Genetics of coxsackievirus virulence.

Abstract

The first reported isolate of the coxsackieviruses occurred in the upstate New York town of Coxsackie (Dalldorf and Sickles 1948). By the mid-late 1950s (Dalldorf 1955), the coxsackie B viruses (CVBs) had been shown to be agents of severe human inflammatory heart muscle disease (myocarditis) (Montgomery et al. 1955; Gear et al. 1956; Javett et al. 1956; van Creveld and de Jager 1956; Verlinde et al. 1956; Fletcher and Brennan 1957; Kibrick and Benirschke 1958; Simenhoff and Ulys 1958). In the intervening years, the CVBs have been confirmed as etiologic agents of, or etiologically linked to, a host of human diseases ranging from flu-like illness through severe inflammatory diseases of the heart and central nervous system (Melnick 1990; Chaps. 2–4 ). Based on molecular detection data, it is estimated that enteroviruses (likely in most cases to be CVBs) are etiologic agents in perhaps 20%–25% of the cases of inflammatory heart disease (or myocarditis) and dilated cardiomyopathy (DCM), although individual reports range from 0%–53% (Bowles et al. 1986; Easton and Eglin 1988; Tracy et al. 1990; Kandolf and Hofschneider 1991; Grasso et al. 1992; reviewed in Martino et al. 1995). DCM alone afflicts approximately five to eight per 100 000 per year worldwide (Williams and Olsen 1985; Manolio et al. 1992). In the aggregate, these data indicate that there are at least 5000 or more occurrences of enterovirus-induced DCM alone per year in the United States.