The host and virus factors that contribute to the pathogenesis and tropism of picornaviruses are manifold1. Some host factors that are involved include cell cycle status, and the innate and adaptive immune responses. On the viral side, one must consider the 5' "cloverleaf that is required for replication, the internal ribosome entry site (IRES) that regulates translation, and various other RNA and protein components whose functions have been analyzed in extraordinary detail. Of course, these two opposing forces do not exist in a vacuum, and it is equally important to consider the interface between host and virus; many picornaviruses exert profound effects on the infected cell, altering cellular apoptosis, autophagy, protein synthesis and other key functions. Thus, the topic is worthy of a book, and cannot be adequately addressed in this short communication. Given the overall focus of the related symposium - Viral Persistence and Latency: Current Concepts and Role in Disease - this extended abstract, and the related presentation, will focus on the persistent / latent infection that is established by one particular picornavirus, coxsackievirus B3 (CVB3). I shall: (i) describe the acute and chronic diseases that are caused by CVB3; (ii) discuss how CVB3 persistence / latency might contribute to chronic disease; (iii) demonstrate that CVB3 evades, with breathtaking efficiency, surveillance by CD8+ T cells, thereby presumably facilitating the establishment and maintenance of a persistent / latent state; and (iv) describe the molecular mechanisms by which the virus achieves this feat.
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