Chapter 21 : Evasion of Innate Host Antiviral Defenses by Picornaviruses

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The family includes a number of medically important viruses, such as poliovirus (PV) and hepatitis A virus (HAV); viruses of significance to veterinary medicine, such as foot-and-mouth disease virus (FMDV); and encephalomyocarditis virus (EMCV), a murine virus with broad capabilities to infect other animal species that has been used widely in studies of the interaction of viruses with the interferon (IFN) system. The remarkable diversity that is evident in these adaptive strategies across the various picornaviral genera suggests that they are relatively recent additions in the evolution of the picornaviruses. In the case of PV and most other picornaviruses, the 3A association appears to be primarily with membranes derived from the ER. The studies described above reveal that the picornaviruses have evolved multiple strategies for evading innate antiviral host defenses, but they are in no way complete for even one member of this large virus family. The diversity of specialized mechanisms of evasion found in only certain groups of viruses, is likely to reflect, at least in part, differences in the tissue tropisms of various picornaviruses, as well as the redundant nature of innate antiviral defenses. Expression of a cleavage-resistant G3PB mutant preserved the ability of the cell to assemble stress granules late in the infection cycle, and also reduced the yields of PV. Although roles for stress granule formation and autophagy in innate cellular defenses against picornaviruses remain speculative, these are likely to be productive lines of future investigation.

Citation: Lemon S. 2009. Evasion of Innate Host Antiviral Defenses by Picornaviruses, p 335-351. In Brasier A, García-Sastre A, Lemon S (ed), Cellular Signaling and Innate Immune Responses to RNA Virus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555815561.ch21
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Figure 1

Basic replication scheme of picornaviruses: (a) virus uptake occurs through a process of receptor-mediated endocytosis leading to release of the positive-strand RNA genome into the cytoplasm; (b) cap-independent translation of the genomic RNA leads to expression of a large polyprotein; (c) the polyprotein is processed into structural (shaded) and nonstructural (not shaded) proteins by a well-coordinated series of viral protease-mediated cleavages; (d) nonstructural proteins assemble as replicase complexes at the 3′ end of the genomic RNA within double-membrane vesicles derived from a reordering of intracellular membranes, and initiate the synthesis of complementary negative-strand RNA, leading to production of dsRNA; (e) multiple copies of positive-strand genomic RNA are transcribed from the negative-strand intermediates; (f) newly synthesized positive-strand progeny assemble with structural proteins to form new viral particles, which are released from the cell through both lytic and nonlytic pathways. Replication occurs within the cytoplasm and involves a number of cellular proteins, some of which are normally localized in the nucleus.

Citation: Lemon S. 2009. Evasion of Innate Host Antiviral Defenses by Picornaviruses, p 335-351. In Brasier A, García-Sastre A, Lemon S (ed), Cellular Signaling and Innate Immune Responses to RNA Virus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555815561.ch21
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Image of Figure 2
Figure 2

Polyprotein organization of viruses within the five major picornaviral genera, showing the general order of the individual mature proteins (L-VP4-VP2-VP3-VP1-2A-2B-2C-3A-3B-3C-3D) that are produced by proteolytic processing directed by virally encoded proteases (shaded proteins). All members of the family express a cysteine protease (3C) that is responsible for most polyprotein processing events. Some genera express additional proteases (2A in enteroviruses and rhinoviruses and L in the aphthoviruses) that act in on the polyprotein and also target cellular proteins that are critical for cellular transcription and/or translation. Precursor proteins may also have specific proteolytic activities, such as 3ABC in the hepatoviruses, which targets MAVS/IPS-1 for cleavage. The amino acid residues flanking each cleavage site are shown for each of the polyproteins and are generally conserved within each picornaviral genus. 3D is the conserved RNA-dependent RNA polymerase. (Modified from reference .)

Citation: Lemon S. 2009. Evasion of Innate Host Antiviral Defenses by Picornaviruses, p 335-351. In Brasier A, García-Sastre A, Lemon S (ed), Cellular Signaling and Innate Immune Responses to RNA Virus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555815561.ch21
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Table 1

Abbreviated list of important members of the family

Citation: Lemon S. 2009. Evasion of Innate Host Antiviral Defenses by Picornaviruses, p 335-351. In Brasier A, García-Sastre A, Lemon S (ed), Cellular Signaling and Innate Immune Responses to RNA Virus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555815561.ch21
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Table 2

Strategies evolved by members of the P for evading innate host antiviral defenses

Citation: Lemon S. 2009. Evasion of Innate Host Antiviral Defenses by Picornaviruses, p 335-351. In Brasier A, García-Sastre A, Lemon S (ed), Cellular Signaling and Innate Immune Responses to RNA Virus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555815561.ch21

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