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Chapter 16 : Host Cell Responses to Coronavirus Infections

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Host Cell Responses to Coronavirus Infections, Page 1 of 2

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Abstract:

This chapter discusses common as well as unique alterations in host gene expression during coronavirus (CoV) infection in vitro, and compares to those in other RNA virus infections. Transcriptional profiling and studies using other approaches have led to a more comprehensive understanding of CoV-induced (immune) responses. The chapter also discusses several common responses on the topics of apoptosis, cell cycle regulation, unfolded-protein response, ubiquitin-proteasome-mediated degradation, autophagy, heterogeneous nuclear ribonucleo-protein (hnRNP)-involved viral transcription, and modulation of cellular translation in more detail. To distinguish reference to genes and associated mRNA from reference to proteins, mouse gene and protein nomenclature has been used.

Citation: Versteeg G, Spaan W. 2008. Host Cell Responses to Coronavirus Infections, p 245-258. In Perlman S, Gallagher T, Snijder E (ed), Nidoviruses. ASM Press, Washington, DC. doi: 10.1128/9781555815790.ch16

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Figure 1

Groups of common differentially regulated genes during CoV infection in vitro. Differentially expressed genes from microarray experiments on CoV infection in vitro were categorized based on their frequency of occurrence among different studies. Genes with altered expression in the majority of the analyzed CoV infections were identified as “common regulated genes.” Since virus-induced changes in host cell morphology often result in changes in gene expression, these studies were organized in lytically and nonlytically infected cells. (a and c) Common regulated genes during nonlytic CoV infections mainly encompass chemokines and IFN-stimulated genes. (b and d) Lytic CoV infection in vitro shows a much more diverse set of common differentially expressed genes. The number of differentially regulated chemokine genes is substantially lower than for nonlytic infections. Induction of IFN and IFN-stimulated genes is completely absent. M.o.i., multiplicity if infection.

Citation: Versteeg G, Spaan W. 2008. Host Cell Responses to Coronavirus Infections, p 245-258. In Perlman S, Gallagher T, Snijder E (ed), Nidoviruses. ASM Press, Washington, DC. doi: 10.1128/9781555815790.ch16
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Figure 2.

Differentially expressed host genes during CoV infection in vitro (nonmicroarray). (a) Nonlytic CoV infections in cells from lymphoid origin resulted in induction of a wide range of CC as well as CXC chemokines partially induced by activation of TLRs. (b) Lytic infections in nonlymphoid cell lines result in less prominent induction of chemokine genes. The more selective induction of a particular subset of chemokine genes is likely cell type dependent. Most of the nonlymphoid cell lines lack TLRs and means to express “specialized” cytokines. Up-regulation of chemokine transcription in these cells is most likely the result of other intracellular interactions between viral components and the host cell. M.o.i., multiplicity of infection; ELISA, enzyme-linked immunosorbent assay.

Citation: Versteeg G, Spaan W. 2008. Host Cell Responses to Coronavirus Infections, p 245-258. In Perlman S, Gallagher T, Snijder E (ed), Nidoviruses. ASM Press, Washington, DC. doi: 10.1128/9781555815790.ch16
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Tables

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Table 1.

Apoptosis induction during CoV infection

Citation: Versteeg G, Spaan W. 2008. Host Cell Responses to Coronavirus Infections, p 245-258. In Perlman S, Gallagher T, Snijder E (ed), Nidoviruses. ASM Press, Washington, DC. doi: 10.1128/9781555815790.ch16

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