Expression of MxA protein in blood lymphocytes discriminates between viral and bacterial infections in febrile children

被引:49
作者
Halminen, M
Ilonen, J
Julkunen, I
Ruuskanen, O
Simell, O
Makela, MJ
机构
[1] UNIV TURKU,TURKU IMMUNOL CTR,FIN-20520 TURKU,FINLAND
[2] UNIV TURKU,DEPT PAEDIAT,FIN-20520 TURKU,FINLAND
[3] UNIV TURKU,DEPT CLIN ALLERGOL,FIN-20520 TURKU,FINLAND
[4] NATL PUBL HLTH INST,DEPT VIROL,HELSINKI,FINLAND
关键词
C-REACTIVE PROTEIN; GENE;
D O I
10.1203/00006450-199705000-00008
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Interferons (IFNs), which are induced by viruses, form an essential part of host's defense systems against viral infections. The antiviral actions of IFNs are mediated by several IFN-inducible gene products, one of which is Mx protein. To evaluate whether MxA protein expression in lymphocytes could function as an indicator of endogenous IFN production in children with acute febrile illness, we analyzed MxA protein levels in peripheral blood lymphocytes by flow cytometry in the acute phase of the disease. Children with a laboratory-confirmed viral infection [respiratory syncytial virus (RSV) in 21, adenovirus in 10, rotavirus in 5, and influenza, herpes simplex, or EBV in 7 other cases] had significantly higher (p < 0.002) MxA protein levels (median fluorescences in different virus groups ranged from 707 to 765) compared with children with a bacterial infection (n = 12, median fluorescence 548). To characterize further MxA protein expression during infections, cells from 41 patients were stimulated in vitro with exogenous IFN-alpha, and the level of MxA protein expression was determined. The rise in MxA staining levels was significantly higher in the group with bacterial infections compared with those with viral infection (p < 0.005), further indicating that the MxA protein levels were already elevated in vivo in patients with viral infections. This study suggests that elevated MxA protein expression levels can be used in the differential diagnosis of bacterial versus viral disease in febrile children.
引用
收藏
页码:647 / 650
页数:4
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