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...