Yan Long Edmund Lui 1,2,3, Peter Timms 2,3, Louise Marie Hafner 2,3, Tuan Lin Tan 4, Kian Hwa Tan 1 & Eng Lee Tan 1,5 SpringerPlus volume 2, Article number: 267 (2013) Cite this article However, in the summers of 2014 and 2016, EV-D68 outbreaks coincided with a spike in polio-like acute flaccid myelitis/paralysis (AFM/AFP) cases. All enteroviruses contain a genome of approximately 7,500 bases and are known to have a high mutation rate due to low-fidelity replication and frequent recombination. https://www.frontiersin.org/articles/10.3389/fmicb.2020.01105 All (+)RNA viruses replicate on distinct membranous domains; however, how they induce and maintain their unique lipid composition is largely unknown. This raised concerns that EV-D68 could be the causative agent of AFM during these recent outbreaks. Enteroviral replication reorganizes the cellular membrane. To investigate whether EV71 replication relies on … by Lisa Bauer, Roberto Manganaro, Birgit Zonsics, Jeroen R P M Strating, Priscila El Kazzi, Moira Lorenzo Lopez, Rachel Ulferts, Clara van Hoey, Maria J Maté, Thierry Langer, Bruno Coutard, Andrea Brancale, Frank J M van Kuppeveld. Upon infection, viral proteins and hijacked host factors generate unique structures called replication organelles (ROs) to replicate their viral genomes. As an important human pathogen, enterovirus type 71 (EV71) is a non-enveloped single-stranded RNA virus, belonging to the family Picornaviridae that has three genotypes (A, B and C) and several sub-genotypes . Enteroviral replication reorganizes the cellular membrane. Characterisation of enterovirus 71 replication kinetics in human colorectal cell line, HT29. Viperin is an important interferon-stimulated gene with a broad antiviral activity against various viruses. Enteroviruses are members of the picornavirus family, a large and diverse group of small RNA viruses characterized by a single positive-strand genomic RNA. Enterovirus 71 (EV71) is a positive-sense single-stranded RNA virus belonging to the Piconavirus family (Ong and Wong 2015).EV71 is one of the main pathogens causing hand, foot, and-mouth disease (HFMD), with frequent outbreaks in the Asia–Pacific region (Chang et al. Enterovirus 71 (EV71) is the main pathogen of the hand, foot, and mouth disease. However, no effective therapy is currently available for treating these infections. In the absence of ACBD3, individually expressed 3A was found in the ER instead of the Golgi, indicating that ACBD3 is required for proper localization of 3A. Enterovirus 71 (EV71) is a nonenveloped, single-stranded positive-sense RNA virus belonging to the genus Enterovirus in the family Picornaviridae, which is the primary cause of hand–foot–mouth disease [].Usually, EV71 infects infants under the age of 5 and results in clinical features of fever heat followed by pharyngitis, oral ulcers and rashes on the hands and feet []. Comments Translation: ... Genome replication occurs in two phases, first the minus strand is synthesized, which is in turn used as template to produce a lot of positive strand RNA genomes. Fluoxetine Inhibits Enterovirus Replication by Targeting the Viral 2C Protein in a Stereospecific Manner. In recent years, EV71 has been the major pathogenic enterovirus responsible for hand-foot-and-mouth disease epidemics in Asia. ) potently inhibited CVB3 replication (Figure 3B), confirming that pharmacological targeting of OSBP can inhibit enterovirus replication. ACS infectious diseases. EV71 3C protein is a 183 amino acid cysteine protease that can cleave most structural and … Ectopic expression of ORF2p proteins derived from diverse enteric enteroviruses sensitizes intestinal cells to the replication of ORF2p-defective EV-A71 and respiratory enterovirus EV-D68. As for ITZ, the 3A[H57Y] mutation in CVB3 provided resistance against OSW-1 (Figure 3B). ITZ Is an Inhibitor of Enterovirus and Cardiovirus Replication We performed a screen of the NCC to identify novel inhibitors of CVB3 replication. The enterovirus genus of the picornavirus family includes a large number of important human pathogens such as poliovirus, coxsackievirus, enterovirus A71, and rhinoviruses. Unexpectedly, the TRIM7-resistant virus has a replication advantage in mice and causes lethal pancreatitis. The formation of replication organelles of enteroviruses is dependent on GBF1 and ARF1 13,18,20,28. ROs promote efficient viral genome replication, coordinate the steps of the viral repli … Enterovirus 2A pro cleaves viral polyproteins and cellular factors, and has multiple roles in regulation of various viral and cellular processes, including viral replication and cytopathogenesis [37, 38], therefore, the possible inhibitory function of quercetin via viral 2Apro was tested. In the present study, we found that enterovirus 71 (EV71) RNA undergoes m 6 A