Abstract
Coxsackieviruses (CV), as all enteroviruses, are small, non-enveloped, icosahedral-shaped capsid viruses. They belong to the family Picornaviridae. This group was named after the town of Coxsackie in New York State (USA) where was recognized the first human case of coxsackievirus infection in the 40s of the XX century. Coxsackie B (CVB) are distinguished from other enteroviruses by ability to infect many types of tissues and organs. This wide tropism reason that these viruses are etiologic agents of large number of different diseases. CVB cause infection of the heart, pleura, pancreas, lungs and liver, causing myocarditis, pleurodynia, pericarditis, pneumonia and hepatitis. They can invade the central nervous system and induce meningitis, encephalitis, or acute flaccid paralysis. They also cause systemic neonatal disease and chronic infections such as type 1 diabetes and chronic myocarditis. This pantropic character of CVB can be determinate by specific virus – receptor interaction, which initiate the infection and viral spread. CVB attach at least two receptor proteins: the coxsackievirus – adenovirus receptor (CAR) and the decay – accelerating factor (DAF). Moreover, other anonymous determinant may play a role in tissue permissiveness and disease severity. This article summarizes the main aspects of Coxsackieviruses B infection: replication, virus-receptor interaction, genetic variability, pathogenesis, epidemiology and diagnostics.