Severe hand, foot and mouth disease associated with Coxsackievirus A10 infections in Xiamen, China in 2015

Chen, Mengyuan; He, Shuizhen; Yan, Qiang; Xue-rong, XU; Wu, Wenhui; Ge, Shuping; Chen, Min; Xia, Ningshao

doi:10.1016/j.jcv.2017.05.011

Cited by 65 publications

(61 citation statements)

References 11 publications

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“…All of these, apart from VP3 Q240 (which is also conserved across non-KRM1-binding viruses) are probably crucial for receptor binding. Capsid residues VP1 23 and 283 identified in clade E CV-A10 viruses implicated in more severe infections, do not directly interact with the receptor but residue 283 could impact on receptor binding by destabilizing the Cterminus of VP1 11 .…”

Section: Resultsmentioning

confidence: 99%

“…More than 20 types of enteroviruses (both species A and B) have been associated with HFMD 9,10 . Earlier outbreaks in the Asia-Pacific region were predominantly caused by EV-A71 and CV-A16 but those attributable to CV-A6 and CV-A10 have become increasingly common in recent years [11][12][13] . CV-A10 shares onlỹ 69% amino acid sequence identity with EV-A71 and CV-A16, resulting in changes in the surface architecture 14 and recognition of a different cell entry receptor.…”

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confidence: 99%

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Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10

et al. 2020

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Coxsackievirus A10 (CV-A10) is responsible for an escalating number of severe infections in children, but no prophylactics or therapeutics are currently available. KREMEN1 (KRM1) is the entry receptor for the largest receptor-group of hand-foot-and-mouth disease causing viruses, which includes CV-A10. We report here structures of CV-A10 mature virus alone and in complex with KRM1 as well as of the CV-A10 A-particle. The receptor spans the viral canyon with a large footprint on the virus surface. The footprint has some overlap with that seen for the neonatal Fc receptor complexed with enterovirus E6 but is larger and distinct from that of another enterovirus receptor SCARB2. Reduced occupancy of a particle-stabilising pocket factor in the complexed virus and the presence of both unbound and expanded virus particles suggests receptor binding initiates a cascade of conformational changes that produces expanded particles primed for viral uncoating.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10

et al. 2020

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“…Since a Coxsackievirus A6 (CVA-6) associated HFMD outbroke in Finland in 2008, several outbreaks caused by CVA-6 were reported in Europe, North America, and Asia [12,[19][20][21][22]. Moreover, Coxsackievirus A10 (CVA-10) had also been identified as the responsible pathogen for a series of HFMD outbreaks [20,23,24]. Guangzhou city is one of the most serious cities in HFMD with high incidence, and the HFMD pathogen spectrum are changing according to previous studies [22,[25][26][27].…”

Section: Introductionmentioning

confidence: 99%

Co-circulation of coxsackieviruses A-6, A-10, and A-16 causes hand, foot, and mouth disease in Guangzhou city, China

Xie

Yang

et al. 2020

BMC Infect Dis

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Background: Hand, foot, and mouth disease (HFMD) is a common infectious disease occurring in children under 5 years of age worldwide, and Enterovirus A71 (EV-A71) and Coxsackievirus A16 (CVA-16) are identified as the predominant pathogens. In recent years, Coxsackievirus A6 (CVA-6) and Coxsackievirus A10 (CVA-10) have played more and more important role in a series of HFMD outbreaks. This study aimed to understand the epidemic characteristics associated with HFMD outbreak in Guangzhou, 2018. Methods: The clinical and laboratory data of 1220 enterovirus-associated HFMD patients in 2018 were analysed in this study. Molecular diagnostic methods were performed to identify its serotypes. Phylogenetic analyses were depicted based on the complete VP1 gene. Results: There were 21 enterovirus serotypes detected in Guangzhou in 2018. Three serotypes of enterovirus, CVA-6 (364/1220, 29.8%), CVA-10 (305/1220, 25.0%), and CVA-16 (397/1220, 32.5%), were identified as the causative pathogens and accounted for 87.3% among all 1220 HFMD patients. In different seasons, CVA-6 was the predominant pathogen of HFMD during autumn, and CVA-10 as well as CVA-16 were more prevalent in summer. Patients infected by CVA-6, CVA-10 or CVA-16 showed similar clinical features and laboratory characteristics, and the ratios of severe HFMD were 5.8, 5.9, and 1.5% in the three serotypes. Phylogenetic analyses of VP1 sequences showed that the CVA-6, CVA-10, and CVA-16 sequences belonged to the sub-genogroup E2, genogroup E, and genogroup B1, respectively. Conclusions: CVA-6, CVA-10, and CVA-16 were the predominant and co-circulated serotypes in Guangzhou China, 2018, which should be the new target for prevention and control of HFMD. Our findings provide useful information for diagnosis, treatment, and prevention of HFMD.

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“…The Enterovirus genus is one of the best-known genera of the Picornavirus family afflicting millions of people each year. Coxsackievirus A10 (CV-A10) belongs to the Enterovirus type A (EV-A) species and has, together with other members such as enterovirus A71 (EV-A71), CV-A16, and CV-A6, been identified as a disease-causing pathogen during recent outbreaks in Asia and Europe (Blomqvist et al, 2010;Lu et al, 2012;Mirand et al, 2012;Yang et al, 2015;Chen et al, 2017). The disease burden of many of these viruses is substantial, with symptoms ranging from rather mild conditions such as herpangina and hand-foot-and-mouth disease (HFMD) to more serious symp-toms such as aseptic meningitis (Lu et al, 2012;He et al, 2013;Liu et al, 2014;Yang et al, 2015;Li et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

KREMEN1 Is a Host Entry Receptor for a Major Group of Enteroviruses

Staring

Hengel

Raaben

et al. 2018

Cell Host & Microbe

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Human type A Enteroviruses (EV-As) cause diseases ranging from hand-foot-and-mouth disease to poliomyelitis-like disease. Although cellular receptors are identified for some EV-As, they remain elusive for the majority of EV-As. We identify the cell surface molecule KREMEN1 as an entry receptor for coxsackievirus A10 (CV-A10). Whereas loss of KREMEN1 renders cells resistant to CV-A10 infection, KREMEN1 overexpression enhances CV-A10 binding to the cell surface and increases susceptibility to infection, indicating that KREMEN1 is a rate-limiting factor for CV-A10 infection. Furthermore, the extracellular domain of KREMEN1 binds CV-A10 and functions as a neutralizing agent during infection. Kremen-deficient mice are resistant to CV-A10-induced lethal paralysis, emphasizing the relevance of Kremen for infection in vivo. KREMEN1 is also essential for infection by a phylogenetic and pathogenic related group of EV-As. Collectively these findings highlight the importance of KREMEN1 for these emerging pathogens and its potential as an antiviral therapeutic target.

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Severe hand, foot and mouth disease associated with Coxsackievirus A10 infections in Xiamen, China in 2015

Cited by 65 publications

References 11 publications

Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10

Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10

Co-circulation of coxsackieviruses A-6, A-10, and A-16 causes hand, foot, and mouth disease in Guangzhou city, China

KREMEN1 Is a Host Entry Receptor for a Major Group of Enteroviruses

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