modification during viral infection, which alters the expression and localization of the methyltransferase and demethylase of m 6 A, and its binding proteins. Phosphatidylinositol 4-kinase IIIβ (PI4KB) is required … Such a diversion of membranes could explain the strong inhibition of the anterograde transport from endoplasmic reticulum (ER) to Golgi complex caused by enterovirus infection (14, 15). Enteroviruses belong to the family Picornaviridae, a highly diverse group of small, non-enveloped, icosahedral-shaped viruses with single positive-strand RNA genomes. Upon infection, viral proteins and hijacked host factors generate unique structures called replication organelles (ROs) to replicate their viral genomes. Enterovirus A71 (EV-A71) is one of the main causative agents of hand-foot-mouth disease (HFMD) and causes serious neurological complications. Enterovirus genome replication occurs at virus-induced structures derived from cellular membranes and lipids. Enterovirus A71 (EVA71) is a human enterovirus belonging to the Picornaviridae family and mostly causes hand-foot-and-mouth disease in infants. However, the effect of viperin on human enteroviruses and the interaction mechanism between EVA71 and viperin remains elusive. This process is initiated by the covalent attachment of uridine monophosphate (UMP) to the terminal protein VPg, yielding VPgpU and VPgpUpU. Enterovirus is a genus of positive-sense single-stranded RNA viruses associated with several human and mammalian diseases. The Transformation of Enterovirus Replication Structures: a Three-Dimensional Study of Single- and Double-Membrane Compartments Authors : Ronald W. A. L. Limpens , Hilde M. van der Schaar , Darshan Kumar , Abraham J. Koster , Eric J. Snijder , Frank J. M. van Kuppeveld , and Montserrat Bárcena Synthesis of negative strand presumably produces dsRNA. At the end of poliovirus life-cycle the host cell is lysed, releasing new virions. The 5' VPg can be cleaved off the genomic RNA by host TBP2, also called “unlinkase” . This creates a pool genomes with a 5’pUp used for translation/replication. Yogarajah T(1), Ong KC(2), Perera D(3), Wong KT(4). 2016).Most HFMD occurs in patients younger than 10 years, and these patient usually have low-grade fever, … The TRIM7-resistant virus has reduced replicative fitness in cultured cells but an unexpected increased fitness advantage in vivo , leading to disseminated infection and severe pathology. All (+)RNA viruses replicate on distinct membranous domains; however, how they induce and maintain their unique lipid composition is largely unknown. Ultrastructural evidence of the membrane donor is lacking, suggesting that … Enteroviruses are members of the family Picornaviridae, which has ∼70 serotypes including poliovirus (types 1, 2 and 3), coxsackievirus A (A1–22 and A24), coxsackievirus B (B1–6), echovirus (1–21 and 24–33) and enterovirus (68–71, 73–78 and 89–91).1 Among the enterovirus strains, enterovirus 71 (EV71) may cause aseptic meningitis, encephalomyelitis or even acute flaccid paralysis similar to paralytic poliomyelitis that is also caused by poliovirus infection.2Currently, no specific antiviral agents … Recombination of two strains of enteroviruses replicating within one cell is a well-known phenomenon. Two recent studies reveal that enteroviruses harness the PI4P–cholestrol exchange cycle driven by OSBP1 protein and PI4 kinase(s), and that blocking the dynamic lipid flow inhibits virus replication. Replication of representative enteroviruses and rhinoviruses was all impaired in ACBD3 knockout cells and PI4KB recruitment by different enterovirus 3A proteins was not observed as well. It was firstly isolated from sputum specimens of infants with central nervous system diseases in California in 1969, and has been repeatedly reported in various parts of the world, especially in the Asia-Pacific region. Replication of all positive strand (+)RNA viruses is obligatorily associated with spatially and chemically distinct membranous replication organelles (RO). These findings reveal a unique mechanism for targeting enterovirus replication and provide molecular insight into the benefits and trade-offs of viral evolution imposed by a host restriction factor. We reveal the mechanism by which TRIM7 suppresses enterovirus replication and demonstrate that TRIM7-mediated inhibition can be overcome by a single point mutation in a viral protein. Althoug… Enterovirus ViralZone main page. Viperin (virus inhibitory protein, endoplasmic reticulum [ER]-associated, IFN-inducible) is one of the few ISGs proven to have direct antiviral activity and can inhibit the replication of multiple viruses, attracting increasing research attention. Neutral lipids are hydrolyzed by LD-associated lipases, including ATGL and HSL. Based on the sequence diversity, they have