Understanding the molecular mechanisms of coxsackievirus B3 genome expression is crucial for developing targeted therapies against viral myocarditis and dilated cardiomyopathy.
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No change to myocarditis management; leaves open mechanism-guided CBV-3 therapeutic design.
Coxsackievirus B3 (CVB-3) belongs to the Picornaviridae family of enterovirus genus of pathogens that cause a great number of human diseases. A viral infection is associated with many pathological states such as: myocarditis, dilated cardiomyopathy, pericarditis, pleurodynia, systemic infection in infants, aseptic meningitis, and pancreatitis. Since viral diseases, especially in their chronic state, are difficult to treat, there has not been as yet, any specific therapeutic developed against coxsackievirus till date. CVB-3 is a single stranded, positive-sense RNA virus that encodes one large open reading frame flanked by two untranslated regions (UTR). The 5NUTR contains an IRES element that directs the translation process and a cloverleaf structure that regulate viral replication. The complementary, 3N terminal region of the replicative strand is also believed to be crucial for the replication of events. The secondary structure RNA elements regulate the most important processes in the viral propagation cycle. The mechanisms that rule the CBV-3 gene expression, its genome structure and the key steps of its viral life cycle are being reviewed in the hope that better knowledge of these processes will lead to better understanding of the molecular biology of CVB-3 and to the design of an effective therapy against this enterovirus.
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Dutkiewicz et al. (2014) studied this question.
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