Ohio Strains of a Virus Pathogenic for Infant Mice (Coxsackie Group). Simultaneous Occurrence With Poliomyelitis Virus in Patients With "Summer Grippe"

Melnick, Joseph L.; Ledinko, Nada; Kaplan, Albert S.; Kraft, Lisbeth M.

doi:10.1084/jem.91.2.185

Cited by 53 publications

(3 citation statements)

References 7 publications

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“…AF081485, M16560, AY752944, X05690, AF114383, AF114384) revealed the heart virus sequence shared highest nt identity (84%) with that of CVB2, strain Ohio-1 (Polacek et al, 1999) with significantly lower identities shared by genomes of the other 5 CVB serotypes (74−75%). The relatively low identity with the prototype CVB2 sequence (and to other prototype CVB genomes) in comparison to the 2002 Kanagawa CVB2 isolates, was not surprising given that the prototype strains circulated more than 50 years ago (Melnick et al, 1950). However, a recently published study of an HEV in type I diabetes patients (Dotta et al, 2007) generated a sequence which shared >99% overall nt identity with the CVB4 prototype strain Benschoten originally isolated in 1951 (Sickles, Feorino, and Plager, 1955), with just one nt mismatch in the 5'NTR.…”

Section: The Nucleotide and Amino Acid Sequences Of The Heart Virus Imentioning

confidence: 99%

5′ terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart

et al. 2008

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Enteroviruses can induce human myocarditis, which can be modeled in mice inoculated with group B coxsackieviruses (CVB) and in which CVB evolve to produce defective, terminally deleted genomes. The 5' non-translated region (NTR) was enzymatically amplified from heart tissue of a fatal case of enterovirus-associated myocarditis in Japan in 2002. While no intact 5' viral genomic termini were detected, 5' terminal deletions ranged in size from 22 to 36 nucleotides. Sequence of the 5' third of this viral genome is of a modern strain, closely related to CVB2 strains isolated in Japan in 2002. A CVB3 chimera containing the 5' NTR with a 22 nt deletion produced progeny virus upon transfection of HeLa cells. When the 5' 22 nucleotide deletion was repaired, the virus induced myocarditis in mice and replicated like wild type virus in murine heart cells. This is the first report of these naturally-occurring defective enteroviral genomes in human myocarditis.

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Section: The Nucleotide and Amino Acid Sequences Of The Heart Virus Imentioning

confidence: 99%

5′ terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart

et al. 2008

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“…The prototype strain CVB2 Ohio-1 (VR-29; ATCC) (56,67) and the CVB2ORD variant (66) were propagated in GMK and RD cells, respectively, as previously described (66).…”

Section: Cells and Virusesmentioning

confidence: 99%

A Single Coxsackievirus B2 Capsid Residue Controls Cytolysis and Apoptosis in Rhabdomyosarcoma Cells

Gullberg

Tolf

Jönsson

et al. 2010

J Virol

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Coxsackievirus B2 (CVB2), one of six human pathogens of the group B coxsackieviruses within the enterovirus genus of Picornaviridae, causes a wide spectrum of human diseases ranging from mild upper respiratory illnesses to myocarditis and meningitis. The CVB2 prototype strain Ohio-1 (CVB2O) was originally isolated from a patient with summer grippe in the 1950s. Later on, CVB2O was adapted to cytolytic replication in rhabdomyosarcoma (RD) cells. Here, we present analyses of the correlation between the adaptive mutations of this RD variant and the cytolytic infection in RD cells. Using reverse genetics, we identified a single amino acid change within the exposed region of the VP1 protein (glutamine to lysine at position 164) as the determinant for the acquired cytolytic trait. Moreover, this cytolytic virus induced apoptosis, including caspase activation and DNA degradation, in RD cells. These findings contribute to our understanding of the host cell adaptation process of CVB2O and provide a valuable tool for further studies of virus-host interactions.Virus infections depend on complex interactions between viral and cellular proteins. Consequently, the nature of these interactions has important implications for viral cell type specificity, tissue tropism, and pathogenesis. Group B coxsackieviruses (CVB1 to CVB6), members of the genus Enterovirus within the family of Picornaviridae, are human pathogens that cause a broad spectrum of diseases, ranging from mild upper respiratory illnesses to more severe infections of the central nervous system, heart, and pancreas (61). These viruses have also been associated with certain chronic muscle diseases and myocardial infarction (2,3,12,13,22).The positive single-stranded RNA genome (approximately 7,500 nucleotides in length) of CVBs is encapsidated within a small Tϭ1, icosahedral shell (30 nm in diameter) comprised of repeating identical subunits made up of four structural proteins (VP1 to VP4). Parts of VP1, VP2, and VP3 are exposed on the outer surface of the capsid, whereas VP4 is positioned on the interior. The virion morphology is characterized by a star-shaped mesa at each 5-fold icosahedral symmetry axis, surrounded by a narrow depression referred to as the "canyon" (69). All six serotypes of CVB can use the coxsackie and adenovirus receptor (CAR) for cell attachment and entry (9,55,82). Some strains of CVB1, -3, and -5 also use decay accelerating factor ([DAF] CD55) for initial attachment to the host cell; however, binding to DAF alone is insufficient to permit entry into the cell (10, 54, 76).Picornaviruses are generally characterized by their cytolytic nature in cell culture. However, several in vivo and in vitro studies have shown that some picornaviruses, e.g., poliovirus, Theiler's murine encephalomyelitis virus, foot-and-mouth disease virus, CVB3, CVB4, and CVB5, may also establish persistent, noncytolytic infections (4,29,35,39,62,74). Recently, it has been shown that the diverse outcomes of picornaviral infections may depend on interactions between the viru...

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“…En el momento de usar los sueros, ya sea en fijacion de complemento o en neutralization se desconselan, se diluyen e inactivan a 60 grades C por 20 minutos (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17).…”

unclassified

Aislamiento y estudio de cuatro virus coxsackie de enfermos de poliomielitis

Steeger¹,

Contreras²,

Santibañez³

1953

Rev. chil. pediatr.

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Ohio Strains of a Virus Pathogenic for Infant Mice (Coxsackie Group). Simultaneous Occurrence With Poliomyelitis Virus in Patients With "Summer Grippe"

Cited by 53 publications

References 7 publications

5′ terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart

5′ terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart

A Single Coxsackievirus B2 Capsid Residue Controls Cytolysis and Apoptosis in Rhabdomyosarcoma Cells

Aislamiento y estudio de cuatro virus coxsackie de enfermos de poliomielitis

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