cord-023053-j061ywrl	2008	In domestic and exotic cats, FIPV is the aetiologic agent of a lethal disease-feline infectious peritonitis (FIP)-characterized by fibrinous serositis, vasculitis, and formation of disseminated pyogranulomas (Wolfe & Griesemer. Laboratory test procedures for detection of coronavirus antibody in feline sera include biological assays such as virus neutralization (VN); non-biological, immunochemical techniques such as indirect immunofluorescence assay (IFA), enzyme-linked immunosorbent assay (ELISA), and kinetics-based ELISA (KELA); and other methods such as agar gel immunodiffusion and passive haemagglutination , though the availability of such tests varies worldwide. The serodiagnostic potential of these assays (i.e., their ability to identify cats with active FIP and/or potential virus carriers/excretors) is thus limited not only by the widespread distribution of serum coronavirus antibody in the feline population, but also by the possibility that non-FIPV coronaviruses may be responsible for some of the seroconversions that they detect.
cord-254291-y8xvh6hs	1998	The sequence of the region located between the S and M glycoprotein genes of the 79-1146 strain of feline infectious peritonitis virus (FIPV) is presented. The inter-structural gene region encodes 3 open reading frames (ORFs), termed ORFs 3a, 3b and 4, with nucleotide sequences conforming to the minimum conserved transcription signal upstream of each. The FIPV interstructural gene region is identical in length when compared to the Insavc-1 strain of canine coronavirus (CCV) but differs from various strains of transmissible gastroenteritis virus (TGEV) by the presence of deletions and insertions. This inter-structural gene region has been examined in the related coronaviruses transmissible gastroenteritis virus (TGEV) and canine coronavirus (CCV) (2±6). The arrangement of the open reading frames (ORFs) in the inter-structural gene region has been described for the FIPV genome (1,7), but detailed sequence has not been presented. The sequence identity between FIPV 79-1146 and the Purdue strain of TGEV in the inter-structural gene region is 90.7%.
cord-255873-18zmvlmk	2014	title: Crystallization and preliminary crystallographic study of Feline infectious peritonitis virus main protease in complex with an inhibitor In this study, the main protease of FIPV in complex with a Michael acceptor-type inhibitor was crystallized. The complex crystals diffracted to 2.5 Å resolution and belonged to space group I422, with unit-cell parameters a = 112.3, b = 112.3, c = 102.1 Å. On the other hand, FIPV efficiently replicates in macrophages/monocytes, leading to feline infectious peritonitis (FIP), a highly lethal systemic granulomatous disease of wild and domestic cats (Addie et al., 2009; Pedersen, 2009; Balint, Farsang, Szeredi et al., 2014; Kipar & Meli, 2014) . Isopropyl -d-1-thiogalactopyranoside was then added to a final concentration of 0.5 mM and the cultures were induced to express FIPV main protease at 289 K for 16 h. A typical diffraction pattern of an FIPV main protease complex crystal collected on beamline BL17U of the Shanghai Synchrotron Radiation Facility (SSRF).
cord-257974-kllqjn68	1988	title: Cultivation techniques for animal coronaviruses: Emphasis on feline infectious peritonitis virus, canine coronavirus, transmissible gastroenteritis virus, and porcine hemagglutinating encephalomyelitis virus Generally these viruses infect epithelial cells of the respiratory tract [human coronavirus (HCV), infectious bronchitis virus (IBV), rat coronavirus (RCV), porcine respiratory coronavirus (PCV)] and epithelial cells of the gastrointestinal tract [bovine coronavirus (BCV), canine eoronavirus (CCV), transmissible gastroenteritis virus {TGEV), turkey coronavirus (TCV), feline enteric coronavirus (FECV), human enteric coronavirus (HECV)]. In addition to CRFK cells, a fetal cat whole fibroblast (FCWF) cell line will support the growth of FIPV, as well as FECV, CCV, and TGEV (28,43t, and corn-Journal of Tissue Culture Methods Vol. 11, No. 2, 1988 parison of antigenic and serologic relatedness of the enteric coronaviruses was done in this cell line ~43). This cell line can be used for primary isolation of virus from clinical specimens and in vitro growth of TGEV It0}.
