Yang K D, Lee C S, Shaio M F
Department of Pediatrics, Tri-service General Hospital, Taipei, Taiwan, R.O.C.
Acta Microbiol Immunol Hung. 1995;42(4):403-7.
Patients with a dengue-1 virus (DV-1) infection followed by another DV-2 infection were reported to have a higher incidence of dengue haemorrhagic fever (DHF). Mononuclear leukocytes (MNLs) are principal cells for DV replication so that we challenge MNLs obtained from non-immune and previously DV-1-infected donors with DV-2 to mimic primary and heterologously secondary DV-2 infections. Production of platelet activating factor (PAF), thromboxane B2 (TxB2), and prostaglandin D2 (PGD2) by MNLs in the DV-2 infections was measured by radioimmunoassay. We found that MNLs, no matter primary or heterologously secondary exposure to DV-2, could release significant amount of PAF, TxB2, and PGD2. PAF but not TxB2 or PGD2 levels released by MNLs were significantly higher in those obtained from previously DV-1-infected donors (75.8 +/- 28.5 vs 21.2 +/- 13.4 pg/ml; p < 0.05). These results suggest that PAF, which is known to enhance inflammatory reactions and to augment platelet aggregation, may in part participate in the pathogenesis of DHF.
据报道,感染登革热1型病毒(DV-1)后又感染另一种DV-2的患者患登革出血热(DHF)的几率更高。单核白细胞(MNLs)是登革热病毒复制的主要细胞,因此我们用DV-2对从非免疫和先前感染过DV-1的供体获得的MNLs进行攻击,以模拟原发性和异源性继发性DV-2感染。通过放射免疫测定法测量DV-2感染中MNLs产生的血小板活化因子(PAF)、血栓素B2(TxB2)和前列腺素D2(PGD2)。我们发现,无论MNLs是原发性还是异源性继发性暴露于DV-2,都能释放大量的PAF、TxB2和PGD2。从先前感染过DV-1的供体获得的MNLs释放的PAF水平显著高于TxB2或PGD2水平(75.8±28.5对21.2±13.4 pg/ml;p<0.05)。这些结果表明,已知能增强炎症反应并增加血小板聚集的PAF可能部分参与了DHF的发病机制。