A review of feline infectious peritonitis virus infection: 1963-2008.

doi:10.1016/J.JFMS.2008.09.008

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A review of feline infectious peritonitis virus infection: 1963-2008.

Journal Article•DOI•

A review of feline infectious peritonitis virus infection: 1963-2008.

Niels C Pedersen¹•Institutions (1)

University of California, Davis¹

01 Apr 2009-Journal of Feline Medicine and Surgery (J Feline Med Surg)-Vol. 11, Iss: 4, pp 225-258

TL;DR: F eline infectious peritonitis (FIP) was first described as an ‘important disorder of cats’ by Holzworth in 1963 and a clinico-pathologic conference on this disorder was published in the following year.

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Abstract: F eline infectious peritonitis (FIP) was first described as an ‘important disorder of cats’ by Holzworth in 1963 at the Angell Memorial Animal Hospital, Boston and a clinico-pathologic conference on this disorder was published in the following year. The disease was thought to be infectious but no specific etiologic agent was identified at the time. Wolfe and Griesemer were the first to propose that FIP was caused by a virus. Zook et al observed virus particles in the tissues of experimentally infected cats, but were unable to characterize the agent. Ward recognized the close similarities of FIP virus (FIPV) in tissues to members of the family Coronaviridae. In 1972 Montali and Strandberg were the first to report that FIPV infection could be either granulomatous (dry, parenchymatous) or effusive (wet, non-parenchymatous). The close genetic relationship of FIPV to coronaviruses of dogs and swine was first reported by Pedersen et al in 1978. Fully virulent FIPV was first propagated in vitro in autochthonous macrophage cultures from experimentally infected cats and later in tissue culture. It was also replicated in the epithelium of intestinal ring cultures. A strain of FIPV (FIPV-UCD1) was first propagated in continuously passsaged Felis catus, whole fetus-4 (Fcwf-4) cells and shown to be virulent when inoculated into cats. The Fcwf-4 cells were later found to be of

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Journal Article•DOI•

Host cell proteases: Critical determinants of coronavirus tropism and pathogenesis

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Jean K. Millet¹, Gary R. Whittaker¹•Institutions (1)

Cornell University¹

16 Apr 2015-Virus Research

TL;DR: This review focuses on the diversity of strategies coronaviruses have evolved to proteolytically activate their fusion protein during spike protein biosynthesis and the critical entry step of their life cycle, and highlights important findings on how proteolytic activation of coronavirus spike influences tissue and cell tropism, host range and pathogenicity.

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753 citations

Journal Article•DOI•

Reversal of the Progression of Fatal Coronavirus Infection in Cats by a Broad-Spectrum Coronavirus Protease Inhibitor

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Yunjeong Kim¹, Hongwei Liu², Anushka C. Galasiti Kankanamalage³, Sahani Weerasekara¹, Duy H. Hua¹, William C. Groutas³, Kyeong-Ok Chang¹, Niels C Pedersen² - Show less +4 more•Institutions (3)

Kansas State University¹, University of California, Davis², Wichita State University³

30 Mar 2016-PLOS Pathogens

TL;DR: It is found that antiviral treatment led to full recovery of cats when treatment was started at a stage of disease that would be otherwise fatal if left untreated, and results indicate that continuous virus replication is required for progression of immune-mediated inflammatory disease of FIP.

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Abstract: Coronaviruses infect animals and humans causing a wide range of diseases. The diversity of coronaviruses in many mammalian species is contributed by relatively high mutation and recombination rates during replication. This dynamic nature of coronaviruses may facilitate cross-species transmission and shifts in tissue or cell tropism in a host, resulting in substantial change in virulence. Feline enteric coronavirus (FECV) causes inapparent or mild enteritis in cats, but a highly fatal disease, called feline infectious peritonitis (FIP), can arise through mutation of FECV to FIP virus (FIPV). The pathogenesis of FIP is intimately associated with immune responses and involves depletion of T cells, features shared by some other coronaviruses like Severe Acute Respiratory Syndrome Coronavirus. The increasing risks of highly virulent coronavirus infections in humans or animals call for effective antiviral drugs, but no such measures are yet available. Previously, we have reported the inhibitors that target 3C-like protease (3CLpro) with broad-spectrum activity against important human and animal coronaviruses. Here, we evaluated the therapeutic efficacy of our 3CLpro inhibitor in laboratory cats with FIP. Experimental FIP is 100% fatal once certain clinical and laboratory signs become apparent. We found that antiviral treatment led to full recovery of cats when treatment was started at a stage of disease that would be otherwise fatal if left untreated. Antiviral treatment was associated with a rapid improvement in fever, ascites, lymphopenia and gross signs of illness and cats returned to normal health within 20 days or less of treatment. Significant reduction in viral titers was also observed in cats. These results indicate that continuous virus replication is required for progression of immune-mediated inflammatory disease of FIP. These findings may provide important insights into devising therapeutic strategies and selection of antiviral compounds for further development for important coronaviruses in animals and humans.

