Key result
EV71 infection links to higher Th2 cytokines, while CA16 associates with elevated Th1 cytokines.
Why the study?
Do different viral pathogens cause distinct clinical and immunological manifestations in children with hand, foot, and mouth disease?
Cross-Sectional (n=60)
No
Do different viral pathogens cause distinct clinical and immunological manifestations in children with hand, foot, and mouth disease?
Answers are grounded in this paper and cite their sources.
Different viral pathogens causing HFMD elicit distinct cytokine and chemokine responses, emphasizing the relevance of exact pathogen determination for understanding immune responses.
Hand, foot, and mouth disease (HFMD), with vesiculae on the hands, feet and mouth, is an infectious disease caused by many viral pathogens. However, the differences of immune response induced by these pathogens are unclear. We compared the clinical manifestations and the levels of immunologic indicators from 60 HFMD patients caused by different viral pathogens to analyze the differences in the immune response. It was shown that Th2 cytokines (IL-4 and IL-10) increased significantly in EV71-infected children; Th1 cytokines (IL-2 and IFN-γ) rose in CA16-infected children; both Th1 and Th2 cytokines elevated in non-EVG-infected children; only individual cytokines (such as IL-10) went up in EVG-infected children. Meanwhile, the antibodies induced by viral infection could not cross-interfere between the different pathogens. These differences might be due to variations in the immune response induced by the individual pathogens or to the pathogenesis of the infections by the individual pathogens.
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Wang et al. (2016) conducted a cross-sectional in Hand, foot, and mouth disease (HFMD) (n=60). Different viral pathogens (EV71, CA16, EVG, non-EVG) vs. Healthy children and comparison across viral groups was evaluated on Levels of immunologic indicators (cytokines and chemokines) and clinical manifestations. EV71 infection was characterized by significantly increased levels of Th2 cytokines (IL-4 and IL-10), while CA16 infection was associated with significantly increased levels of Th1 cytokines (IL-2 and IFN-γ).
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