In 1981 Pattison et al detected a parvovirus-like agent (PVLA) in sera from six children with sickle cell anaemia (SCA) who had had aplastic crises. Evidence of PVLA infection has since been found in eight more cases of SCA in the U.K. (Anderson, 1982), 24 in Jamaica (Serjeant et al, 1981) and six in the U.S.A. (Rao et al, 1983). Similar crises associated with PVLA infection have also been reported in hereditary spherocytosis (HS) by Kelleher et al(l982), in pyruvate kinase deficiency (PK) by Duncan & Kertz (1982), and in untransfused thalassaemia intermedia by Rao et al (1 8 3). PVLA infection probably occurs worldwide, 9 having been identified in West Africa (Pattison, 1983, unpublished observation) and Australia (Schneerson et al, 1980, quoting Cossart); as well as in the U.K., the U.S.A. and Jamaica. Together these findings suggest that PVLA could be the cause of most aplastic crises in haemolytic anaemias. A retrospective study of published reports of aplastic crises in HS between 1935 and 1964 concluded that they might all have been manifestations of infection by a single agent which could have been PVLA (Mortimer, 1983). Automonous animal parvoviruses are known to have an affinity for rapidly
British Journal of Haematology – Wiley
Published: Nov 1, 1983
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