Viral and Host Factors that Contribute to Pathogenicity of Enterovirus 71

Abstract

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.

Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

“…The occurrence of apoptosis is well documented in EV-A71 in both neuronal and non-neuronal cells [23,26]. Various cytokines are expressed in EV-A71-infected hosts, including IL-4, IL-5, IL-6, IL-10, IL-2, TNF-α, IFN-γ, IL-13, IL-1β and macrophage inflammatory protein 1 alpha (MIP-1α) [27]. Pro-inflammatory responses with significant increases of IFN-β, IL-6, chemokine (C-C motif) ligand 5 (CCL5) and interferon gamma-induced protein 10 (IP-10) in the EV-A71-infected HT-29 intestinal cell line were also reported [28].…”

High-affinity interaction of hnRNP A1 with conserved RNA structural elements is required for translation and replication of enterovirus 71

“…[8][9][10] Like other members of the Picornaviridae family, the mechanism of ITAF-mediated protein synthesis remains unknown, partly due to a paucity of structural and mechanistic descriptions of function as a site of recognition for trans factors or form longrange interactions with a distant site within the IRES. Both postulates were in agreement with the contemporary virological and phylogenetic studies on polioviruses.…”

“…6,7 Given their limited coding capacity, picornaviruses coordinate these different viral RNA functions through mechanisms that co-opt host proteins. 6,8,9 human enterovirus 71 (eV71) is an emerging pathogen of infectious disease and a serious threat to public health. currently, there are no antivirals or vaccines to slow down or prevent eV71 infections, thus underscoring the urgency to better understand mechanisms of host-enterovirus interactions.…”

Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome

“…Since its first identification in 1969, enterovirus 71 (EV71) has caused many epidemics in the world, especially in the Asia-Pacific region, manifested by hand, foot, and mouth disease (HFMD) (Huang et al, 2012). Infection with EV71 can lead to severe neurological complications such as encephalitis, acute flaccid paralysis, and pulmonary edema in children .…”