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Genomic regions of coxsackievirus B3 associated with cardiovirulence
Author(s) -
Lee Cheol,
Maull Elizabeth,
Chapman Nora,
Tracy Steve,
Gauntt Charles
Publication year - 1997
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199707)52:3<341::aid-jmv18>3.0.co;2-l
Subject(s) - virology , coxsackievirus , enterovirus , biology , picornaviridae , virus , medicine
The molecular basis for cardiovirulence in the coxsackievirus B3 (CVB3) genome was examined in a murine model of acute myocarditis. Infectious cDNAs representing a highly cardiovirulent coxsackievirus B3 (CVB3 m ) and a noncardiovirulent (CVB3 0 ) virus were used to construct infectious chimeric cDNAs. Assays of the resulting recombinant viruses for cardiovirulence in adolescent male CD‐1 mice showed that the 5′ nontranslated region (5′ NTR) of the CVB3 m genome plays the major role in determining cardiovirulence and that the genomic region encoding the capsid proteins has a minor additive effect in increasing cardiovirulence. Nucleotide sequences in the 5′ NTR of CVB3 m and CVB3 0 differ at 23 positions; 14 are located in four stemloop motifs of the secondary structure and may influence the cardiovirulent phenotype by regulating RNA or protein synthesis. A comparison of predicted amino acid sequences of capsid proteins in CVB3 m and CVB3 0 identified two amino acids as potential candidate contributors to cardiovirulence, i.e., amino acids at positions A207 (Asn‐Asp) in the puff structure of the E‐F loop of VP2 and A566 (Gln‐Glu) in the C terminal of VP3 at the external surface. The data from this study and published literature support the conclusion that cardiovirulence of a CVB3 can depend on several regions of the genome. J. Med. Virol. 52:341–347, 1997. © 1997 Wiley‐Liss, Inc.