Key result
Viral and host factors, including cell tropism, cell death mechanisms, and host immune responses, contribute to the pathogenesis and disease progression of Enterovirus 71 infections.
This review summarizes the mechanisms of EV71 disease progression, focusing on cell tropism, cell death, and host immune responses.
May guide EV71 intervention research; leaves open clinical validation studies.
The single-stranded RNA virus enterovirus 71 (EV71), which belongs to the Picornaviridae family, has caused epidemics worldwide, particularly in the Asia-Pacific region. Most EV71 infections result in mild clinical symptoms, including herpangina and hand, foot and mouth disease. However, serious pathological complications have also been reported, especially for young children. The mechanisms of EV71 disease progression remain unclear. The pathogenesis of adverse clinical outcomes may relate to many factors, including cell tropism, cell death and host immune responses. This article reviews the recent advances in the identification of factors determining EV71 cell tropism, the associated mechanisms of viral infection-induced cell death and the interplay between EV71 and immunity.
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Huang et al. (2012) conducted a review in Enterovirus 71 (EV71) infection. Enterovirus 71 (EV71) infection was evaluated. Viral and host factors, including cell tropism, cell death mechanisms, and host immune responses, contribute to the pathogenesis and disease progression of Enterovirus 71 infections.
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