B19 evolving picture of disease

Abstract

Parvovirus B19 first came to light in plasma from healthy blood donors and it was several years before it was associated with any disease at all. The wide spectrum of illness now attributed to B19 includes Fifths Disease of childhood, aplastic anaemia, arthritis and hydrops fetalis. Two pathogenic mechanisms are responsible. Immune complexes which circulate in very large amounts at the height of acute infection produce the rash and arthritis which characterise epidemics of disease in school children and young adults. The exquisite tissue trophism of the virus targets cells (probably pronormoblasts) of the erythroid lineage. Virus replication is dependent upon host cell turnover and is greatly increased in patients with haemolytic anaemia and in these patients the virus induced arrest of erythropoeisis quickly translates into aplastic crisis. The stem cells appear to be insusceptible to infection and these patients recover rapidly and completely as soon as antibody appear and virus is cleared from the circulation. In pregnancy B19 may cross the placenta and produce mid-trimester hydrops fetalis. Fetal loss has also been attributed to infection early in pregnancy and there an; hints of myocarditis as a specific feature of B19 infection of the infant. The latest addition to the spectrum of parvovirus related disease occurs in immune compromised individuals where chronic viraemia is associated with chronic aplastic anaemia and/or thrombocytopenia. As integration of viral DNA is the first step in replication of all parvoviruses these clinical findings raise the possibility that they are due to reactivation rather than primary infection. It seems that the clinical spectrum of B19 infection is not yet completely unfolded with its many diverse streams of interest.