been divided into 15 species: enterovirus A to L and rhinovirus A to C. Human enteroviruses containing four enterovirus species (A to D) and three rhinovirus species (A to C) infect millions of people worldwide every year. This dsRNA may be the replicative form of picornaviruses. All (+)RNA viruses replicate on distinct membranous domains; however, how they induce and maintain their unique lipid composition is largely unknown. Like all enteroviruses, CVB3 kills its host cell and thereby causes a “cytopathic effect” (CPE). Therefore, effective drugs to prevent and treat EV-A71 infections are urgently needed. Enterovirus is a genus of positive-sense single-stranded RNA viruses associated with several human and mammalian diseases. Enteroviruses are named by their transmission-route through the intestine (enteric meaning intestinal). Serologic studies have distinguished 71 human enterovirus serotypes on the basis of antibody neutralization tests. Enteroviruses, like other RNA viruses, evolve rapidly with short replication times, large population sizes, high mutation rates due to the lack of proofreading by the RNA-dependent RNA polymerase, and frequent recombination events [4–6]. We screened the NCC by microscopically observing which compounds prevented the Two recent studies reveal that enteroviruses harness the PI4P–cholestrol exchange cycle driven by OSBP1 protein and PI4 kinase(s), and that blocking the dynamic lipid flow inhibits virus replication. (+)RNA viruses from the Enterovirus genus of the Picornaviridae family include important human pathogens such as poliovirus, Coxsackie viruses, enterovirus 71 and D68, among others. The first step in the replication of the plus-stranded poliovirus RNA is the synthesis of a complementary minus strand. Like all enteroviruses, CVB3 kills its host cell, and thereby causes a ‘cytopathic effect’ (CPE). Enteroviruses Engage Lipid Droplets to Support the Development of the Replication Organelles. However, the origin of these replication organelles (ROs) remains uncertain. Lipid droplets (LDs) are formed in association with the ER membrane and support basic cellular metabolism in uninfected cells. We show that the highly conserved WIGHPV domain of ORF2p is important for ORF2p-dependent viral intestinal infection. ITZ is an inhibitor of Enterovirus and Cardiovirus replication We performed a screen of the NCC to identify novel inhibitors of CVB3 replication. Enterovirus cis-acting replication element is a small RNA hairpin in the coding region of protein 2C as the site in PV1(M) RNA that is used as the primary template for the in vitro uridylylation. Replication of all positive strand (+)RNA viruses is obliga-torily associated with spatially and chemically distinct membranous replication organelles (RO). Enterovirus genomes are smaller than many … Like all other positive-strand RNA viruses, genome replication of enteroviruses occurs on rearranged membranous structures called replication organelles (ROs). Enterovirus A71 and coxsackievirus A16 show different replication kinetics in human neuronal and non-neuronal cell lines. Two recent studies reveal that enteroviruses harness the PI4P-cholestrol exchange cycle driven by OSBP1 protein and PI4 kinase(s), and that blocking the dynamic lipid flow inhibits virus replication. Author information: (1)Department of Pathology, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia. Akin to ITZ, OSW-1 inhibited all enteroviruses tested as well as EMCV, but not ERAV (data not shown). To assess the potential neurotropism of EV-D68, we … virus replication. Several findings suggest that enteroviruses transform membranes of the secretory pathway into their replication structures. These results reveal a mechanism of enterovirus replication that involves a selective strategy for recruitment of PI4KB to the RNA replication sites.IMPORTANCE Enterovirus 71, like other human enteroviruses, replicates its genome within host cells, where viral proteins efficiently utilize cellular machineries. While multiple factors are involved, it is largely unclear how viral replication is controlled. Enterovirus D68 (EV-D68) has historically been associated with respiratory illnesses. Collectively, our work unravels the sequential appearance of distinct enterovirus-induced replication structures, elucidates their detailed 3-D architecture, and provides the basis for a model for their transformation during the course of infection.IMPORTANCE: Positive-strand RNA viruses hijack specific intracellular membranes and remodel them into special structures that support viral RNA … (+)RNA viruses from the Enterovirus genus of the Picornaviridae family include important human pathogens such as poliovirus, Coxsackie viruses, enterovirus 71 and D68, among others.
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