FCoV Viral Sequences of Systemically Infected Healthy Cats Lack Gene Mutations Previously Linked to the Development of FIP
Mirjam Lutz,
Aline R. Steiner,
Valentino Cattori,
Regina Hofmann-Lehmann,
Hans Lutz,
Anja Kipar,
Marina L. Meli
Affiliations
Mirjam Lutz
Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Aline R. Steiner
Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Valentino Cattori
Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Regina Hofmann-Lehmann
Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Hans Lutz
Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Anja Kipar
Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Marina L. Meli
Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland
Feline Infectious Peritonitis (FIP)—the deadliest infectious disease of young cats in shelters or catteries—is induced by highly virulent feline coronaviruses (FCoVs) emerging in infected hosts after mutations of less virulent FCoVs. Previous studies have shown that some mutations in the open reading frames (ORF) 3c and 7b and the spike (S) gene have implications for the development of FIP, but mainly indirectly, likely also due to their association with systemic spread. The aim of the present study was to determine whether FCoV detected in organs of experimentally FCoV infected healthy cats carry some of these mutations. Viral RNA isolated from different tissues of seven asymptomatic cats infected with the field strains FCoV Zu1 or FCoV Zu3 was sequenced. Deletions in the 3c gene and mutations in the 7b and S genes that have been shown to have implications for the development of FIP were not detected, suggesting that these are not essential for systemic viral dissemination. However, deletions and single nucleotide polymorphisms leading to truncations were detected in all nonstructural proteins. These were found across all analyzed ORFs, but with significantly higher frequency in ORF 7b than ORF 3a. Additionally, a previously unknown homologous recombination site was detected in FCoV Zu1.
