Assessment of the IFN-β response to four feline caliciviruses: Infection in CRFK cells

- We first cloned and identified the feline IFN-β promoter sequence and PRD motifs.
- FCV strains (3/4) could not activate the IFN-β promoter in vitro.
- Induction of the IFN-β promoter by FCV 2280 infection depended on viral dsRNA.
- Over-expression of IFN-β before exposure to the virus reduced viral yields.

Feline calicivirus (FCV) is a highly contagious pathogen with a widespread distribution. Although the cat genome has been sequenced, little is known about innate immunity in cats, which limits the understanding of FCV pathogenesis. To investigate the IFN-β response during FCV infection in CRFK cells, we first cloned and identified the feline IFN-β promoter sequence and the positive regulatory domain (PRD) motifs, which shared a high similarity with human and porcine IFN-β promoters. Next, we found that infections with FCV strains F9, Bolin and HRB-SS at the 100 or 1000 TCID50 doses could not activate the IFN-β promoter at 12 and 24 h post-infection. Only strain 2280 infection at a 1000 TCID50 dose could induce the IFN-β promoter mainly through IRF3 and partially through NF-κB, at 24 h post-infection. However, the IFN response occurred much later and was smaller in magnitude compared with that following Sendai virus (SeV) infection. Further, we found that induction of the IFN-β promoter by FCV 2280 infection depended on dsRNA and not on viral proteins. Finally, we examined whether the IFN-β response had an antiviral effect against FCV replication. The over-expression of IFN-β before exposure to the virus reduced viral yields by a range of 2.2-3.2 log10TCID50, but its over-expression at 12 h post-infection did not inhibit FCV replication. Our results indicate that some FCV strains cannot induce IFN-β expression in vitro, which may be a potential factor for FCV survival in cats. Whether this is important in evading the host interferon response in vivo must be investigated.