cord-258374-qht98q0l	2009	title: Neutrophil survival factors (TNF-alpha, GM-CSF, and G-CSF) produced by macrophages in cats infected with feline infectious peritonitis virus contribute to the pathogenesis of granulomatous lesions Furthermore, it was investigated whether macrophages, one of the target cells of FIPV infection, produce neutrophil survival factors (TNF-alpha, GM-CSF, and G-CSF). The neutrophil survival rates were significantly increased in the presence of the culture supernatant of macrophages infected with the mixture of FIPV and MAb 6-4-2 compared to those in the presence of other supernatants (Fig. 5) . When SPF-cat-derived alveolar macrophages were infected with a mixture of FIPV and MAb 6-4-2, the intracellular TNF-alpha, GM-CSF, and G-CSF mRNA levels increased (Fig. 6 ). These cytokine mRNA levels were also elevated in macrophages infected with FIPV and MAb 6-4-2, clarifying the presence of neutrophil survival factors in the macrophage culture supernatant. It was suggested that: (1) FIPV-infected macrophages release TNF-alpha, GM-CSF, and G-CSF in response to virus replication, and (2) these cytokines act on neutrophils and prolong their survival.
cord-258684-lq4knxgf	2020	Hydroxychloroquine (HCQ) is a drug approved by several countries to treat malaria and immune-mediated diseases in humans, and its antiviral effects on other viral infections (e.g., SARS-CoV-2, dengue virus) have been confirmed. Interestingly, the combination of 100 μM of HCQ and 10(4) U/mL of recombinant feline IFN-ω (rfIFN-ω, veterinary registered drug) increased its antiviral activity against type I FIPV infection. As shown in Figure 4 , type I FIPV replication was significantly inhibited by HCQ and rfIFN-ω, and the combination of these drugs strongly decreased the replication of virus. As shown in Figure 4 , type I FIPV replication was significantly inhibited by HCQ and rfIFN-ω, and the combination of these drugs strongly decreased the replication of virus. As shown in Figure 4 , type I FIPV replication was significantly inhibited by HCQ and rfIFN-ω, and the combination of these drugs strongly decreased the replication of virus.
cord-263165-bv4dh9eu	1990	The recent detection of previously unknown coronaviruses or mutants, like the "Porcine Epidemic Diarrhea"-virus (PEDV) and the TGE-like "Porcine Respiratory Coronavirus" (PRCV) on one hand and new knowledge about pathogenetic mechanisms, for example in FIPV-infections, on the other hand are the basis for this review article. For diagnosis TGEV antigen can be detected by immunofluorescence in the small intestine of piglets at an early stage of disease, by virus isolation in tissue culture or by ELISA. As it causes a respiratory infection and does not replicate in the enteric tract, it was named "Respiratory Variant" of TGEV [16] and recently "Porcine respiratory coronavirus". Pedersen [51] assumed that not only the properties of the infecting virus strain were responsible for the outcome of the disease, but that also the immunologic situation of the host and the type and degree of developing immunity may be of great importance. Natural infection with the Porcine Respiratory Coronavirus induces protective lactogenic immunity against Transmissible Gastroenteritis
cord-267014-3vi7pgvr	1992	Abstract The genomic organization at the 3′ end of canine coronavirus (CCV) and feline enteric coronavirus (FECV) was determined by sequence analysis and compared to that of feline infectious peritonitis virus (FIPV) and transmissible gastroenteritis virus (TGEV) of swine. Amplification of cDNA was performed by the polymerase chain reaction (PCR) as described (Kawasaki and Wang, 1989) , after the addition of synthetic oligonucleotide 178, 5''-GATGACACACAGGlTGAG-3'', which is identical to the carboxyl-terminus of the nucleocapsid (N) protein gene of FIPV (nucleotides 1945-l 962; Vennema et a/., 1991) . The nucleotide sequences flanking the ORFs 6a and 6b of FIPV and CCV and ORF 7 of TGEV were aligned to design primers for cDNA synthesis and polymerase chain reaction (PCR) amplification. The recombinant expression products were compared to the proteins produced in CCV-, FECV-, and FIPV-infected cells, which were analyzed similarly (Fig. 6) .
cord-269986-jdcw59r2	2009	Here we show that infection of primary blood-derived feline mononuclear cells by FIPV WSU 79-1146 and FIPV-DF2 leads to rapid activation of the p38 MAPK pathway and that this activation regulates production of the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). FIPV-induced p38 MAPK activation was observed in primary feline blood-derived mononuclear cells individually purified from multiple SPF cats, as was the inhibition of TNF-alpha production by pyridinyl imidazole inhibitors. To determine whether viral replication was required for FIPV-induced p38 MAPK activation, UV-inactivated virus was added to PFBM cells and analyzed by western blot as described above (Fig. 1B) . Overall these data indicate that production of the pro-inflammatory cytokine TNF-alpha in FIPVinfected PFBM cells is regulated by activation of the p38 MAPK pathway. In this study we show that infection by FIPV causes a rapid activation the p38 MAPK pathway in PFBM cells, and that this process directly regulates production of the pro-inflammatory cytokines TNF-alpha and IL-1 beta.
