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The ability of cultured human synovial cells derived from synovial membrane and cartilage to support the replication of human parvovirus B19 was assessed. No viral DNA synthesis nor viral antigens were detected suggesting that B19 virus is not capable of replicating in synovial cells. The significance of this finding in relationship to the pathogenesis of parvovirus arthritis is discussed.
Human parvovirus B19 is a member of the autonomous parvoviridae but in contrast to other members of the genus has not been shown to agglutinate red blood cells. We now report that the virus agglutinates red cells of primate origin, though with plasma-derived virus this activity is masked by the presence of an IgM-like inhibitor. This observation is consistent with the presence on the erythroid precursor target cell of a specific receptor for parvovirus B19.
A chemiluminescence dot blot hybridization assay was used for the detection of B19 parvovirus DNA in human sera by using digoxigenin-labeled probes. The probes were revealed immunoenzymatically by use of anti-digoxigenin Fab fragments conjugated with alkaline phosphatase. The chemiluminescence signal was obtained by reacting the labeled probe-target complex with an enzyme-triggerable dioxetane substrate. The emitted photons were detected with instant photographic films. In the search for B19 parvovirus DNA, 2,808 serum samples were analyzed.
To produce parvovirus B19 antigen for diagnostic purposes, partially overlapping segments covering the genes encoding the viral structural proteins VP1 and VP2 were cloned into expression vectors. The constructs were induced in Escherichia coli, resulting in the expression of beta-galactosidase fusion proteins. In immunoblotting experiments with sera from patients with erythema infectiosum, immunoglobulin G (IgG) and IgM antibodies bound to a single polypeptide of 235 amino acids at the N terminus of VP1. The DNA fragment encoding this polypeptide was amplified by the polymerase chain reaction and cloned into an expression vector. The viral capsid antigen expressed in E. coli was purified by preparative agarose gel electrophoresis and used in IgG and IgM solid-phase enzyme immunoassays. Comparison with reference gamma- and mu-capture radioimmunoassays using whole virus antigen showed that these antibody tests are suitable for the serodiagnosis of human infections caused by parvovirus B19.
A 59 year old woman presented with an influenza-like illness preceding signs and symptoms strongly suggestive of systemic lupus erythematosus (SLE), which progressed over several months. Owing to these influenza-like symptoms, a viral cause of her illness was sought. Human parvovirus B19 serology was positive and antibodies to DNA were detected by two different methods. This patient is believed to be the first report of human parvovirus B19 infection coinciding with the onset of SLE. The evidence for B19 virus and the part it plays in autoimmunity and arthritis is discussed.
AIMS: To compare the use of biotinylated and digoxigenin labelled probes for diagnosis of human fetal parvovirus B19 infection in formalin fixed, paraffin wax embedded tissues; and to assess the cellular distribution of the virus in positive cases. METHODS: Sections of lung tissue from 23 cases of anatomically normal non-immune fetal hydrops presenting between 1984 and 1989, and from 13 control cases of hydrops due to chromosomal abnormality were probed for B19 DNA by in situ hybridisation using both biotinylated and digoxigenin labelled probes. The distribution of the virus was then investigated in all cases of fetal B19 infection confirmed in this laboratory to date (n = 11) by combining in situ hybridisation for viral DNA (using the digoxigenin system) with immunohistological labelling for a range of cellular antigens. RESULTS: Five unequivocal cases of B19 infection were identified among the 23 fetuses with unexplained hydrops using both probe labels. When combined with data from previous studies of the period 1974-1983, the results indicate that B19 infection was responsible for 27% of cases of anatomically normal non-immune hydrops and 8% of all cases, of non-immune hydrops presenting to this hospital over 15 years. False positive signal was seen in an additional three cases, using biotinylated probes. Digoxigenin labelled probes gave greater specificity and permitted detailed investigation of tissues high in endogenous biotin. Though most cells containing B19 DNA colabelled as erythroid precursors, viral DNA was frequently detected within mononuclear-phagocytic cells. In three cases viral signal was also found within occasional myocardial cells labelled by antibody to desmin. CONCLUSIONS: A relatively high proportion of cases of anatomically normal, non-immune hydrops are caused by B19 infection. Digoxigenin is a more reliable probe label than biotin for in situ hybridisation in archival fetal tissues. Double labelling for cellular antigens and viral nucleic acid is a powerful technique for investigating virus-host cell interactions, and provides evidence that cell types other than those of erythroid lineage may have a role in human fetal parvovirus infection.
