Disease relevance of Enterovirus B, Human

• Acute enterovirus infections were diagnosed by measuring IgM class antibodies against coxsackievirus B5 (series 1) and a mixture of coxsackievirus B3, coxsackievirus A16, and echovirus 11 antigens (series 2) [1].
• Binding of echovirus 1 (EV1, a nonenveloped RNA virus) to the alpha2beta1 integrin on the cell surface is followed by endocytic internalization of the virus together with the receptor [2].
• RmcB did not protect HeLa cells from infection by poliovirus, echovirus 6, or coxsackievirus A18 [3].
• In addition, in Vero cells infected with CVB3, echovirus (EV)11, or EV12, increased tyrosine phosphorylation of a 200-kDa protein was detected 6 h p.i. Herbimycin A, a specific inhibitor of Src-like protein tyrosine kinases, was shown to inhibit virus-induced tyrosine phosphorylations and to reduce the production of progeny virions [4].
• We show here that the receptor for coxsackie B viruses and adenoviruses 2 and 5 (CXADR) is expressed in mouse germ cells, suggesting the possibility that these viruses could infect germ cells [5].

High impact information on Enterovirus B, Human

• Identification of the integrin VLA-2 as a receptor for echovirus 1 [6].
• Echovirus 16 was recovered from a throat swab of one hospitalized player and from the CSF of another [7].
• HBB alone also protects Coxsackie A 9, but not echo virus 9-infected animals, whereas guanidine alone is ineffective in either case [8].
• Mouse cells transfected with the CD55 clone bind echovirus 7, and this binding is blocked by the anti-receptor mAb [9].
• Integrins are cell surface receptors for several microbial pathogens including echovirus 1 (EV1), a picornavirus [10].

Chemical compound and disease context of Enterovirus B, Human

• This was accompanied by a large rise in the creatine phosphokinase level and a rise in echovirus 9 titers from 1:16 to greater than 1:256 during a two-week period [11].
• The arginine at position 17 of VPg could not be exchanged with any other amino acid without loss of viability, whereas the lysine at position 20, an amino acid conserved among all known polioviruses, coxsackieviruses, and echoviruses, was replaceable with several neutral amino acids and even with glutamic acid [12].
• Echoviruses bind heparan sulfate at the cell surface [13].
• This possibility was confirmed by the clinical course of ECG change, with elevated CPK and lactate dehydrogenase and a slightly elevated antibody titer for echovirus [14].
• Purified recombinant protein containing SCR domains 2, 3, and 4, but lacking the serine/threonine rich region, was shown to block infection of susceptible cells by echovirus 7 [15].

Biological context of Enterovirus B, Human

• Binding sites for both collagen and echovirus 1 have been mapped to the I domain within the alpha2 subunit of the VLA-2 alpha2beta1 heterodimer [16].
• In this study, we use surface plasmon resonance to study the affinity and kinetics of the interaction of echovirus 11 with its cellular receptor decay-accelerating factor (CD55) [17].
• Nucleotide sequences of nine epidemic strains [belonging to echovirus serotypes 4 (E4), 7 (E7) and 30 (E30)] in the two genomic regions (300 nt of VP1 and 520 nt of 3D polymerase) were compared to prototype and field strains, and phylogenetic trees were generated from alignments [18].
• In this study, RNA extracts of CNS tissue from 28 patients with ALS-MND and 7 controls were assayed by nested polymerase chain reaction (PCR) using primers to the 5'-untranslated region (UTR) of the enterovirus (EV) genome which is highly conserved between EVs including PV, echovirus and coxsackie viruses [19].
• In particular, there was no evidence for associations between ICA status at diagnosis and either sex, race, family history of IDDM, HLA-DR phenotype, antibody titers to Coxsackie B viruses, immunoglobulin levels, C-peptide and glycosylated hemoglobin concentrations, or insulin requirements [20].

Anatomical context of Enterovirus B, Human

• HeLa cells specifically lost the capacity to bind echovirus 7 when treated with phosphatidylinositol-specific phospholipase C, an enzyme that releases GPI-anchored proteins from the cell surface, indicating that the virus receptor, like DAF, is a GPI-anchored protein [21].
• Despite great similarity in the structure and replication of coxsackievirus B3 (CBV3), echovirus 1 (EV1), and poliovirus 1 (PV1), the ability of these viruses to infect human peripheral blood mononuclear cells (PBMC), and B (Raji), T (Molt-4) and monocytic (U-937) cell lines differed markedly [22].
• Since E9/Barty does not replicate or replicates only poorly in mice older than about 5 days, and expression of the vitronectin receptor is reported to be down-regulated in striated muscle tissue during development, it is suggested that susceptibility of mice to this echovirus infection is controlled by the availability of alpha(v)beta3 integrin [23].
• Primary endothelial cells were highly susceptible to several serotypes of enteroviruses (coxsackievirus A13, echoviruses 6, 7, 11, 30, and poliovirus 1) [24].
• Lymphocytotoxicity power, as well as the ability of each drug to influence secondary humoral (against sheep red blood cells or diphtheria anatoxin) or cell-mediated (against PPD and Coxsackie A9 virus) immunity were searched [25].

Gene context of Enterovirus B, Human

• Human cardiac inflammatory responses triggered by Coxsackie B viruses are mainly Toll-like receptor (TLR) 8-dependent [26].
• In contrast to FAC localization and collagen adhesion results, VLA-2-dependent binding and infection by echovirus were unaffected by either alpha 2 cytoplasmic domain deletion or exchange with other cytoplasmic domains [27].
• Remarkably, RasGAP is cleaved during infections with different strains of coxsackievirus B3 as well as with echovirus 11 and echovirus 12, yielding a 104-kDa protein fragment [28].
• Specifically, it was found that CAV1, -11, -13, -15, -17 to -22, and -24 are classified together with polioviruses and enterovirus 70, whereas the rest of the CAVs are classified along with coxsackie B viruses, echoviruses, and the rest of the other enteroviruses [29].
• This latter finding was supported by a greater frequency of antibodies to Coxsackie-B viruses in the DR4 cases at presentation [30].

Analytical, diagnostic and therapeutic context of Enterovirus B, Human

• We present here a structure for echovirus (EV) type 12 bound to DAF using cryo-negative stain transmission electron microscopy and three-dimensional image reconstruction to 16-A resolution, which we interpreted using the atomic structures of EV11 and DAF [31].
• Recent sequence analysis revealed that the human pathogen echovirus 22 (EV22) is genetically distant from all the other picornaviruses studied to date (T. Hyypiä, C. Horsnell, M. Maaronen, M. Khan, N. Kalkkinen, P. Auvinen, L. Kinnunen, and G. Stanway, Proc. Natl. Acad. Sci. USA 89:8847-8851, 1992) [32].
• Filters containing diatomaceous earth modified by in situ precipitation of a combination of ferric chloride and aluminum chloride adsorbed greater than 80% of enteroviruses (poliovirus 1, echovirus 5, and coxsackievirus B5) and coliphage MS2 present in tap water at ambient pH (7.8 to 8.3), even after filtration of 100 liters of tap water [33].
• The virus isolates were initially identified as echovirus 4 (E4) on the basis of immunofluorescence staining with anti-E4 and anti-E30 (Bastianni prototype) monoclonal antibodies [34].
• The echovirus type 11 IgM ELISA appears to have considerable laboratory diagnostic potential when a rising antibody level cannot be demonstrated in paired sera or when virus is not cultured [35].

References