Chapter 35 : Persistent Infections by Picornaviruses

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Viral persistence is currently one of the main public health problems. It depends on specific virus and host factors and particularly on the capacity of the virus to escape the immune defense. Some picornaviruses establish persistent infections in their natural animal hosts, while others are suspected to be responsible for chronic human diseases. This chapter focuses on the aspects relating to virus persistence. Theiler's murine encephalomyelitis virus (TMEV) persistence appears to be required for immune-mediated demyelination. During the chronic phase, the number of infected cells is always low, there are only small amounts of capsid proteins in infected cells, and viral RNA replication seems to be blocked at the minus-strand RNA synthesis step. Encephalomyocarditis virus (EMCV), another cardiovirus, establishes persistent infections in human erythroleu-kemic K562 cells. B group coxsackieviruses (CVBs) induce different effects in different types of cultured human renal cells, and interestingly, CVB1, -3, -4, and -5 established persistent infections in glomerular mesangial cells, which failed to develop cytopathic effects (CPE). The authors have started to study the molecular mechanisms of poliovirus (PV) persistence in HEp-2c cells because this cell model can be used for both lytic and persistent PV strains, allowing the identification of viral determinants involved in persistence. Persistent picornavirus infections are valuable models for understanding complicated pathologies resulting from persistent viral infections.

Citation: Colbère-Garapin F, Pelletier I, Ouzilou L. 2002. Persistent Infections by Picornaviruses, p 437-448. In Semler B, Wimmer E (ed), Molecular Biology of Picornavirus. ASM Press, Washington, DC. doi: 10.1128/9781555817916.ch35

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Tumor Necrosis Factor alpha
Theiler's Murine Encephalomyelitis
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Image of FIGURE 1

Principal events in the persistent FMDV infection of BHK-21 cells. The graph summarizes the data presented in several articles ( ). ts, temperature sensitive.

Citation: Colbère-Garapin F, Pelletier I, Ouzilou L. 2002. Persistent Infections by Picornaviruses, p 437-448. In Semler B, Wimmer E (ed), Molecular Biology of Picornavirus. ASM Press, Washington, DC. doi: 10.1128/9781555817916.ch35
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Image of FIGURE 2

Simplified models of persistent PV infection in neuroblastoma IMR-32 cells (star shapes) and HEp-2 cells (large hexagons). The majority of PV strains (small white hexagons) are able to establish persistent infections in IMR-32 cells ( ). Virus and cell coevolution occurs, leading to the selection of PVpi (small black hexagons). PVpi and PV mutants carrying particular PVpi determinants are ableto establish persistent infections in HEp-2 cells ( ). During the establishment of persistent PV infection, cellular factors are of crucial importance in the IMR-32 cell model, whereas viral determinants play the principal role in the HEp-2 cell model ( ).

Citation: Colbère-Garapin F, Pelletier I, Ouzilou L. 2002. Persistent Infections by Picornaviruses, p 437-448. In Semler B, Wimmer E (ed), Molecular Biology of Picornavirus. ASM Press, Washington, DC. doi: 10.1128/9781555817916.ch35
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Persistent picornavirus infection with virus production in vivo

Citation: Colbère-Garapin F, Pelletier I, Ouzilou L. 2002. Persistent Infections by Picornaviruses, p 437-448. In Semler B, Wimmer E (ed), Molecular Biology of Picornavirus. ASM Press, Washington, DC. doi: 10.1128/9781555817916.ch35
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Poliovirus persistence in human cell lines

Citation: Colbère-Garapin F, Pelletier I, Ouzilou L. 2002. Persistent Infections by Picornaviruses, p 437-448. In Semler B, Wimmer E (ed), Molecular Biology of Picornavirus. ASM Press, Washington, DC. doi: 10.1128/9781555817916.ch35

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