Genetic test fingers viral, bacterial infections: Method could help doctors treat children's fevers

By differentiating between bacterial and viral fevers, a new test may help doctors decide whether to prescribe antibiotics.

Fevers are a common symptom of many infectious diseases, but it can be difficult to tell whether viruses or bacteria are the cause. By measuring gene activity in the blood of 22 sick children, Gregory Storch, a pediatrician and infectious disease researcher at Washington University in St. Louis and colleagues were able to distinguish bacteria-sparked fevers from ones kindled by viruses. The activity of hundreds of genes changed as the children’s immune systems responded to the pathogens, but the team found that gauging the response of just 18 genes could correctly distinguish between viral and bacterial infections about 90 percent of the time. The gene activity test could also determine, for viral infections, which specific microbes caused the illness, the team reports July 15 in the Proceedings of the National Academy of Sciences...

Gene expression profiles in febrile children with defined viral and bacterial infection

Abstract
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.

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