Group B Coxsackieviruses

1. Front Matter

   Pages i-xix

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2. CVB Genetics

   1. Coxsackieviruses and Quasispecies Theory: Evolution of Enteroviruses

      • E. Domingo, V. Martin, C. Perales, C. Escarmis

      Pages 3-32

   2. Comparative Genomics of the Coxsackie B Viruses and Related Enteroviruses

      • M. Steven Oberste

      Pages 33-47

   3. Group B Coxsackievirus Virulence

      • Steven Tracy, C. Gauntt

      Pages 49-63

3. CVB Entry and Replication

   1. The Coxsackievirus and Adenovirus Receptor

      • P. Freimuth, L. Philipson, S. D. Carson

      Pages 67-87

   2. Coxsackievirus B RNA Replication: Lessons from Poliovirus

      • P. Sean, B. L. Semler

      Pages 89-121

   3. CVB Translation: Lessons from the Polioviruses

      • J. M. Bonderoff, R. E. Lloyd

      Pages 123-147

   4. Preferential Coxsackievirus Replication in Proliferating/Activated Cells: Implications for Virus Tropism, Persistence, and Pathogenesis

      • R. Feuer, J. L. Whitton

      Pages 149-173

4. Host-Virus Interaction

   1. The Impact of CVB3 Infection on Host Cell Biology

      • D. Marchant, X. Si, H. Luo, B. McManus, D. Yang

      Pages 177-198

   2. Host Immune Responses to Coxsackievirus B3

      • S. Huber

      Pages 199-221

   3. Pediatric Group B Coxsackievirus Infections

      • J. R. Romero

      Pages 223-239

   4. CVB-Induced Pancreatitis and Alterations in Gene Expression

      • A. I. Ramsingh

      Pages 241-258

   5. The CVB and Etiology of Type 1 Diabetes

      • Kristen M. Drescher, Steven Tracy

      Pages 259-274

   6. Persistent Coxsackievirus Infection: Enterovirus Persistence in Chronic Myocarditis and Dilated Cardiomyopathy

      • N. M. Chapman, K. -S. Kim

      Pages 275-292

   7. Autoimmunity in Coxsackievirus Infection

      • N. R. Rose

      Pages 293-314

   8. CVB Infection and Mechanisms of Viral Cardiomyopathy

      • K. U. Knowlton

      Pages 315-335

5. Back Matter

   Pages 337-340

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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.

• CVB entry
• CVB genetics
• CVB infection
• CVB replication
• autoimmunity
• chronic myocarditis
• chronic pancreatitis
• coxsackievirus-adenovirus receptor
• enterovirus persistence
• infection
• infections
• poliovirus
• quasispecies theory
• virus

• University of Nebraska Medical Center, Omaha, USA

  Steven Tracy

• National Center for Immunization & Respiratory Diseases, Atlanta, USA

  M. Steven Oberste

• Creighton University School of Medicine, Omaha, USA

  Kristen M. Drescher