We report three cases of systemic lupus erythematosus (SLE) associated with necrotizing histiocytic lymphadenitis (Kikuchi's disease) and immunologically proven human parvovirus B19 infection. Simultaneous occurrence of SLE and Kikuchi's disease was a characteristic of the three cases. Kikuchi's disease is an uncommon disease that usually affects young women and is characterized by painless unilateral cervical lymph-node enlargement. T-cell regions of affected lymph nodes are exclusively involved with patchy paracortical necrosis surrounded by a polymorphous cell population of histiocytes and macrophages. However, lymphadenopathy in patients with SLE may be histologically indistinguishable from Kikuchi's necrotizing lymphadenitis. The cause of Kikuchi's disease remains uncertain, although infectious agents have been proposed. A positive IgM-specific anti-human parvovirus B19 antibody test in our three cases suggests that B19 can induce a necrotizing histiocytic lymphadenitis and possibly a clinical SLE flare. High-dose (1 mg/kg/day) and medium-dose (0.5 mg/kg/day) oral prednisone was an effective treatment for constitutional and visceral symptoms of Kikuchi's and SLE diseases.
Parvovirus B19 DNA can be detected by polymerase chain reaction with double primer pairs (nested PCR). Recent infection was documented by a retrospective serological study using Parvoscan-B19 enzyme linked immunosorbent assay (EIA) for detection of B19 human parvovirus IgM and IgG antibodies in serum or plasma specimens. In 3 families B19 outbreaks caused aplastic crises necessitating blood transfusion in 5 children and 1 adult with hereditary sphaerocytosis. Four members from 2 of the families had clinically overt haemolytic anaemia prior to the event. Two members in another family presented with an aplastic crisis disclosing the underlying chronic haemolytic disease. All 7 patients were identified as PCR positive in serum samples taken 3-14 days after the onset of symptoms. Comparison with dot blot hybridization revealed detectable DNA in only 2/3 PCR positive patients. Thus, nested PCR is more sensitive than the dot blot hybridization method and is therefore a suitable complement to the antibody assay for identifying recent B19 infection.
A case of bone marrow necrosis associated with a serologically documented recent Parvovirus B 19 infection which preceded the development of PH1+ acute lymphoblastic leukemia is reported. No conclusions can be drawn on the basis of a single case but the question of the role of human Parvovirus B19 in the pathogenesis of bone marrow necrosis is discussed. It is suggested that the virus may act as a co-factor for the induction of bone marrow necrosis, in some cases.
A seven months old boy was admitted to hospital for investigation and treatment of severe anaemia. The final diagnosis was hereditary spherocytosis. When, six weeks later, he developed an aplastic crisis, serological criteria provided evidence of recent human parvovirus B19 infection. The same disease was detected in the family. Human parvovirus B19 is shown to be of particular interest in aplastic crisis.
The pathogenic human parvovirus B19 has extreme tropism for human erythroid progenitor cells and has resisted cultivation in conventional cell lines. We report first propagation of this virus in an erythropoietin-dependent strain of a megakaryoblastic leukemia cell line called UT-7. Virus protein was present in about 5% of cells after 1 week of culture. Appropriate ratios of major and minor capsid proteins were determined by immunoblot, and newly synthesized capsid protein was detected by immunoprecipitation of radioactively labeled cell lysates. High molecular weight monomer and dimer intermediates were detected by Southern analysis, indicating active viral replication. Approximately 1,000 genome copies were present per infected cell, and at the optimal multiplicity of infection 20- to 50-fold more virus was produced than inoculated. Virus propagation only occurred in UT-7 cells that were adapted to growth in erythropoietin; virus signal was not detected in UT-7 cells adapted for growth in granulocyte-macrophage colony-stimulating factor or interleukin-3, even with exposure to erythropoietin for several days. Infectious virus was detected in cultures as long as 3 months after inoculation. Despite persistence, there was no evidence of viral integration on Southern analysis. This cell line may prove useful for the production of infectious virus and in the analysis of B19 parvovirus persistence, cytotoxicity, and permissivity.
