The immune response to parvovirus B19 exposure in previously seronegative and seropositive individuals.

Little information is available on the immune response to parvovirus B19 after the administration of contaminated blood products. In the present study, we found that levels of B19 IgG in B19-seropositive recipients protect against reinfection and, after transfusion with pooled plasma containing B19 DNA (1.6 x 10(8) IU/mL), increase from 19-39 IU/mL to 50-100 IU/mL.

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

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 beta-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.

B cell memory is directed toward conformational epitopes of parvovirus B19 capsid proteins and the unique region of VP1.

Background: Loss of antibody reactivity against linear epitopes of parvovirus B19 (B19) capsid proteins VP1 and VP2 occurs after infection; however, it is unclear whether B cell memory is established against linear epitopes.

Methods: B cell enzyme-linked immunospot assay was used to evaluate B19-specific B cell memory in volunteer donors (n=22).

Results: B cell memory is maintained against conformational epitopes of VP2 and is absent against linear epitopes of VP2.

Ex vivo cytokine responses against parvovirus B19 antigens in previously infected pregnant women.

Parvovirus B19 infection is a significant cause of fetal death. The aim of this study was to investigate the role of maternal immune status in modulating susceptibility to fetal B19 infection. Peripheral blood was obtained from pregnant women (n = 199) with no clinical evidence of recent B19 infection.