Occurrence of infection with a parvovirus-like agent in children with sickle cell anaemia during a two-year period.

Abstract

SUMMARY The occurrence of infection with a parvovirus-like agent during the period April 1979-May 1981 in children attending a single sickle cell clinic in London was investigated. Virus was detected in serum by counter-current immunoelectrophoresis (CIE) and immunoelectron microscopy (IEM). Viral antibody was detected by CIE and specific IgM antibody by an IgMantibody capture assay. Of the 68 children studied nine presented in aplastic crisis and evidence of infection with the parvovirus-like agent at the time of the crisis was found in all nine. Eighteen of the other children were antibody-positive at some time during the study. In 11 children there was no evidence of recent infection; however, two of these had a history of aplastic crisis in previous years. The other seven seroconverted during the course of the study but did not show any haematological effects. Five of these had a primary infection, one appeared to have reinfection and in the seventh there were insufficient data to distinguish between the two. Possible explanations for the difference between those presenting with aplastic crisis and those with asymptomatic seroconversion are discussed.In 1975 Cossart et al described the presence of parvovirus-like particles in the sera of 11 persons.' Nine were healthy blood donors, one was a case of ,acute hepatitis and one had been given a renal transplant a week earlier. The serum from one of the healthy blood donors was designated B19. Subsequently a similar virus was found in the serum of two blood donors2 (one of whom felt unwell and vomited several times and the other complained of myalgia at about the time of the viraemia) and in two patients with a short febrile illness.3We recently reported45 an association between a virus which cross-reacts with that found in serum B 19 and aplastic crises in children with sickle cell anaemia (SCA). In order to minimise morbidity and mortality children with SCA are admitted to hospital promptly for observation and investigation even when they are suffering apparently minor illness. Investigation of these patients after admission to hospital includes the taking of serum samples for

Characterization of the Genome of the Agent of Erythrocyte Aplasia Permits its Classification as a Human Parvovirus

“…Following this description sporadic cases of infection were reported in association with febrile illness Shneerson et al, 1980) but the nature of this agent and its pathological significance in man remained obscure. With the identification of a defined syndrome of serious clinical illness attributable to infection with this virus Serjeant et al, 1981) interest has been revived; it is now clear that in patients with chronic haemolytic anaemias, infection with this agent results in a transient interruption in the production of erythrocytes, leading to a profound but self-limiting anaemia (Anderson et al, 1982a;Duncan et al, 1983;Kelleher et al, 1983;Rao et al, 1983), the so-called 'aplastic crisis'. This pattern of pathological changes affecting the rapidly dividing cells of the erythrocyte series is reminiscent of the changes seen in rapidly dividing tissues of other species infected with animal parvoviruses, such as leukopenia and enteritis in cats and dogs, and foetal death and abnormality in pigs.…”

Human Parvovirus B19

“…While the anemia may be lethal, the aplastic crisis itself is usually terminated by the appearance of specific antibodies and thus rarely lasts for more than 2 weeks. In predisposed individuals 70 to 80% of aplastic episodes are caused by B19 infection (7,59,179). The annual incidence is 1 to 5%, predominantly affecting children and representing a unique event in life (7,59).…”

“…The annual incidence is 1 to 5%, predominantly affecting children and representing a unique event in life (7,59). Aplastic crisis usually presents with pallor, weakness, and lethargy, and patients are highly viremic, thereby posing a risk of transmission to others (7,26,59).…”

Biological and Immunological Relations among Human Parvovirus B19 Genotypes 1 to 3

“…The viral capsid proteins were stained with a 1:1,000-diluted mouse monoclonal antibody (69), and the NS protein was stained with a 1:500-diluted human monoclonal antibody (22) for 60 min at room temperature in a moist chamber. The primary antibodies were then visualized by 1:30-or 1:50-diluted fluorescein isothiocyanate-conjugated secondary antibodies [polyclonal rabbit anti-mouse immunoglobulins (Dako A/S, Denmark) or AffiniPure F(abЈ) 2 Fragment Goat anti-Human IgG (HϩL) (Jackson Immunoresearch Laboratories, Inc., West Grove, PA), respectively] applied for 30 min. After being washed, the cells were mounted with Vectashield mounting medium containing DAPI (4Ј,6Ј-diamidino-2-phenylindole) counterstain and observed with a Zeiss Axioplan 2 fluorescence microscope.…”

“…The virus replicates in erythroid progenitor cells of bone marrow (49,64), causing aplastic crisis in patients with hemolytic anemia of various etiologies (2,53,56). During pregnancy, B19 can be transmitted from the infected mother to the fetus and cause fetal hydrops and death (9).…”