Despite 30 years of vaccination the prevalence of feline calicivirus (FCV) infection remains the same, at 30%. This is due to the high variability of the virus and the high mutation rate of RNA viruses. FCV is a non-enveloped, positive sense RNA virus of the genus Vesivirus. Previously, FCV-5 mutants that are resistant to inactivation by incubation with the fJAM-A soluble receptor were identified. The native FCV-5 virus and capsid mutants underwent an increase in hydrophobicity after incubation with fJAM-A, and it was proposed that this increase in hydrophobicity is due to a conformational change in the viral capsid that is important for membrane association and genome release. The specific mechanism of entry for FCV is not well understood. I produced the resistant capsid mutants in a genomic background expressing the FCV-5 capsid proteins and the FCV-Urbana non-structural proteins. I found that the FCV5Urbana virus was inactivated by incubation with fJAM-A. Capsid mutants of FCV5-Urbana were shown to be resistant to inactivation by fJAM-A when incubated for 30 minutes at 37°C. Preincubation at 4°C for 3 hours let to inactivation of FCV-Urbana and the FCV5-Urbana capsid mutants. These findings suggest that a tectonic effect occurs after pre-incubation of FCV with fJAM-A at 4°C for 3 hours. Further characterization of these mutations and their effect on the virus's ability to retain infectivity after incubation with soluble fJAM-A could further our understanding of infectious entry for FCV. Identifying protein interactions necessary for genome release and association with membranes would provide greater understanding of infectious entry for members of the family Caliciviridae.