Brazilian fitness programme registers health benefits

Fioravanti, Carlos

doi:10.1016/s0140-6736(12)61201-x

Cited by 11 publications

(6 citation statements)

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“…However, EV-A71 infections are also associated to severe neurological complications (such as encephalitis, aseptic meningitis and poliomyelitis-like syndrome) and acute pulmonary edema, which may be highly limiting and fatal particularly in children under the age of 5 years [5,6]. In 2010, a large outbreak of HFMD in China resulted in an estimated 1.7 million cases and 905 deaths [7] and an outbreak in Cambodia in 2012 resulted in the death of 54 children [8,9]. A sub-genogroup C4 EV-A71-inactivated vaccine has recently been approved in China, but worldwide coverage and long-term protection still need to be addressed [10–12].…”

Section: Introductionmentioning

confidence: 99%

Viral engagement with host receptors blocked by a novel class of tryptophan dendrimers that targets the 5-fold-axis of the enterovirus-A71 capsid

et al. 2019

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Enterovirus A71 (EV-A71) is a non-polio neurotropic enterovirus with pandemic potential. There are no antiviral agents approved to prevent or treat EV-A71 infections. We here report on the molecular mechanism by which a novel class of tryptophan dendrimers inhibits (at low nanomolar to high picomolar concentration) EV-A71 replication in vitro . A lead compound in the series (MADAL385) prevents binding and internalization of the virus but does not, unlike classical capsid binders, stabilize the particle. By means of resistance selection, reverse genetics and cryo-EM, we map the binding region of MADAL385 to the 5-fold vertex of the viral capsid and demonstrate that a single molecule binds to each vertex. By interacting with this region, MADAL385 prevents the interaction of the virus with its cellular receptors PSGL1 and heparan sulfate, thereby blocking the attachment of EV-A71 to the host cells.

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Section: Introductionmentioning

confidence: 99%

Viral engagement with host receptors blocked by a novel class of tryptophan dendrimers that targets the 5-fold-axis of the enterovirus-A71 capsid

et al. 2019

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“…EV71 was first isolated from a sick child in California in 1969, and EV71 outbreaks subsequently occurred in Europe in the 1970s. Currently, HFMD is a major endemic infectious disease, with over one million cases annually in China and Southeastern Asia [ 3 , 5 – 7 ]. So far, the factors that determine the age-dependent susceptibility of children to EV71 infection remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

TLR3 Signaling in Macrophages Is Indispensable for the Protective Immunity of Invariant Natural Killer T Cells against Enterovirus 71 Infection

et al. 2015

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Enterovirus 71 (EV71) is the most virulent pathogen among enteroviruses that cause hand, foot and mouth disease in children but rarely in adults. The mechanisms that determine the age-dependent susceptibility remain largely unclear. Here, we found that the paucity of invariant natural killer T (iNKT) cells together with immaturity of the immune system was related to the susceptibility of neonatal mice to EV71 infection. iNKT cells were crucial antiviral effector cells to protect young mice from EV71 infection before their adaptive immune systems were fully mature. EV71 infection led to activation of iNKT cells depending on signaling through TLR3 but not other TLRs. Surprisingly, iNKT cell activation during EV71 infection required TLR3 signaling in macrophages, but not in dendritic cells (DCs). Mechanistically, interleukin (IL)-12 and endogenous CD1d-restricted antigens were both required for full activation of iNKT cells. Furthermore, CD1d-deficiency led to dramatically increased viral loads in central nervous system and more severe disease in EV71-infected mice. Altogether, our results suggest that iNKT cells may be involved in controlling EV71 infection in children when their adaptive immune systems are not fully developed, and also imply that iNKT cells might be an intervention target for treating EV71-infected patients.

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“…Globally, two patterns of EV71 outbreaks have been reported: small-scale outbreaks with low mortality and large-scale outbreaks with high mortality. The latter pattern occurred in Bulgaria in 1975, in Hungary in 1978, in Malaysia in 1997, in Taiwan in 1998, in Singapore in 2000, in Vietnam in 2005, in Brunei in 2006, in China since 2007, and recently in Cambodia in 2012[ 1 , 4 , 5 ]. Since the 1998 epidemic, Taiwan Centers for Disease Control has established national enterovirus surveillance system and EV71 has been detected as an endemic disease with cyclical nationwide epidemics every 3–4 years[ 1 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Reemergence of Enterovirus 71 Epidemic in Northern Taiwan, 2012

et al. 2015

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BackgroundEnterovirus 71 (EV71) belongs to picornavirus family and could be classified phylogenetically into three major genogroups (A, B and C) including 11 genotypes (A, B1-B5 and C1-C5). Since 1997, EV71 has caused large-scale of epidemics with neurological complications in Asian children. In Taiwan, nationwide EV71 epidemics with different predominant genotypes have occurred cyclically since 1998. A nationwide EV71 epidemic occurred again in 2012. We conducted genetic and antigenic characterizations of the 2012 epidemic.MethodsChang Gung Memorial Hospital (CGMH) is a medical center in northern Taiwan. In CGMH, specimens were collected from pediatric inpatients with suspected enterovirus infections for virus isolation. Enterovirus isolates were serotyped and genotyped and sera from EV71 inpatients were collected for measuring neutralizing antibody titers.ResultsThere were 10, 16 and 99 EV71 inpatients identified in 2010, 2011 and 2012, respectively. There were 82 EV71 isolates genotyped, which identified 17 genotype C4a viruses and 65 genotype B5 viruses. The genotype B5 viruses were not detected until November 2011 and caused epidemics in 2012. Interestingly, the B5-2011 viruses were genetically distinguishable from the B5 viruses causing the 2008 epidemic and are likely introduced from China or Southeastern Asia. Based on antigenic analysis, minor antigenic variations were detected among the B5-2008, B5-2011, C4a-2008 and C4a-2012 viruses but these viruses antigenically differed from genotype A.ConclusionsGenotype B5 and C4a viruses antigenically differ from genotype A viruses which have disappeared globally for 30 years but have been detected in China since 2008. Enterovirus surveillance should monitor genetic and antigenic variations of EV71.

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Brazilian fitness programme registers health benefits

Cited by 11 publications

References 0 publications

Viral engagement with host receptors blocked by a novel class of tryptophan dendrimers that targets the 5-fold-axis of the enterovirus-A71 capsid

Viral engagement with host receptors blocked by a novel class of tryptophan dendrimers that targets the 5-fold-axis of the enterovirus-A71 capsid

TLR3 Signaling in Macrophages Is Indispensable for the Protective Immunity of Invariant Natural Killer T Cells against Enterovirus 71 Infection

Reemergence of Enterovirus 71 Epidemic in Northern Taiwan, 2012

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