McElroy et al. (2014) used multiplex assays and other laboratory tests to examine serum samples banked from the 2000–2001 Ebola virus outbreak affecting Gulu, a small town in northern Uganda, for pediatric-specific biomarkers.1 From the results, they hoped to establish useful measures for prognosis and treatment appropriate to children and to find out if the course of Ebola virus disease differs in younger patients.
The research team gathered banked samples from 55 pediatric cases (defined as being younger than 21 years old) to compare with samples from 50 adults in the same outbreak, all with laboratory-confirmed Ebola virus infection. They prioritized novel biomarker testing to maximize information from the limited sample volumes available, attempting to measure 55 serum analytes from each case where possible. The scientists analyzed the samples for biomarkers of inflammation, acute phase response, endothelial function and coagulopathy, in addition to analyzing serum biochemistry and noting outcome, clinical signs and viremia as stated in records from each patient.
Once analyzed, they found that both adults and children had similar viral loads. Although viremia was greater in those who died from Ebola virus infection, the difference was not significant for pediatric patients. For individuals with sufficient samples for onward testing, the case fatality rate was lower among the pediatric patients greater than five years of age versus the adults, whereas all children under the age of five died.
McElroy and coworkers did not observe any age-specific differences in serum biochemistry; neither did they note correlations between these analytes and disease outcome.
The research team did, however, find evidence for age-specific differences in other biomarkers for disease progression in the children, indicating that different pathophysiological processes might occur with pediatric Ebola virus infection. For example, raised levels of both IL-10 and IP-10 predicted death in pediatric cases, while an elevated RANTES concentration correlated well with survival. The team also found that in pediatric patients, acute phase markers SAA and IgG were elevated and reflected clinical signs, but this was not seen in adults. Other prognostic indicators for pediatric survival included sICAM and sVCAM—both were raised, indicating an overactive endothelial response in children as compared to adults—and PAI-1, a marker of coagulopathy, that was elevated and even more so with pediatric death.
In summary, McElroy et al. suggest that the age-specific biomarker alterations illustrated by their study show that children and adults respond differently to Ebola virus infection. These disparities highlight areas in which treatment can be tailored specifically to children, namely in suppression of endothelial response and support for the immune system, thus further improving pediatric survival from infection.
1. McElroy, A.K., et al. (2014, October) “Biomarker correlates of survival in pediatric patients with Ebola virus disease,” Emerging Infectious Diseases, 20(10), doi: http://dx.doi.org/10.3201/eid2010.140430.
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