Expression of Feline Infectious Peritonitis (FIP) Coronavirus Antigens on the Surface of Feline Macrophage-Like Cells

Jacobse-Geels, H. E. L.; Horzinek, Marian C.

doi:10.1007/978-1-4615-9373-7_37

Cited by 2 publications

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“…10,28 FCoV infection may increase the synthesis of complement factors in macrophages, and antibody-mediated lysis of infected macrophages in or around vessels may enhance the inflammatory reaction. 10,11,43,45 However, although all these features may well participate in the disease, they seem not to induce the vasculitis in FIP.…”

Section: Discussionmentioning

confidence: 99%

“…7,15 FCoV- 1 Present address: Department of Veterinary Pathology, Faculty of Veterinary Science, University of Liverpool, Liverpool, UK infected circulating monocytes are considered as responsible for viral dissemination within the host. 10,11,28,44 Furthermore, the demonstration of FCoV antigen within intravascular leukocytes and among cells in the lesions of vasculitis in a previous experimental study suggested that the infected monocyte mediates the development of FIP lesions. 44 The degree of macrophage infection and viral replication within infected cells in vitro, however, is associated with the virulence of FCoV strains.…”

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Morphologic Features and Development of Granulomatous Vasculitis in Feline Infectious Peritonitis

et al. 2005

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Abstract. Feline infectious peritonitis (FIP) is a fatal, coronavirus (CoV)-induced systemic disease in cats, characterized by granulomas in organs and granulomatous vasculitis. This study describes the morphologic features of granulomatous vasculitis in FIP as well as its development in the course of monocyte-associated feline CoV (FCoV) viremia in five naturally infected Domestic Shorthair cats with FIP. Monocyte-associated FCoV viremia was demonstrated by immunohistology, RNA in situ hybridization, and electron micropscopy. Granulomatous phlebitis at different stages of development was observed. Vasculitic processes ranged from attachment and emigration of FCoV-infected monocytes to vascular/perivascular granulomatous infiltrates with destruction of the vascular basal lamina. Monocytes as well as perivascular macrophages were activated because they were strongly positive for CD18 and expressed cytokines (tumor necrosis factor-␣ and interleukin-1␤) and matrix metalloproteinase-9. In addition, general activation of endothelial cells, represented by major histocompatibility complex II upregulation, was observed in all cases. These results confirm FIP as a monocyte-triggered systemic disease and demonstrate the central role of activated monocytes in FIP vasculitis.Key words: Cats; feline coronavirus; feline infectious peritonitis; granulomatous vasculitis; monocyte-associated viremia; phlebitis.Feline infectious peritonitis (FIP) is a well-known and widely distributed coronavirus (CoV)-induced systemic disease in cats, characterized by fibrinous to granulomatous serositis with protein-rich effusions in body cavities and granulomatous inflammatory lesions in several organs. 24,45 Not the most obvious finding, but one of its morphologic hallmarks is a granulomatous to necrotizing phlebitis and periphlebitis. 8,16,24,43 Up till now, the pathogenesis of FIP is largely undetermined.Feline CoV (FCoV) is transmitted via the fecal-oral route and primarily infects enterocytes. 28 Despite the generally high prevalence of FCoV infection among the cat population, especially in multicat facilities, FIP morbidity is low and rarely surpasses 5%. 1,7,28 FIP seems to develop in the individual infected animal when FCoV acquires virulence by deletions in open reading frames 3 and 7, coding for nonstructural proteins of unknown function, which occur as mutations primarily during replication in the infected host. 39 Most infected cats develop an FCoV viremia that can be detected by reverse transcriptase-polymerase chain reaction (RT-PCR) on isolated (and cultivated) monocytes regardless of the development of FIP. 7,15 FCoV-1 Present address: Department of Veterinary Pathology, Faculty of Veterinary Science, University of Liverpool, Liverpool, UK infected circulating monocytes are considered as responsible for viral dissemination within the host. 10,11,28,44 Furthermore, the demonstration of FCoV antigen within intravascular leukocytes and among cells in the lesions of vasculitis in a previous experimental study suggested that the inf...

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Section: Discussionmentioning

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Morphologic Features and Development of Granulomatous Vasculitis in Feline Infectious Peritonitis

et al. 2005

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“…128 Subsequently, the macrophage cell line Felis catus whole fetus-4 (Fcwf-4) has predominantly been used for virus propagation. 90,128 In his recent review article, based on more than 40 years of work in the field, Pedersen 136 speculated on the reason for the likely emergence of FIP in the 20th century. He considered as the most relevant potential factors the evolution of the feline CoV (FCoV) alongside CoV of pigs and dogs, the development of virulent FIP virus mutations from enteric FCoV that had only evolved at that stage, and the changes in keeping and especially breeding of cats due to their increasing popularity as pets.…”

Section: Historymentioning

confidence: 99%

Feline Infectious Peritonitis

2014

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Feline infectious peritonitis (FIP) is one of the most important fatal infectious diseases of cats, the pathogenesis of which has not yet been fully revealed. The present review focuses on the biology of feline coronavirus (FCoV) infection and the pathogenesis and pathological features of FIP. Recent studies have revealed functions of many viral proteins, differing receptor specificity for type I and type II FCoV, and genomic differences between feline enteric coronaviruses (FECVs) and FIP viruses (FIPVs). FECV and FIP also exhibit functional differences, since FECVs replicate mainly in intestinal epithelium and are shed in feces, and FIPVs replicate efficiently in monocytes and induce systemic disease. Thus, key events in the pathogenesis of FIP are systemic infection with FIPV, effective and sustainable viral replication in monocytes, and activation of infected monocytes. The host's genetics and immune system also play important roles. It is the activation of monocytes and macrophages that directly leads to the pathologic features of FIP, including vasculitis, body cavity effusions, and fibrinous and granulomatous inflammatory lesions. Advances have been made in the clinical diagnosis of FIP, based on the clinical pathologic findings, serologic testing, and detection of virus using molecular (polymerase chain reaction) or antibody-based methods. Nevertheless, the clinical diagnosis remains challenging in particular in the dry form of FIP, which is partly due to the incomplete understanding of infection biology and pathogenesis in FIP. So, while much progress has been made, many aspects of FIP pathogenesis still remain an enigma.

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Expression of Feline Infectious Peritonitis (FIP) Coronavirus Antigens on the Surface of Feline Macrophage-Like Cells

Abstract: Indications pathogenesis of reported (1,2). predominant if vivo.

Cited by 2 publications

References 2 publications

Morphologic Features and Development of Granulomatous Vasculitis in Feline Infectious Peritonitis

Morphologic Features and Development of Granulomatous Vasculitis in Feline Infectious Peritonitis

Feline Infectious Peritonitis

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