一项研究报告说，血液中的基因表达特征可以帮助区别幼儿的发热是由病毒还是由细菌造成的。发热是病毒和细菌感染的一个常见症状，但是发热源常常在临床检查中不那么显而易见。Gregory Storch及其同事研究了发热儿童的血液是否表现出了病毒和细菌的特定基因表达特征，这些特征可能在区别这两种发热源方面有用。这组作者分析了来自各种病毒或细菌感染阳性的30名发热儿童以及35名没有发热但是其中一些人呈病毒感染阳性的儿童的基因表达数据。这组作者发现不发热的病毒阳性和病毒阴性的儿童的特征谱是相互难以区分的，并且有别于发热儿童的特征谱。此外，这项分析揭示出了发热儿童的特定病毒感染——诸如疱疹病毒、腺病毒或肠道病毒——以及急性细菌感染的独特特征；这些特征比区分细菌和病毒感染的传统的白细胞计数更准确。这组作者说，这些发现提示血液基因表达分析可能会成为理解儿童发热来源的一种有用的工具。（生物谷Bioon.com）
生物谷推荐的英文摘要
PNAS DOI：10.1073/pnas.1302968110
Gene expression profiles in febrile children with defined viral and bacterial infection
Xinran Hua, Jinsheng Yub, Seth D. Crosbyb, and Gregory A. Storcha
Viral infections are common causes of fever without an apparent source in young children. Despite absence of bacterial infection, many febrile children are treated with antibiotics. Virus and bacteria interact with different pattern recognition receptors in circulating blood leukocytes, triggering specific host transcriptional programs mediating immune response. Therefore, unique transcriptional signatures may be defined that discriminate viral from bacterial causes of fever without an apparent source. Gene expression microarray analyses were conducted on blood samples from 30 febrile children positive for adenovirus, human herpesvirus 6, or enterovirus infection or with acute bacterial infection and 22 afebrile controls. Blood leukocyte transcriptional profiles clearly distinguished virus-positive febrile children from both virus-negative afebrile controls and afebrile children with the same viruses present in the febrile children. Virus-specific gene expression profiles could be defined. The IFN signaling pathway was uniquely activated in febrile children with viral infection, whereas the integrin signaling pathway was uniquely activated in children with bacterial infection. Transcriptional profiles classified febrile children with viral or bacterial infection with better accuracy than white blood cell count in the blood. Similarly accurate classification was shown with data from an independent study using different microarray platforms. Our results support the paradigm of using host response to define the etiology of childhood infections. This approach could be an important supplement to highly sensitive tests that detect the presence of a possible pathogen but do not address its pathogenic role in the patient being evaluated.