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198 citations

Cites background from "A review of feline infectious perit..."

...Seemingly innocuous coronavirus infection can also be turned deadly by changing its tropism, exemplified by mutation of feline enteric coronavirus (FECV) to feline infectious peritonitis virus (FIPV) [10, 11]....
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...Feline infectious peritonitis (FIP) has intrigued researchers for half a century since its first description in the 1960s [10]....
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...FIP is a leading cause of death among young cats under 2 years of age and estimated to kill 1 in 100 to 300 cats worldwide [10, 26]....
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Journal Article•DOI•

Feline Infectious Peritonitis Still an Enigma

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Anja Kipar¹, Anja Kipar², Marina L. Meli²•Institutions (2)

University of Liverpool¹, University of Zurich²

01 Mar 2014-Veterinary Pathology

TL;DR: 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.

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Abstract: 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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177 citations

Cites background from "A review of feline infectious perit..."

...Weber, unpublished data), suggesting that the actual involvement of the eyes is generally underestimated.(136) FIP lesions are occasionally seen at unusual sites, such as the tunica vaginalis in cats with peritonitis, the skin, or the testicle....
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...However, evidence of subclinical or protracted disease over a period of weeks to months has been reported.(136) Also, an experimental longitudinal study demonstrated recurring waves of clinical disease, where fever and weight loss coincided with T-cell depletion and increased viral loads in the blood....
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...FIP, together with panleukopenia and viral infections of the upper respiratory tract, is one of the leading infectious causes of death in cats.(136) However, despite the generally high prevalence of FCoV infection in the cat population, which can exceed 90% in multicat environments, FIP morbidity is low and rarely surpasses 5% of infected cats....
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...Outbreaks are defined by the occurrence of FIP in more than 10% of cats in high-prevalence establishments, but the percentage can be lower in an environment with generally very low FIP prevalence.(41,136,141) In this context, a closer look into an ‘‘artificially induced’’ FIP outbreak that we monitored a number of years ago is of interest....
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...Finally, it is well known that although FECVs are endemic in cat populations, FIP develops only sporadically, providing further strong evidence that FIPVs are generally not transmitted horizontally from cat to cat but emerge de novo in each cat that succumbs to FIP.(136) FCoVs exhibit in vivo genetic diversity, as shown by the frequent occurrence of viral quasispecies both in individual infected animals and in infected cats from the same household....
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Journal Article•DOI•

An update on feline infectious peritonitis: Virology and immunopathogenesis

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Niels C Pedersen¹•Institutions (1)

University of California, Davis¹

01 Aug 2014-Veterinary Journal

TL;DR: After a half century, FIP remains one of the last important infections of cats for which there is no single diagnostic test, no vaccine and no definitive explanations for how virus and host interact to cause disease.

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Abstract: Feline infectious peritonitis (FIP) continues to be one of the most researched infectious diseases of cats. The relatively high mortality of FIP, especially for younger cats from catteries and shelters, should be reason enough to stimulate such intense interest. However, it is the complexity of the disease and the grudging manner in which it yields its secrets that most fascinate researchers. Feline leukemia virus infection was conquered in less than two decades and the mysteries of feline immunodeficiency virus were largely unraveled in several years. After a half century, FIP remains one of the last important infections of cats for which we have no single diagnostic test, no vaccine and no definitive explanations for how virus and host interact to cause disease. How can a ubiquitous and largely non-pathogenic enteric coronavirus transform into a highly lethal pathogen? What are the interactions between host and virus that determine both disease form (wet or dry) and outcome (death or resistance)? Why is it so difficult, and perhaps impossible, to develop a vaccine for FIP? What role do genetics play in disease susceptibility? This review will explore research conducted over the last 5 years that attempts to answer these and other questions. Although much has been learned about FIP in the last 5 years, the ultimate answers remain for yet more studies.

