Coxsackie B virus.

Abstract

Coxsackie B virus (CVB) was first isolated in the late 1940s in Coxsackie, New York, and is now known to be widespread worldwide. Infections are common and show some seasonal variation as infections are more common during the summer and early fall. The virus particle is small, nonenveloped, and contains a positive single-stranded RNA genome. The virus attaches to a cellular receptor (often the Coxsackie-adenovirus receptor, CAR) on the cell surface and is then internalized via endocytic vesicles after which the virus uncoats and the RNA genome is delivered across the endosomal membrane into the cytoplasm. Genome translation produces a single polyprotein which is processed into capsid and nonstructural proteins. The nonstructural proteins aid in the production of a negative-strand RNA, which serves as a template for synthesis of new positive-strand RNA molecules, and facilitate virion assembly. Newly synthesized capsid proteins appear in the cytoplasm concomitantly with the appearance of membranous tubulovesicular structures linked to active replication sites. Progeny viruses are typically spread to other cells after lysis of the infected cells, although nonlytic spread has also been reported. The majority of CVB infections are asymptomatic or associated with mild symptoms of the common cold. Occasionally, the CVBs cause severe disease, and infections of neonates can have a fatal outcome.