Steven Tracy – författare

The group B coxsackieviruses have a long and colorful history, dating to the early days of virology as we now know it. In the late 1940s, ultracentrifugation and electron microscopy were new, high-tech tools and suckling mice were suppla- ing monkeys as the virus isolation vessel of choice. Viruses were, often as not, still referred to as “filterable agents. ” The rampage of paralytic poliomyelitis epid- ics in the previous 20 or so years had spurred national investment in infectious disease research, resulting in an unprecedented period of virus discovery, eclipsed only a few years later once cell culture became the preferred method to isolate and identify mammalian viruses. The coxsackieviruses were isolated from feces of patients with paralytic poliomyelitis and nonparalytic poliomyelitis (aseptic meningitis), causing disease in suckling mice, but not in adult mice or monkeys. They were considered to be related to the polioviruses on the basis of their physical properties, such as virion size, acid and ether resistance, and temperature stability in 50% glycerol, and were classified into groups A and B by the nature of the disease induced in mice: flaccid paralysis by group A viruses and spastic paralysis by those of group B. Our knowledge of the group B coxsackieviruses has progressed dramatically in the past 60 years.

The group B coxsackieviruses have a long and colorful history, dating to the early days of virology as we now know it. In the late 1940s, ultracentrifugation and electron microscopy were new, high-tech tools and suckling mice were suppla- ing monkeys as the virus isolation vessel of choice. Viruses were, often as not, still referred to as “filterable agents. ” The rampage of paralytic poliomyelitis epid- ics in the previous 20 or so years had spurred national investment in infectious disease research, resulting in an unprecedented period of virus discovery, eclipsed only a few years later once cell culture became the preferred method to isolate and identify mammalian viruses. The coxsackieviruses were isolated from feces of patients with paralytic poliomyelitis and nonparalytic poliomyelitis (aseptic meningitis), causing disease in suckling mice, but not in adult mice or monkeys. They were considered to be related to the polioviruses on the basis of their physical properties, such as virion size, acid and ether resistance, and temperature stability in 50% glycerol, and were classified into groups A and B by the nature of the disease induced in mice: flaccid paralysis by group A viruses and spastic paralysis by those of group B. Our knowledge of the group B coxsackieviruses has progressed dramatically in the past 60 years.

The group B coxsackieviruses have a long and colorful history, dating to the early days of virology as we now know it. In the late 1940s, ultracentrifugation and electron microscopy were new, high-tech tools and suckling mice were suppla- ing monkeys as the virus isolation vessel of choice. Viruses were, often as not, still referred to as “filterable agents. ” The rampage of paralytic poliomyelitis epid- ics in the previous 20 or so years had spurred national investment in infectious disease research, resulting in an unprecedented period of virus discovery, eclipsed only a few years later once cell culture became the preferred method to isolate and identify mammalian viruses. The coxsackieviruses were isolated from feces of patients with paralytic poliomyelitis and nonparalytic poliomyelitis (aseptic meningitis), causing disease in suckling mice, but not in adult mice or monkeys. They were considered to be related to the polioviruses on the basis of their physical properties, such as virion size, acid and ether resistance, and temperature stability in 50% glycerol, and were classified into groups A and B by the nature of the disease induced in mice: flaccid paralysis by group A viruses and spastic paralysis by those of group B. Our knowledge of the group B coxsackieviruses has progressed dramatically in the past 60 years.

S. TRACY Late in the 1940s, a virus was isolated from a young patient with a flaccid par­ alysis in the sleepy Hudson River town of Coxsackie in the state of New York. Within the next few years, it was apparent that this and other similar viruses were not polioviruses but were indeed a new group of viruses, viruses that by the mid- 1950s had been found to be commonly associated with pediatric inflammatory heart disease. Two groups of coxsackieviruses (A and B) were differentiated on the basis of the type of paralysis induced in suckling mice by these viruses. Group B coxsackieviruses, because of their primacy as etiologic agents of human acute viral myocarditis and its relatively common sequela, dilated cardiomyopathy, are the focus of this volume. of the century approaches, the massive international effort to eradi­ As the end cate polioviruses through vaccination as causes of human disease has been success­ ful in the Western Hemisphere and in many parts of Europe, and it is expected that worldwide eradication may be achieved within the near future. While this is wonderful news, there are sadly no similar efforts being planned to combat the numerous other human enteroviruses that daily incur widespread morbidity and mortality throughout the world. While this is due in part to the lack of specific know­ ledge about the other human enteroviruses, it is also due to the perceptions of industry that there is insufficient profit to be made by developing these vaccines.