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Abstract:

Caliciviruses and astroviruses, along with rotavirus, are regarded as important causes of viral gastroenteritis. Surveillance studies using recently developed molecular diagnostic methods have also highlighted the importance of human astroviruses and other underreported pathogens as important causes of pediatric acute gastroenteritis. Epidemiological information on human caliciviruses and astroviruses is providing data required to assess the economic burden of the disease and justify the development of prevention strategies, including vaccination. A section describes what is now known about the activation of innate responses after both human and nonhuman calicivirus infections, and specifically emphasizes the effect that innate antiviral responses might have on restricting human norovirus propagation in vitro. To date, the role of innate immunity in controlling infections caused by caliciviruses has been demonstrated for murine norovirus (MNV) and porcine enteric calicivirus (PEC), but only limited data are available to confirm this for human noroviruses. As positive-sense RNA viruses, there are several steps in the replication cycle of caliciviruses and astroviruses where the cellular antiviral machinery could detect foreign viral components. Exploration of the interplay between caliciviruses and astroviruses and the interferon (IFN) response not only will help us to better understand viral pathogenesis but also can result in novel vaccination strategies and therapies. This chapter concludes with a few remarks meant to stimulate discussion and future studies to better understand the interplay between calicivirus and astrovirus infections and the cellular antiviral responses.

Citation: Guix S, Estes M. 2009. and , p 389-402. 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.ch24

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Figure 1

Current proposed model for calicivirus and astrovirus life cycle. The entry process in both calicivirus and astrovirus infection following receptor binding on the cell surface is poorly understood. Adsorptive endocytosis was described as the most probable mechanism by which astroviruses enter susceptible cells ( ), and recently it has been shown that FCV enters the cell by clathrin-mediated endocytosis and that acidification is required for uncoating of the genome and access to the cytoplasm ( ). Once uncoated in the cytoplasm, genomic RNA is translated as a polyprotein. Cleavage of the polyprotein results in the individual non-structural proteins (nsp) necessary for replication. Viral replication complexes assemble in close association with intracellular membranes, resulting in the formation of both genomic and subgenomic positive-sense RNAs. Large quantities of subgenomic RNAs are used to synthesize high levels of capsid proteins. While it is known that both genomic and subgenomic RNAs are encapsidated into virions of animal caliciviruses, it is still unclear whether this occurs for human caliciviruses and astroviruses.

Citation: Guix S, Estes M. 2009. and , p 389-402. 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.ch24
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Figure 2

Detection of Norwalk virus capsid protein expression by immunofluorescence in Huh7 cells transfected with wild-type NV RNA isolated from human volunteer stool samples. Low-magnification images are shown. Prior to NV RNA transfection, cell monolayers were incubated for 3 h at 37°C with supernatant (SN) from cultures that had been mock-transfected, or transfected with poly(I:C), a carrier RNA used as a negative control, or wild-type NV RNA for 24 h. After NV RNA transfection, SNs used for the pretreatment of cells were further incubated with cells until immunostaining was performed at 48 h posttransfection. The number in each panel indicates the average number plus or minus standard deviation of NV-positive cells per transfected well after transfecting 3 wells of a 48-well plate for each condition. The asterisk denotes statistically significant differences ( < 0.05) after the average numbers of NV-positive cells in each condition were compared by Student’s test.

Citation: Guix S, Estes M. 2009. and , p 389-402. 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.ch24
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Tables

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Table 1

Highlights of innate responses induced by caliciviruses and astroviruses

Citation: Guix S, Estes M. 2009. and , p 389-402. 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.ch24

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