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Review
. 2013 Sep;63(3):230-6.
doi: 10.1016/j.cyto.2013.05.007. Epub 2013 Jun 10.

Enter at your own risk: how enteroviruses navigate the dangerous world of pattern recognition receptor signaling

Katharine G Harris  1 , Carolyn B Coyne
Affiliations
Review

Enter at your own risk: how enteroviruses navigate the dangerous world of pattern recognition receptor signaling

Katharine G Harris et al. Cytokine. 2013 Sep.

Abstract

Enteroviruses are the most common human viral pathogens worldwide. This genus of small, non-enveloped, single stranded RNA viruses includes coxsackievirus, rhinovirus, echovirus, and poliovirus species. Infection with these viruses can induce mild symptoms that resemble the common cold, but can also be associated with more severe syndromes such as poliomyelitis, neurological diseases including aseptic meningitis and encephalitis, myocarditis, and the onset of type I diabetes. In humans, polarized epithelial cells lining the respiratory and/or digestive tracts represent the initial sites of infection by enteroviruses. Control of infection in the host is initiated through the engagement of a variety of pattern recognition receptors (PRRs). PRRs act as the sentinels of the innate immune system and serve to alert the host to the presence of a viral invader. This review assembles the available data annotating the role of PRRs in the response to enteroviral infection as well as the myriad ways by which enteroviruses both interrupt and manipulate PRR signaling to enhance their own replication, thereby inducing human disease.

Keywords: Enterovirus; RIG-I-like receptor; Toll-like receptor; Type I IFN.

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Figures

Figure 1
Figure 1. Schematic of the EV genome
The positive sense single stranded RNA genome undergoes IRES dependent translation into a single polypeptide. This polypeptide is then processed into individual viral proteins by two viral proteases: 2Apro and 3Cpro (shown in red), as indicated by arrows. These viral proteases also act upon a wide range of host cell proteins.
Figure 2
Figure 2. Interference of PRR-mediated signaling by EVs
EVs have evolved multiple mechanisms to attenuate and/or modulate PRR signaling at a number of diverse stages. This results in a reduction of type I IFN production and/or NF-κB mediated transcription and allows the virus to evade detection by the innate immune system.
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