Abstract
The expression and production of type 1 interferon is the classic cellular response to virus infection. In addition to this antiviral response, virus infection also stimulates the production of proinflammatory mediators. In this review, the pathways controlling the induction of inflammatory genes and the roles that these inflammatory mediators contribute to host defense against viral pathogens will be discussed. Specific focus will be on the role of the chemokine receptor CCR5, as a signaling receptor controlling the activation of pathways leading to virus-induced inflammatory gene expression.
Highlights
Macrophages are a differentiated monocytic cell type within the innate immune system that have a well-defined role in the host response against viral infection [1,2]
In searching for mechanisms that would allow for the activation of each of the signaling cascades that selectively control the expression of inflammatory genes in macrophages, we showed that pharmacological inhibitors and dominant negative mutants of the Src family kinases (SFKs) attenuate Encephalomyocarditis Virus (EMCV)-stimulated expression of inducible nitric oxide synthase (iNOS), COX-2, and IL-1 in macrophages [68]
The studies outlined in this review provide evidence that CCR5 functions as an integral cell surface signaling receptor that participates in signaling events leading to the expression of the inflammatory genes iNOS, COX-2, and IL-1 by macrophages in response to EMCV infection
Summary
Macrophages are a differentiated monocytic cell type within the innate immune system that have a well-defined role in the host response against viral infection [1,2]. In addition to NF-B, at least one secondary signaling pathway, selective for each target gene, is required for inflammatory gene expression by macrophages The differences in responses are likely to be cell type and virus specific
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