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161 citations

Cites background from "A review of feline infectious perit..."

...Over 100 published articles concerning FIP have appeared in the world’s literature since the last extensive review of the disease (Pedersen, 2009)....
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...macrophages and also contribute to a type III hypersensitivity (antibody-mediated or Arthus-type) vasculitis (Pedersen, 2009)....
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...Our knowledge of the pathogenesis of FIP remains at a very basic level (Pedersen, 2009; Myrrha et al., 2011)....
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...Antibodies enhance the uptake and replication of FIPVs in macrophages and also contribute to a type III hypersensitivity (antibody-mediated or Arthus-type) vasculitis (Pedersen, 2009)....
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...FIP is a relatively new disease of cats and only became clinically significant in the late 1950s (Pedersen, 2009)....
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Journal Article•DOI•

Spike Protein Fusion Peptide and Feline Coronavirus Virulence

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Hui-Wen Chang¹, Herman Egberink¹, Rebecca A. Halpin², David J. Spiro², Peter J. M. Rottier¹ - Show less +1 more•Institutions (2)

Utrecht University¹, J. Craig Venter Institute²

01 Jul 2012-Emerging Infectious Diseases

TL;DR: Mutations can occur erratically and accompany tropism changes, resulting in unpredictable new diseases, and the environment can change rapidly to accommodate these changes.

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Abstract: Coronaviruses are well known for their potential to change their host or tissue tropism, resulting in unpredictable new diseases and changes in pathogenicity; severe acute respiratory syndrome and feline coronaviruses, respectively, are the most recognized examples. Feline coronaviruses occur as 2 pathotypes: nonvirulent feline enteric coronaviruses (FECVs), which replicate in intestinal epithelium cells, and lethal feline infectious peritonitis viruses (FIPVs), which replicate in macrophages. Evidence indicates that FIPV originates from FECV by mutation, but consistent distinguishing differences have not been established. We sequenced the full genome of 11 viruses of each pathotype and then focused on the single most distinctive site by additionally sequencing hundreds of viruses in that region. As a result, we identified 2 alternative amino acid differences in the putative fusion peptide of the spike protein that together distinguish FIPV from FECV in >95% of cases. By these and perhaps other mutations, the virus apparently acquires its macrophage tropism and spreads systemically.

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155 citations

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BASIC and clinical immunology

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Daniel P. Stites, Abba I. Terr

01 Jan 1976

TL;DR: This text and review has been updated and revised since the last edition in 1974 and features include emphasis on normal immunologic function and disease processes.

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Abstract: This text and review has been updated and revised since the last edition in 1974. The normal immunologic function and disease processes are presented clearly. New features include emphasis on normal immunologic function and disease processes; a new immunotherapy section describing drugs and other therapies; an updated immunologic laboratory tests section featuring new methods and techniques; a chapter on molecular genetic techniques for clinical analysis of the immune system; and numerous illustrations. This work is intended for students, physicians and biotechnology professionals.

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Zoo and wild animal medicine

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Murray E. Fowler

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TL;DR: Zoo and wild animal medicine / , Zoo and wildAnimal medicine /, مرکز فناوری اطلاعات و اشاوρزی

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Abstract: Zoo and wild animal medicine / , Zoo and wild animal medicine / , مرکز فناوری اطلاعات و اطلاع رسانی کشاورزی

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In vivo enhancement of dengue virus infection in rhesus monkeys by passively transferred antibody.

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Scott B. Halstead¹•Institutions (1)

University of Hawaii at Manoa¹

01 Oct 1979-The Journal of Infectious Diseases

TL;DR: The demonstration of antibody dependence of dengue virus infection in subhuman primates--a complex, outbred experimental host--supports the hypothesis that the severity of d Dengue in humans is regulated by antibody.

