Outbreak of aseptic meningitis due to ECHO-9 in northern Kyushu island in the summer of 1997.
(1/17)
An outbreak of aseptic meningitis caused by echovirus type 9 (ECHO-9) occurred between June and August 1997 in the Chikugo area, Fukuoka, Japan. Clinical manifestations and laboratory data of 317 children with aseptic meningitis were analyzed. The age of the patients ranged from 1 month to 12 years with the highest incidence in 4 years old children. The male: female ratio was 2.0:1.0. Symptoms of the meningitis included fever (100%), headache (89.5%) and nausea and/or vomiting (85.6%). Skin rash was not frequent (2.2%) in contrast to previous reports of ECHO 9 infections. The number of white blood cells (WBC) in cerebrospinal fluid (CSF) ranged from 10 to 3,493 cells/microliter (median; 412 cells/microliter). The neutrophils were more than 50% of the WBC in CSF in one-fourth of the patients at diagnosis. Enteroviruses were identified from CSF utilizing virus culture and enterovirus-specific RT-PCR, and ECHO-9 infection was determined by antibody titer of paired sera. Finally 44 patients were diagnosed virologically or serologically as aseptic meningitis caused by ECHO-9. Sequence analysis revealed that two strains of ECHO-9 isolated from CSF in this epidemic were closely related to ECHO-9 virulent strain Barty. (+info)
Integrin alpha(v)beta3 (vitronectin receptor) is a candidate receptor for the virulent echovirus 9 strain Barty.
(2/17)
The enterovirus echovirus 9 strain Barty (E9/Barty) is pathogenic for newborn mice as well as for humans. In contrast to the apathogenic prototype strain Hill, strain Barty encodes an RGD motif in the C-terminal part of the structural protein VP1. Data are presented that show that E9/Barty binds its target cells via contact of the RGD motif to the alpha(v)beta3 integrin (vitronectin receptor), whereas prototype Hill uses a different, still unidentified receptor site. Furthermore, virus titres of murine muscle tissue were compared after infection of newborn and 1-, 2-, 3- and 12-week-old mice. The replication capacity of the virus decreased dramatically with age of the infected mice. 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. (+info)
Echovirus-9 protein 2C binds single-stranded RNA unspecifically.
(3/17)
Polypeptide 2C is essential for picornavirus replication. Although many data on multiple functions of this highly conserved protein are available, the mechanism of RNA binding is still obscure. In this work, protein 2C of echovirus-9 strain Barty was expressed as a histidine-tagged protein in E. coli followed by nondenaturing purification to homogeneity. After incubation of 2C protein with different kinds of RNA fragments, binding was shown in gel retardation assays. Competition experiments revealed that 2C targets linear RNA unspecifically; however, single-stranded linear DNA does not react with this protein. In contrast to poliovirus, protein 2C of echovirus-9 only recognizes RNA with a low content of secondary structures. This may be a first hint of a different binding specificity of 2C in echo- and polioviruses. (+info)
Acute onset of type I diabetes mellitus after severe echovirus 9 infection: putative pathogenic pathways.
(4/17)
Enterovirus infections have been implicated in the development of type I diabetes mellitus. They may cause beta cell destruction either by cytolytic infection in the pancreas or indirectly by contributing to autoimmune reactivity. We sought evidence for these 2 mechanisms in a case of acute-onset diabetes mellitus that occurred during severe echovirus 9 infection. The virus was isolated and administered to cultured human beta cells. No viral proliferation was observed, and no beta cell death was induced, while parallel exposure to Coxsackie B virus serotype 3 resulted in viral proliferation and massive beta cell death. Although the viral protein 2C exhibited a sequence similar to that of the beta cell autoantigen glutamic acid decarboxylase (GAD(65)), no cross-reactive T cell responses were detected. The patient did not develop antibodies to GAD(65) either. Absence of evidence for direct cytolytic action or an indirect effect through molecular mimicry with GAD(65) in the present case raises the possibility of another indirect pathway through which enteroviruses can cause diabetes mellitus. (+info)
Successful treatment of enterovirus-infected mice by 2-(alpha-hydroxybenzyl)-benzimidazole and guanidine.
(5/17)
Echo virus 9- or Coxsackie A 9-infected newborn mice are protected from paralysis and death by combined treatment with nontoxic concentrations of HBB plus guanidine. HBB alone also protects Coxsackie A 9, but not echo virus 9-infected animals, whereas guanidine alone is ineffective in either case. Protection is due to inhibition of virus multiplication via the antiviral activity of these selective inhibitors. Treatment must be begun at the latest 48 h after virus inoculation. 3 days of treatment are sufficient if started at the time of virus inoculation. Failure of protection after treatment with one compound alone is not due to rapid development of drug-resistant virus mutants. Infected, successfully treated mice may develop a solid immunity. (+info)
Outbreaks of aseptic meningitis associated with echoviruses 9 and 30 and preliminary surveillance reports on enterovirus activity--United States, 2003.
(6/17)
Aseptic or viral meningitis is the most common type of meningitis and is associated with an estimated 26,000--42,000 hospitalizations each year in the United States. Enteroviruses are the most common cause of aseptic meningitis. Echovirus 9 (E9) and echovirus 30 (E30) have been associated frequently with outbreaks of aseptic meningitis. During March 2003, several state public health departments noted increased reports of aseptic meningitis and, as of August 7, seven states (Arizona, California, Georgia, Idaho, Oregon, South Carolina, and Texas) had reported outbreaks associated with either E9 or E30. This report summarizes the epidemiologic features of the aseptic meningitis outbreaks in five states (Arizona, California, Georgia, Idaho, and South Carolina) and provides an overview of enterovirus activity in the United States during January 1--August 7. Enteroviruses, E9 and E30 in particular, should be considered in the differential diagnosis of persons with aseptic meningitis. (+info)
Aseptic meningitis outbreak associated with echovirus 9 among recreational vehicle campers--Connecticut, 2003.
(7/17)
Aseptic meningitis is an inflammation of the tissues covering the brain and spinal cord and caused by a virus, most frequently an enterovirus. In August 2003, the Connecticut Department of Public Health (CDPH) received a report of three viral meningitis cases among recreational vehicle (RV) campers staying at a campground in northeastern Connecticut. CDPH, assisted by CDC, conducted an investigation, which 1) identified a total of 12 cases of aseptic meningitis and 24 cases of enterovirus-like illness among 201 campers interviewed, 2) demonstrated how transmission of enterovirus from persons with mild illness contributed to the aseptic meningitis outbreak, and 3) determined that crowded conditions inside RVs and in the campground swimming pool likely facilitated spread of enterovirus. Pool operators should check chlorine and pH levels frequently, particularly during peak pool occupancy; adults should take precautions against passing enterovirus to children, who are at greater risk for severe illness. (+info)
Acid stability of hepatitis A virus.
(8/17)
The acid stability of unpurified and highly purified hepatitis A virus (HAV) was tested and compared with that of poliovirus type 1, coxsackievirus types A9 and B1 and echovirus type 9. Only HAV had a high residual infectivity after 2 h of exposure to pH 1 at room temperature, remaining infectious for up to 5 h. At 38 degrees C, pH 1, HAV remained infectious for 90 min. Highly purified HAV was found to be infectious for 8 h at pH 1 and room temperature. This indicates that the increased stability is not due to protection by cellular material attached to the virus, but is a virus-specific marker. Under the same conditions, at pH 1 and room temperature, unpurified and highly purified HAV antigens were traceable for 5 and 4 h respectively. (+info)