Detection of antibodies and antigens of human parvovirus B19 by enzyme-linked immunosorbent assay

Abstract

Acute-phase serum from a patient with aplastic crisis provided sufficient human parvovirus B19 to make a monoclonal antibody against B19 and to develop antigen and immunoglobulin M (IgM) and IgG antibody detection enzyme-linked immunosorbent assays (ELISAs). The indirect capture antibody method was used for all three assays. Antigen was detected in 8 of 29 sera drawn within 2 days of onset of illness from patients with aplastic crisis. These sera had high titers of virus by electron microscopy and DNA hybridization and had no detectable B19 antibody. Antigen was not detected in serum specimens that had low titers of B19 DNA and had B19 antibody. With the IgM ELISA, we detected B19 IgM in over 85% of clinical cases of aplastic crisis and fifth disease and less than 2% of controls. The prevalence of B19 IgG antibodies increased with age. Approximately 2% of children <5 years of age and 49% of adults >20 years of age had B19 IgG antibodies. The B19 antibody ELISAs are sensitive and specific tests to detect B19 infections. Human parvovirus B19 was identified and characterized in 1975 by Cossart et al. while they were evaluating assays for hepatitis B virus in serum (11). Initially, studies to identify the clinical and epidemiological characteristics of B19 infections used counterimmunoelectrophoresis tests. Counter immunoelectrophoresis and later, a more sensitive radioimmunoassay (RIA), showed that B19 infection was associated with aplastic crisis in patients with hemolytic anemias in 1981 (31), with fifth disease in 1983 (6), with stillbirths in 1984 (8, 20), and with arthritis in 1985 (30, 33). The antibody assays require B19 antigen (P), and since B19 has not been grown in tissue culture or in laboratory animals, sera from humans remain the sole source of this antigen (7). Recently, the development of DNA hybridization assays (5, 9) has improved our ability to detect the virus, but immunoglobulin G (IgG) and IgM antibody assays remain the most sensitive way to detect B19 infection (5). An epidemiological investigation of simultaneous outbreaks of aplastic crisis and fifth disease in Ohio in the spring of 1984 (30a; T.

Seroepidemiology of Human Bocavirus in Hokkaido Prefecture, Japan

“…The overall seroprevalence rate and the age group-specific rate of anti-B19 antibody titers are shown in Table 3. These rates are consistent with previously reported data (4,14,22,25,46), indicating that the VP1 protein of B19 was properly prepared. The existence of HBoV IFA-positive and B19 IFA-negative or HBoV IFAnegative and B19 IFA-positive serum samples indicates that the anti-HBoV and anti-B19 sera did not cross-react with each other ( Table 1).…”

Molecular and phylogenetic analyses of human Parvovirus B19 isolated from Brazilian patients with sickle cell disease and β‐thalassemia major and healthy blood donors

“…This epidemiological pattern may result from a combination of factors that facilitate B19V transmission, such as presence of highly viremic patients, nosocomial spread, transfusion-related transmission, and absence of well-defined diagnostic and therapeutic procedures [Regaya et al, 2007]. In the examined Brazilian region, the overall B19V seroprevalence was similar to that reported in the USA [Anderson et al, 1986], and Japan [Shiraishi et al, 1985], and significantly higher than that of some South eastern Asian countries (Hong Kong, Singapore, Taiwan) [Lim et al, 1997].…”

Epidemiologic study of human parvovirus B19 infection in East China

“…The aa 550-580 are shown with mutations of P558S and Y573G. results showed that the overall B19V IgG antibody presence is between 21.9% and 41.8% in various populations in the greater metropolitan area of Hangzhou, East China, which is lower than the rate ($60%) reported in adults worldwide [Nunoue et al, 1985;Anderson et al, 1986;Cohen and Buckley, 1988;Lim et al, 1997;Lin et al, 1999]. This result indicates that a large percentage of the population ($60%) in this area has not been exposed to B19V, and thus individuals living in this area might be at a high risk of becoming infected with B19V.…”

“…Since the first discovery of B19V in 1974 [Heegaard and Brown, 2002], B19V infection has been reported worldwide [McOmish et al, 1993;Jordan et al, 1998;Aubin et al, 2000;Heegaard et al, 2001;Thomas et al, 2003]. The presence of B19V antibody ranges from $20% in young children to $80% in people >60 years [Nunoue et al, 1985;Anderson et al, 1986;Cohen and Buckley, 1988;Lim et al, 1997;Lin et al, 1999]. The presence of B19V DNA in healthy blood donors could be as high as 1% [Azzi et al, 1999].…”