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Abstract: Five pairs of juvenile, dengue virus-susceptible rhesus monkeys were given normal or dengue-immune human cord-blood serum injected intravenously to a final dilution of 1:300. The pool of immune human cord-blood serum had a titer of antibody to dengue type 2 virus (D2V) of 1:140 in the plaque-reduction neutralization test and a titer of human monocyte infection enhancement of greater than 1:2,000,000. Fifteen minutes after inoculation of serum, animals were infected with D2V (strain no. 16681). Daily titers of viremia were always higher in the animals that had received antiserum to D2V than in animals that had received normal cord-blood serum. Ratios of infection enhancement ranged from 2.7 to 51.4. The demonstration of antibody dependence of dengue virus infection in subhuman primates--a complex, outbred experimental host--supports the hypothesis that the severity of dengue in humans is regulated by antibody.

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424 citations

Journal Article•DOI•

Feline Coronavirus Type II Strains 79-1683 and 79-1146 Originate from a Double Recombination between Feline Coronavirus Type I and Canine Coronavirus

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A. A. P. M. Herrewegh¹, Ingrid M.B Smeenk¹, Marian C. Horzinek¹, Peter J. M. Rottier¹, Raoul J. de Groot¹ - Show less +1 more•Institutions (1)

Utrecht University¹

01 May 1998-Journal of Virology

TL;DR: The data show that the type II FCoVs have arisen from double recombination events: additional crossover sites were mapped in the ORF1ab frameshifting region of strain 79-1683 and in the 5′ half of ORF 1b of strains 79-1146.

...read moreread less

Abstract: Recent evidence suggests that the type II feline coronavirus (FCoV) strains 79-1146 and 79-1683 have arisen from a homologous RNA recombination event between FCoV type I and canine coronavirus (CCV). In both cases, the template switch apparently took place between the S and M genes, giving rise to recombinant viruses which encode a CCV-like S protein and the M, N, 7a, and 7b proteins of FCoV type I (K. Motowaka, T. Hohdatsu, H. Hashimoto, and H. Koyama, Microbiol. Immunol. 40:425-433, 1996; H. Vennema, A. Poland, K. Floyd Hawkins, and N. C. Pedersen, Feline Pract. 23:40-44, 1995). In the present study, we have looked for additional FCoV-CCV recombination sites. Four regions in the pol gene were selected for comparative sequence analysis of the type II FCoV strains 79-1683 and 79-1146, the type I FCoV strains TN406 and UCD1, the CCV strain K378, and the TGEV strain Purdue. Our data show that the type II FCoVs have arisen from double recombination events: additional crossover sites were mapped in the ORF1ab frameshifting region of strain 79-1683 and in the 5' half of ORF1b of strain 79-1146.

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361 citations

Journal Article•DOI•

Feline Infectious Peritonitis Viruses Arise by Mutation from Endemic Feline Enteric Coronaviruses

[...]

Harry Vennema¹, Amy Poland¹, Janet E Foley¹, Niels C Pedersen¹•Institutions (1)

University of California, Davis¹

30 Mar 1998-Virology

TL;DR: It was concluded that FIPVs evolved as mutants of FECVs, and the order of descent is from FECV to FIPV.

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349 citations

"A review of feline infectious perit..." refers background in this paper

...Functional mutations in several of the accessory genes, including 3c and 7b, do not appear to prevent replication either in vitro(39) or in vivo.(29,40) There is no evidence that certain strains of FECV are more likely to mutate to FIPVs, but this needs to be more thoroughly studied....
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...The mutation responsible for the FIPV biotype is consistently found in the 3c gene, which encodes a small protein of unknown function (NC Pedersen, UC Davis, 2009, manuscript submitted).(29) The mutations are usually SNPs causing premature stop codons or deletion mutations that negate or significantly truncate the 3c gene product....
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...Damaging mutations within an accessory gene of FECV (ORF 3c) are known to be associated with the FECV / FIPV mutation in cats.(29) The participation of both host and virus factors are important for the development of SARS in a rat model, with increased virulence in old compared to young rats, as in humans....
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