Detection of parvovirus B19 DNA, antigen, and particles in the human fetus

Clewley, J. P.; Cohen, B. J.; Field, Anne M.

doi:10.1002/jmv.1890230409

Cited by 63 publications

(19 citation statements)

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“…Dot blot hybridisation (DBH) -A 10% homogenate of fetal tissue was prepared and DNA extracted as described by Clewley et al (1987) except that the extracted DNA was applied to nitrocellulose filters and the blots were hybridised with a 32P-labelled B19 probe. The probe was made from the 5.2 Kb Eco RI fragment excised from the B19/pGem-1 plasmid (Mori et al 1989).…”

Section: Methodsmentioning

confidence: 99%

“…The infection is diagnosed by the detection of IgM antibodies in both maternal and fetal blood (Knott et al 1984) but, in some cases, maternal anti-B19 IgM can no longer be detected when hydrops fetalis develops (Bond et al 1986. In most of the reported cases, DNA detection in fetal tissues is the method of choice for diagnosis (Clewley et al 1987, Salimans et al 1989. Electron microscopy has also been used , Knisely et al 1988, Naides & Weiner 1989.…”

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confidence: 99%

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Human parvovirus B19 infection and hydrops fetalis in Rio de Janeiro, Brazil

Cubel¹,

Garcia²,

Pegado³

et al. 1996

Mem. Inst. Oswaldo Cruz

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Section: Methodsmentioning

confidence: 99%

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Human parvovirus B19 infection and hydrops fetalis in Rio de Janeiro, Brazil

Cubel¹,

Garcia²,

Pegado³

et al. 1996

Mem. Inst. Oswaldo Cruz

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“…B19 can be transmitted transplacentally from an infected mother to her fetus, which may lead to non-immune fetal hydrops (NIHF), spontaneous abortion or intrauterine fetal death (IUFD) (Clewley et al, 1987;Miller et al, 1998; Skjoldebrand-Sparre et al, 2000). The P blood group antigen, which serves as a receptor for B19, has been detected on cells of the villous trophoblast of placental tissues in varying amounts during the course of pregnancy.…”

Section: Infectivity Transmission and Epidemiologymentioning

confidence: 99%

Advances in the biology, diagnosis and host–pathogen interactions of parvovirus B19

Corcoran

Doyle

2004

Journal of Medical Microbiology

153

103

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Increased recognition of parvovirus B19 (B19), an erythrovirus, as a significant human pathogen that causes fetal loss and severe disease in immunocompromised patients has resulted in intensive efforts to understand the pathogenesis of B19-related disease, to improve diagnostic strategy that is deployed to detect B19 infection and blood-product contamination and, finally, to elucidate the nature of the cellular immune response that is elicited by the virus in diverse patient cohorts. It is becoming clear that at least three related erythrovirus strains (B19, A6/K71 and V9) are circulating in the general population and that viral entry into target cells is mediated by an expanding range of cellular receptors, including P antigen and â-integrins. Persistent infection by B19 is emerging as a contributory factor in autoimmune disease, a hypothesis that is constrained by the detection of B19 in the skin of apparently healthy individuals. B19 infection during pregnancy may account for thousands of incidences of fetal loss per annum in Europe, North America and beyond, yet there is currently only minimal screening of pregnant women to assess serological status, and thereby risk of infection, upon becoming pregnant. Whilst major advances in diagnosis of B19 infection have taken place, including standardization of serological and DNA-based detection methodologies, blood donations that are targeted at high-risk groups are only beginning to be screened for B19 IgG and DNA as a means of minimizing exposure of at-risk patients to the virus. It is now firmly established that a Th1-mediated cellular immune response is mounted in immunocompetent individuals, a finding that should contribute to the development of an effective vaccine to prevent B19 infection in selected high-risk groups, including sickle-cell anaemics. Parvovirus B19In 1975, Yvonne Cossart discovered what was to become known as human parvovirus B19 (B19) (Cossart et al., 1975). B19 was first associated with disease in 1981, when it was linked to an aplastic crisis in a patient with sickle-cell disease. It has since been shown to cause erythema infectiosum (EI) (fifth disease of childhood), spontaneous abortion and some forms of acute arthritis (Anderson et al., 1983; Kinney et al., 1988;Woolf & Cohen, 1995).B19 is a small, non-enveloped, ssDNA virus and, like all parvoviruses, the capsid proteins are arranged with icosahedral symmetry. B19 is 20-25 nm in diameter and has a genome of 5 . 6 kb (Clewley, 1984;Cotmore & Tattersall, 1984). The B19 capsid consists of an 83 kDa minor structural protein, VP1, and a 5 kDa major structural protein, VP2. VP2 makes up about 95 % of the total capsid, with VP1 accounting for the remaining 5 % . The sequences of the two proteins are collinear, with VP2 being identical to the carboxyl-terminus of VP1; however, VP1 comprises an additional 227 aa domain that is unique to the amino-terminal (Fig. 1). To the left of these sequences on the B19 genome is the ORF for a non-structural protein, NS1, which encodes a protein product of 7...

