Abstract
Enterovirus 71 (EV71) is one of the most common intestinal virus that causes hand, foot, and mouth disease (HFMD) in infants and young children (mostly ≤5 years of age). Generally, children with EV71-infected HFMD have mild symptoms that resolve spontaneously within 7-14 days without complications. However, some EV71-infected HFMD cases lead to severe complications such as aseptic meningitis, encephalitis, acute flaccid paralysis, pulmonary edema, cardiorespiratory complication, circulatory disorders, poliomyelitis-like paralysis, myocarditis, meningoencephalitis, neonatal sepsis, and even death. The mechanism of EV71 pathogenesis has been studied extensively, and the regulation of host immune responses is suspected to aggravate EV71-induced severe complications. Recently, several cytokines or chemokines such as TNF-α, IFN-γ, IL-1β, IL-18, IL-33, IL-37, IL-4, IL-13, IL-6, IL-12, IL-23, IL-27, IL-35, IL-10, IL-22, IL-17F, IL-8, IP-10, MCP-1, G-CSF, and HMGB1 have been reported to be associated with severe EV71 infection by numerous research teams, including our own. This review is aimed at summarizing the pathophysiology of the cytokines and chemokines with severe EV71 infection.
Highlights
Enterovirus 71 (EV71) is one of the most common and neurotropic intestinal virus that causes hand, foot, and mouth disease (HFMD) in infants and young children
These results suggest that HFMD infected with EV71 can cause encephalitis
There were 11 severe EV71-infected HFMD cases with neurologic complications, such as brainstem encephalitis and aseptic meningitis, and 3 children died from a combination of acute pulmonary edema and heart and respiratory failure in Shandong, China, in 2007 [8]
Summary
Enterovirus 71 (EV71) is one of the most common and neurotropic intestinal virus that causes hand, foot, and mouth disease (HFMD) in infants and young children (mostly ≤5 years of age). There were 11 severe EV71-infected HFMD cases with neurologic complications, such as brainstem encephalitis and aseptic meningitis, and 3 children died from a combination of acute pulmonary edema and heart and respiratory failure in Shandong, China, in 2007 [8]. High levels of TNF-α were detected in severe patients with complications (including brainstem encephalitis, neurogenic pulmonary edema, and sepsis) at disease onset, and decreased with disease progression [10]. The serum levels of IFN-γ elevated a lot in patients with brainstem encephalitis and pulmonary edema [17], which suggests that IFN-γ may be involved in the progress of EV71-caused severe complications
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