Viral and host proteins involved in picornavirus life cycle

Abstract

Picornaviruses cause several diseases, not only in humans but also in various animal hosts. For instance, human enteroviruses can cause hand-foot-and-mouth disease, herpangina, myocarditis, acute flaccid paralysis, acute hemorrhagic conjunctivitis, severe neurological complications, including brainstem encephalitis, meningitis and poliomyelitis, and even death. The interaction between the virus and the host is important for viral replication, virulence and pathogenicity. This article reviews studies of the functions of viral and host factors that are involved in the life cycle of picornavirus. The interactions of viral capsid proteins with host cell receptors is discussed first, and the mechanisms by which the viral and host cell factors are involved in viral replication, viral translation and the switch from translation to RNA replication are then addressed. Understanding how cellular proteins interact with viral RNA or viral proteins, as well as the roles of each in viral infection, will provide insights for the design of novel antiviral agents based on these interactions.

Figure 1

Schematic of the enterovirus genome, the polyprotein products and their major functions. A diagrammatic representation of the enterovirus genome is shown. The 11 mature polypeptides are shown, together with the three main cleavage intermediates. The main biological functions are included for each polypeptide. UTR, untranslated region; IRES, internal ribosome entry site; VPg, viral protein genome-linked.

Figure 2

Structural features of type I, II, III, and IV picornavirus IRES elements. RNA secondary structures of four types base on M-fold software. (A). Enteroviruses (PV, CVB3 and EV71) and rhinoviruses contain type I IRES elements. (B). Aphthoviruses (FMDV) and cardiovirus (EMCV and TMEV) contain type II IRES elements. (C). HAV contains type III IRES element. (D). porcine reschovirus serotype 1 (PTV-1) contains type IV IRES element.