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“…Globoside is present not only on cells of the erythroid lineage but also on the surface of placental syncytiotrophoblast and cytotrophoblast cells (17). The presence of the globoside receptor on trophoblast cells may play a role in transmission of the virus across the placenta.B19 infection of pregnant women can lead to vertical transmission of virus to the fetus with outcomes that include spontaneous abortion, fetal anemia, nonimmune hydrops fetalis, and intrauterine fetal death (6,15,23,26,31,36). Although B19 is capable of causing congenital infection, numerous clinical studies show clearly that the majority of women who become infected with B19 during pregnancy deliver healthy infants (9,20,27,29,37).…”

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Placental Cellular Immune Response in Women Infected with Human Parvovirus B19 during Pregnancy

Jordan

Huff

DeLoia

2001

Clin Diagn Lab Immunol

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Human parvovirus B19 can cause congenital infection with variable morbidity and mortality in the fetus and neonate. Although much information exists on the B19-specific antibody response in pregnant women, little information is available describing the cell-mediated immune (CMI) response at the maternal-fetal interface. The focus of this study was to characterize the CMI response within placentas from women who seroconverted to B19 during their pregnancies and compare it to controls. Immunohistochemical techniques were used to identify the various immune cells and the inflammatory cytokine present within placental tissue sections. Group 1 consisted of placentas from 25 women whose pregnancies were complicated by B19 infection; 6 women with good outcome (near-term or term delivery), and 19 with poor outcome (spontaneous abortion, nonimmune hydrops fetalis, or fetal death). Group 2 consisted of placentas from 20 women whose pregnancies were complicated with nonimmune hydrops fetalis of known, noninfectious etiology. Group 3 consisted of placentas from eight women whose pregnancies ended in either term delivery or elective abortion. The results of the study revealed a statistically significant increase in the number of CD3-positive T cells present within placentas from group 1 compared to group 2 or 3 (13.3 versus 2 and 1, respectively) (P < 0.001). In addition, the inflammatory cytokine interleukin 2 was detected in every placenta within group 1 but was absent from all placentas evaluated from groups 2 and 3. Together, these findings demonstrate evidence for an inflammation-mediated cellular immune response within placentas from women whose pregnancies are complicated with B19 infection.The placenta plays an integral barrier role in limiting congenital viral infections (18). However, some viruses, transmitted via the blood, are able to circumvent this barrier. Virus within maternal blood reaches the intervillous space and makes intimate contact with the placental trophoblast layer, which can lead to virus transmission across that protective barrier to the fetal side. Transmission can occur through breaks in the placental barrier, via endocytosis or receptormediated transfer.The P blood group antigen globoside is the main cellular receptor for B19 (3,4). Globoside is present not only on cells of the erythroid lineage but also on the surface of placental syncytiotrophoblast and cytotrophoblast cells (17). The presence of the globoside receptor on trophoblast cells may play a role in transmission of the virus across the placenta.B19 infection of pregnant women can lead to vertical transmission of virus to the fetus with outcomes that include spontaneous abortion, fetal anemia, nonimmune hydrops fetalis, and intrauterine fetal death (6,15,23,26,31,36). Although B19 is capable of causing congenital infection, numerous clinical studies show clearly that the majority of women who become infected with B19 during pregnancy deliver healthy infants (9,20,27,29,37). The risk of fetal demise appears to be greatest when infecti...

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Detection of parvovirus B19 DNA, antigen, and particles in the human fetus

Cited by 63 publications

References 23 publications

Human parvovirus B19 infection and hydrops fetalis in Rio de Janeiro, Brazil

Human parvovirus B19 infection and hydrops fetalis in Rio de Janeiro, Brazil

Advances in the biology, diagnosis and host–pathogen interactions of parvovirus B19

Placental Cellular Immune Response in Women Infected with Human Parvovirus B19 during Pregnancy

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