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目的：研究人微小病毒 Ｂ１９（ Ｈ Ｐ Ｖ Ｂ１９）引致胎肝造血细胞凋亡及凋亡相关基因表达的变化，初步探讨 Ｈ Ｐ Ｖ Ｂ１９ 引起死胎的机理． 方法：采用原位末端标记法对２５ 例石蜡包埋死胎肝脏组织（其中 Ｈ Ｐ Ｖ Ｂ１９ Ｄ Ｎ Ａ 阳性者 １０ 例， Ｈ Ｐ Ｖ Ｂ１９ Ｄ Ｎ Ａ 阴性者１５ 例）进行细胞凋亡检测，并用免疫组化方法检测ｂｃ１２，ｂａｘ 表达情况． 结果：１０ 例 Ｈ Ｐ Ｖ Ｂ１９ Ｄ Ｎ Ａ 阳性死胎肝脏组织中 ８ 例明显可见造血细胞的凋亡，６ 例 ｂａｘ 表达阳性． １５ 例 Ｈ Ｐ Ｖ Ｂ１９ Ｄ Ｎ Ａ 阴性死胎肝脏组织中仅 ２ 例有造血细胞的凋亡，２ 例ｂａｘ 表达阳性，２５ 例均未检出ｂｃ１２ 的表达．结论： Ｂ１９ 感染可能诱导胎肝造血细胞的凋亡，这为可能是该病毒引起胎儿死亡的重要机制．
OBJECTIVE: To study the changes of apoptosis and related gene expression in fetal liver hematopoietic cells induced by human parvovirus B19 (H P V B19), and to investigate the mechanism of H P V B19 induced stillbirth. Methods: Twenty-five paraffin-embedded fetal liver tissues (including 10 H P V B19 D N A positive and 15 H P V B19 D N A negative) were detected by in situ end labeling. Immunohistochemical detection of bcl-2, bax expression. Results: The apoptosis of hematopoietic cells was obvious in 8 of 10 Hp V B19 D N A positive dead fetus liver tissues, and 6 of them were positive for bax. In 15 cases of H P V B19 D N A negative fetal dead liver tissue, only 2 cases of apoptosis of hematopoietic cells, 2 cases of bax expression was positive, 25 cases were not detected bc1 2 expression. Conclusion: B19 infection may induce apoptosis of fetal liver hematopoietic cells, which may be an important mechanism of fetal death caused by the virus.