, 44 in 1987 and 33 in 1992, derived from 67 patients with erythema infectiosum, fever and/or non-specific exanthem and aplastic crisis in persons with hereditary spherocytosis. Each patient had been confirmed of B19 parvovirus infection by other methods as radio immunoassay and/or enzyme-linked immunosolvent assay for B19-IgG and IgM using other antigens and by detection of B19-genome DNA using the polymerase chain reaction. Days of the illness of every serum were confirmed including before infection to 216 days after onset. Sera from 23 patients with measles, Kawasaki disease and rubella were selected for controls, and those patients who had not been infected with B19 parvovirus. Tests were carried out by enzyme immunoassay, indirect method for IgG and IgM capture method. In a total of 103 specimens after onset of symptoms B19-IgG was positive in yearly specimens, and B19-IgM was also positive in all acute phase sera. B19-IgG in most of all sera was kept in peak level up to 216 days after onset. B19-IgM increased rapidly in acute phase and seemed to disappear within one to 5 months after onset. Thirty-seven specimens including 14 obtained at state before infection and 23 controls were completely negative for both B19-IgG and IgM.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Viral↗

PubMed1993

Erythrocyte P antigen: cellular receptor for B19 parvovirus.

The pathogenic human parvovirus B19 replicates only in erythroid progenitor cells. This virus was shown to bind to blood-group P antigen, as measured by hemagglutination. Erythrocytes lacking P antigen were not agglutinated with B19. Purified P antigen (globoside) blocked the binding of the virus to erythroid cells and the infectivity of the virus in a hematopoietic colony assay. Target cells were protected from infection by preincubation with monoclonal antibody to globoside. Knowledge of a parvovirus receptor has implications for understanding the pathogenesis of parvovirus infections and for the use of parvoviruses in gene therapy.

Antibodies, Monoclonal↗

PubMed1996

Evaluation of serological assays for identification of parvovirus B19 immunoglobulin M.

Three different enzyme immunoassays (EIAs) (Parvoscan-B19, IBL parvovirus B19, and IDEIA parvovirus B19) and one immunofluorescence assay (Biotrin Parvo B19 IFA) were evaluated for detection of parvovirus B19 immunoglobulin M (IgM) antibodies in 203 clinical serum samples. An IgM antibody capture radioimmunoassay was used as a reference test. Serum specimens obtained from patients with clinical symptoms suggestive of parvovirus B19 infections were used to evaluate the sensitivities of the assays, which were shown to be comparable for the Biotrin IFA and IDEIA (97%) and lower for the other two EIAs (90%). In order to test the specificity of the assays, clinical serum samples with IgM antibodies against other viruses were examined, as well as sera with rheumatoid factor activity and sera from healthy pregnant women. The specificities of B19 IgM antibody detection were 96% for the Biotrin IFA, 96% for IDEIA, 90% for Parvoscan, and 88% for the IBL assay. These results show that all four assays can be recommended for diagnostic purposes, although false-positive results may be seen with other acute viral infections, healthy pregnant women, and rheumatoid factor-positive samples.

Adolescent↗

PubMed2003

Evidence of parvovirus replication in cerebral neurons of cats.

The correlation between parvovirus infections and lesions in the central nervous system other than cerebellar hypoplasia was studied in 100 cats. The animals were necropsied with a history of various diseases, one third showing typical clinical and pathomorphological signs of panleukopenia. In 18 cats polyclonal antiserum against canine parvovirus consistently labeled neurons mainly in diencephalic regions, whereas the cerebellar cortex remained negative in all cases. In situ hybridization with digoxigenin-labeled minus-sense RNA probes, hybridizing with monomer-replicative form DNA or mRNA, revealed positive signals in nuclei of several neurons of the brain, again excluding the cerebellum. PCR applied to formalin-fixed and paraffin-embedded brain tissue and intestinal tissues of the diseased cats and subsequent DNA sequence analysis yielded canine parvovirus type 2 (CPV-2)-like sequences in the central nervous system. Two aspects of these findings are intriguing: (i). parvoviruses appear to be capable of replicating in neurons, cells that are considered to be terminally differentiated and (ii). CPV-like viruses of the old antigenic type CPV-2 appear to be able to infect cats.

Animals↗

PubMed1996

DNA double-strand break repair functions defend against parvovirus infection.

We measured parvovirus replication and sensitivity to X-ray damage in nine CHO cell lines representing a variety of DNA repair deficiencies. We found that parvovirus replication efficiency increases with radiosensitivity. Parvovirus replication is disrupted at an early stage of infection in DNA repair-proficient cells, before conversion of the single-stranded viral DNA genome into the double-stranded replicative form. Thus, status of the DNA repair machinery inversely correlates with parvovirus replication and is proportional to the host's ability to repair X-ray-induced damage.

Animals↗