Cell and tissue tropism of enterovirus 71 and other enteroviruses infections

Jing-Yi Lin,Shin-Ru Shih

doi:10.1186/1423-0127-21-18

Abstract

Enterovirus 71 (EV71) is a member of Picornaviridae that causes mild and self-limiting hand, foot, and mouth disease (HFMD). However, EV71 infections can progress to polio-like paralysis, neurogenic pulmonary edema, and fatal encephalitis in infants and young children. Large EV71 outbreaks have been reported in Taiwan, China, Japan, Malaysia, Singapore, and Australia. This virus is considered a critical emerging public health threat. EV71 is an important crucial neurotropic enterovirus for which there is currently no effective antiviral drug or vaccine. The mechanism by which EV71 causes severe central nervous system complications remains unclear. The interaction between the virus and the host is vital for viral replication, virulence, and pathogenicity. SCARB2 or PSGL-1 receptor binding is the first step in the development of viral infections, and viral factors (e.g., 5′ UTR, VP1, 3C, 3D, 3′ UTR), host factors and environments (e.g., ITAFs, type I IFN) are also involved in viral infections. The tissue tropism and pathogenesis of viruses are determined by a combination of several factors. This review article provides a summary of host and virus factors affecting cell and tissue tropism and the pathogenesis of enteroviruses.

Highlights

Enterovirus 71 (EV71), a member of the family Picornaviridae, poses a persistent global public health threat
EV71 infections typically cause hand, foot, and mouth disease (HFMD) or herpangina; EV71 has been implicated as the etiological agent in several largescale outbreaks of severe neurological complications in children worldwide [1]
In 1998, an EV71 epidemic occurred in Taiwan, with the virus infecting over 120000 people and killing 78 children

Summary

Introduction

Enterovirus 71 (EV71), a member of the family Picornaviridae, poses a persistent global public health threat. They observed that a single amino acid, residue 145 of the viral capsid protein (VP1-145), determines whether a virus binds to PSGL1, and that it functions by influencing the orientation of a nearby lysine residue (VP1-244) on the virus surface They proposed that VP1-145 controls virus tropism by changing the accessibility of the positivelycharged lysine side chain of VP1-244 to the negatively charged, sulfated N-terminus of PSGL-1. Because virus infection initiates after viruses bind to a receptor on the cell surface, cellular receptors for viruses have been considered the primary determinants of tissue tropism. Roles of microRNAs in the interaction network between virus and host In addition to host proteins and viral genome diversity, some small RNAs have been reported to be involved in regulating viral replication and translation in viral life cycles [60,61,62,63]. MiR10a* was detectable in the cardiac tissue of suckling Balb/c mice, suggesting that miR10a* might affect CVB3 replication during its cardiac infection [61]

Conclusion

15. Stanway G

48. Schneider-Schaulies J

66. Knowlton KU