The age-specific prevalence of human parvovirus immunity in Victoria, Australia compared with other parts of the world

Abstract

The age-specific immunity to human parvovirus infection was estimated in Victoria, Australia using prospectively collected samples from the Royal Children's Hospital, the Royal Women's Hospital and the Australian Red Cross Blood Service and from sera stored at the Victorian Infectious Diseases Reference Laboratory (VIDRL). All testing was performed at VIDRL using a commercial enzyme-linked immunosorbent assay (Biotrin). Of the 824 sera tested, 28% of those drawn from people aged 0-9 years contained protective antibodies to human parvovirus. This rose to 51% in the next decade of life. There was then a slow rise to about 78% immunity over 50 years of age. An analysis of all requests for parvovirus serology at VIDRL from 1992 to 1998 suggested that parvovirus tended to occur in 4-year cycles, with 2 epidemic years followed by 2 endemic years. A review of published reports of parvovirus immunity suggested that parvovirus infection may be more common, with a correspondingly higher proportion of the community immune, in temperate as opposed to tropical countries.

Seroprevalence of parvovirus B19 infection in daycare educators

“…It reinforces the importance of prevention of parvovirus B19 infection in pregnant women and especially that of the recent recommendation of the Society of Obstetricians and Gynaecologists of Canada (SOGC) to assess a pregnant woman's immunity to parvovirus B19 [10]. The association of parvovirus B19 seropositivity with age is consistent with population-based studies in the United Kingdom and Australia [11,12]. This trend can be explained by the fact that parvovirus B19 antibodies last for life [10].…”

Parvovirus B19 and the Kidney

“…Acquisition is often during childhood and continues at lower rates throughout adulthood such that between 70 and 85% of adults show serologic evidence of past infection (14,15). Infectivity shows seasonal variation in temperate climates, being more common in winter and spring.…”

Etiopathogenesis of aplastic anemia in children: a case control study

“…15 Therefore parvovirus B19 infection can result in transient aplastic crises, congenital or acquired pure red cell aplasia and also idiopathic thrombocytopenic purpura. [13][14][15][16][17][18][19][20] The second hypothesis is based on immunological mediation. In virus associated haemophagocytic syndrome with acute parvo B19 infection, raised cytokines such as interferon γ would impair regulation of the phagocyte system, resulting in pancytopenias and/or decreased haematopoiesis.…”