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Abstract
Laboratory cats were infected with a serotype I cat-passaged field strain of FIP virus (FIPV) and peritoneal cells harvested 2–3 weeks later at onset of lymphopenia, fever and serositis. Comparison peritoneal cells were collected from four healthy laboratory cats by peritoneal lavage and macrophages predominated in both populations. Differential mRNA expression analysis identified 5621 genes as deregulated in peritoneal cells from FIPV infected versus normal cats; 956 genes showed > 2.0 Log2 Fold Change (Log2FC) and 1589 genes showed < −2.0 Log2FC. Eighteen significantly upregulated pathways were identified by InnateDB enrichment analysis. These pathways involved apoptosis, cytokine–cytokine receptor interaction, pathogen recognition, Jak-STAT signaling, NK cell mediated cytotoxicity, several chronic infectious diseases, graft versus host disease, allograft rejection and certain autoimmune disorders. Infected peritoneal macrophages were activated M1 type based on pattern of RNA expression. Apoptosis was found to involve large virus-laden peritoneal macrophages more than less mature macrophages, suggesting that macrophage death played a role in virus dissemination. Gene transcripts for MHC I but not II receptors were upregulated, while mRNA for receptors commonly associated with virus attachment and identified in other coronaviruses were either not detected (APN, L-SIGN), not deregulated (DDP-4) or down-regulated (DC-SIGN). However, the mRNA for FcγRIIIA (CD16A/ADCC receptor) was significantly upregulated, supporting entry of virus as an immune complex. Analysis of KEGG associated gene transcripts indicated that Th1 polarization overshadowed Th2 polarization, but the addition of relevant B cell associated genes previously linked to FIP macrophages tended to alter this perception.
Highlights
Macrophages are the main host cell supporting FIP virus (FIPV) replication in vivo [1]
Pathways identified by InnateDB Eighteen pathways were up-regulated in peritoneal cells harvested from the ascites fluid of cats with experimentally-induced FIP by InnateDB analysis at a significance of Padjusted < 0.05 (Table 2)
Most of the genes were those associated with monocytes-macrophages, Th1 cell functions, and apoptosis, mirroring the present findings
Summary
Macrophages are the main host cell supporting FIPV replication in vivo [1]. It is important to study how FIPV infected macrophages respond to infection, because they mediate the resultant immune/inflammatory responses. It appears that virus may spread to distant sites within these cells, as similar appearing infected macrophages dominate in organs such as the brain [2, 3]. Attempts to mimic this infection in vitro have relied heavily on monocyte/. Antibodies to feline coronavirus (FECV or FIPV) enhance virus infection both in vitro [7] and in vivo [8]. The antibodies that mediate macrophage infection have been shown to Watanabe et al Vet Res (2018) 49:81 be the same as those that inhibit FIPV infection in CRFK or Fcwf-4 cell in vitro and enhance the infectivity of FIPV in monocyte/macrophage cultures [9]
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