The molecular epidemiology of parvovirus B19

Abstract

Parvovirus B19, the only known parvovirus pathogenic for humans, is a common infectious agent, causing erythema infectiosum in children, post-infection arthropathy in adults, transient aplastic crisis in patients with shortened red cell survival and chronic bone marrow failure in immunosuppressed patients. B19 infection has also been associated with a diverse group of clinical manifestations including hydrops fetalis, congenital red cell aplasia, vasculitis syndromes, glomerulonephritis with nephrotic syndrome, meningitis, encephalopathy, peripheral neuropathy, myocarditis and hepatitis. B19 does not propogate well in conventional cell culture but B19 DNA from clinical samples has been amplified using molecular cloning or PCR. Analysis of isolates has revealed genetic diversity, and a workable strategy for strain classification has been devised to study the molecular epidemiology of B19 infection. The particular genotype endemic in Japan during the outbreak of 1981–1982 was replaced in the outbreak of 1986–1987 by a different genotype similar to B19 strains isolated in the USA and Europe during 1978–1986, suggesting the possibility of global transmission of B19. Sequence heterogeneity between B19 strains isolated from each case of persistent infection (infected fetuses and a persistently-infected patient with arthralgia and chronic fatigue syndrome) is probably accounted for by the many rounds of replication necessary to maintain a prolonged infection. Isolation of a new B19 genotype from a particular disease (e.g. encephalopathy) and replacement of genotype during persistent infection would seem to be the platform from which to launch further studies to associate particular genotypes with particular clinical manifestations of infection.