The human parvovirus B19 agent causes infectious erythema (fifth disease). However, a wide range of other pathological manifestations may also be seen: atypical exanthema, ARD (also obstructive forms, e.g. bronchiolitis), acute gastroenteritis, chronic anemia or aplastic crises (in constitutional or malignant hematological diseases or immunological deficiency), arthralgia/arthritis (e.g. rheumatoid arthritis, jcA), diseases of the central nervous systems (e.g. febrile convulsions in young children), lymphadenopathies (e.g. lymphadenitis mesenterialis or pseudoappendicitis); prenatal infection can lead to fetal death (not malformations!). Infection occurring concomitantly with vaccination may suggest complications of the latter. To clarify the true etiological situation, modern laboratory investigations are then required. Vaccination against parvovirus B19 (initially indicated in the case of non-immune girls and women wanting children) is a desirable future development.
Antibodies against H-1 and X14 parvoviruses were found 13.71 and 9.14%, respectively, of 350 sera from women affected by repeated abortions or still-births. On the contrary, only 2.66 and 1.66% of 300 control sera were positive to the two viruses. The difference in the incidence of antibodies appears highly significant (p greater than 0.001). Therefore a possible role of the parvoviruses in inducing abortions or still-births in humans is suggested.
During 1987 and 1988, we identified 9 adults at the Medical and Rheumatology Services of the University of Iowa Hospitals and Clinics who had a clinical diagnosis of fifth disease; 8 of the 9 had symptoms of joint involvement. Another 12 adults with serologic positivity for anti-parvovirus B19 IgM antibody presented with polyarthralgia/polyarthritis. Patients were usually found to be seronegative for rheumatoid factor, and none developed nodules or erosive disease. Many patients with chronic disease met criteria for a diagnosis of rheumatoid arthritis. A diagnosis of parvovirus B19 infection should be considered during the initial visit of patients with polyarthralgia/polyarthritis.
Half of the genomic DNA of the human parvovirus (B19) was cloned in the plasmid pBR322. The cloned DNA was used as a molecular probe for the detection of parvovirus in serum by means of a dot hybridization test. In an assay of 26 samples, the dot hybridization test was found to be of comparable sensitivity and to be as rapid as radioimmunoassay for viral antigen detection; it is potentially useful as a diagnostic test.
Human parvovirus B19 commonly infects children, causing erythema infectiosum (fifth disease). However, there is a significant adult population which has not been exposed to the virus and, consequently, does not have protective antibody. Recent reports have associated B19 infection during pregnancy with fetal death, although normal outcome of pregnancy is more common. To characterise further the role of B19 infection in fetal deaths, a series of laboratory investigations has been undertaken on tissues obtained at autopsy. These have demonstrated the presence of virion-sized DNA by Southern blotting, viral antigen by radioimmunoassay, and viral particles by electron microscopy, all from tissues of hydrops fetalis. These data confirm that the human parvovirus B19 can cross the placenta and replicate in fetal tissues.
We report the findings on an HIV-positive patient found to be infected with human parvovirus B19. In a comparative study of sequential sera, direct electron microscopy (EM) had the same sensitivity as DNA hydridization for the detection of the virus. EM did not require specific reagents and also yielded information on the state of the virus; i.e., whether random or complexed, and the type of antibody involved. The presence of parvovirus complicated the judgement as to drug treatment. This case also highlighted the importance of diagnosing the presence of opportunistic viral infections that have no, or low-grade, pathogenic activity.
Sera from inhabitants of Belém, Pará (542 sera), Brazil and of members of 3 Brazilian tribes--Tiriyo/Alto Paru (near Surinam) (212 sera), Xicrin (128 sera), and Mekranoiti (121 sera)--of different age and sex groups were tested for the presence of specific antibody against human parvovirus (B19) (RIA) and rubella virus (latex agglutination test). Parvovirus (B19) IgG was found in 42.6% of the population sample from Belém but in only 4.7 to 10.7% of the members of the tribes. Rubella virus antibody was found in 72.7% of the sera from Belém but approaching a prevalence of 85-90% in age groups above 20 years. In the tribes rubella virus antibody was detected in 36.9 to 72.6% of all sera. There were remarkable sex differences of antibody prevalence in several age groups of the population from Belém and of the tribal populations. About a quarter of the skin rashes in Belém that were not attributable to infections with rubella, measles, or arboviruses were caused by recent B19 infections.