Objectives: intrauterine parvovirus B19 infection is related to non-immune
hydrops fetalis, the pathogenesis of which is based on the strict tropism o
f B19 for erythroid precursor cells and the massive destruction of the infe
cted erythroid cells, although the mechanism of B19-induced cytotoxicity ha
s not been studied in detail, The purpose of this study is to provide empir
ical evidence that B19 induces apoptosis of erythroid cells both in vitro a
nd in vivo.
Methods: we analysed culture cells infected in vitro by B19 and tissues of
nine cases of hydrops fetalis caused by B19 intrauterine infection by histo
logical and biological methods,
Results: cells infected in vitro by B19 showed nuclear changes characterist
ic of apoptosis by light microscopic examination and DNA extracted from the
infected cells was fragmented. Electron microscopic examination showed the
nuclei of infected cells contained crescent-shaped clumps of heterochromat
in with increased density and double staining with anti-B19 antibody and te
rminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphat
e-digoxigenin nick-end labeling (TUNEL) confirmed apoptosis of individual c
ells. Tissues of cases of hydrops fetalis caused by B19 contained erythroid
cells with nuclear inclusions and characteristic nuclear changes of apopto
sis by light microscopy The double-staining confirmed apoptosis of erythroi
d cells in the tissues. Immunohistochemical analysis with antibodies agains
t cellular factors involved in apoptosis showed that caspase3, p53 and p21
were positive in infected cells.
Conclusions: these data indicate that B19 infection causes apoptosis of inf
ected cells and cellular factors, caspase3, p53 and p21, may play important
roles in the apoptotic pathway induced by B19.