cord-271831-vekok62k	2005	Feline infectious peritonitis virus (FIPV) (Coronaviridae) causes the most lethal viral infection in cats: FIP. In this study, infection kinetics (titres and antigen expression) of FIPV 79-1146, and FECV 79-1683, were determined in peripheral blood monocytes from 3 donor cats and compared to those in Crandell feline kidney (CrFK) cells. Two coronaviruses are described in cats: feline infectious peritonitis virus (FIPV) and feline enteric coronavirus (FECV). Within this population of 19 cats, the monocytes isolated from 9 cats showed a continuous increase in viral antigen positive cells during a 24 hour time span after inoculation with FIPV. Monocytes from 9 cats did not sustain both FIPV and FECV infection since the number of viral antigen positive cells dropped after 6 or 12 hpi (third pattern). In an infection kinetics study where another cell type, feline peritoneal macrophages, was used, different results in the antigen expression kinetics were obtained [29] .
cord-274673-tjzlssal	1989	authors: De Groot, Raoul J.; Van Leen, Robert W.; Dalderup, Mieke J.M.; Vennema, Harry; Horzinek, Marian C.; Spaan, Willy J.M. title: Stably expressed FIPV peplomer protein induces cell fusion and elicits neutralizing antibodies in mice Abstract We have established bovine papilloma virus (BPV)-transformed mouse C127 cell lines that synthesize the peplomer protein of the feline infectious peritonitis virus (FIPV) strain 79-1146. Mice immunized with whole lysates of the transformed cells produced FIPV-neutralizing antibodies as shown by plaque reduction. Mammalian cell lines expressing the FIPV peplomer gene would provide a convenient source of protein to dissect the role of E2 in FIP. It is shown that the expression product induces fusion of FIPV-permissive feline cells and is immunogenic in mice. (b) Glyoxal-denatured RNA extracted from noninduced (lane 2) and heat-shock-induced (lane 3) RM(-)I 7 cells was separated on 0.8% agarose gels, transferred to a nylon membrane, and hybridized to a nick-translated 4.5-kbBamHl fragment containing the complete FIPV E2 gene.
cord-275225-fvq8hezk	2012	The quantitative sg-mRNA detection method revealed more than 10-50,000 times increase of the M gene sg-mRNA in organ materials of feline infectious peritonitis cases, compared to those of the enteric FCoV variants present in the faeces of normal, healthy cats. The quantitative sg-mRNA detection method revealed more than 10-50,000 times increase of the M gene sg-mRNA in organ materials of feline infectious peritonitis cases, compared to those of the enteric FCoV variants present in the faeces of normal, healthy cats. These results indicate the applicability of the new P-sg-QPCR test as a powerful novel tool for the better detection and quantitation of FCoV and for the improved diagnosis of feline infectious peritonitis, this important disease of the Felidae, causing serious losses in the cat populations at a global scale. The detailed analysis of the feline infectious peritonitis positive cat samples by SYBR-Green QPCR method revealed that the following organs harbour FCoV most frequently: lungs 6/6 (100%), liver 6/6 (100%), kidney 10/11 (90.9%), mesenteric lymph node 18/20 (90%), spleen 16/20 (80%) and gut 15/10 (66.7%).
cord-276617-chgjpg0v	2008	The present study shows that: (1) the ratio of peripheral blood sIg(+) CD21(−) B-cells was higher in cats with FIP than in SPF cats, (2) the albumin-to-globulin ratio has negative correlation with the ratio of peripheral blood sIg(+) CD21(−) B-cell, (3) cells strongly expressing mRNA of the plasma cell master gene, B-lymphocyte-induced maturation protein 1 (Blimp-1), were increased in peripheral blood in cats with FIP, (4) mRNA expression of B-cell differentiation/survival factors, IL-6, CD40 ligand, and B-cell-activating factor belonging to the tumor necrosis factor family (BAFF), was enhanced in macrophages in cats with FIP, and (5) mRNAs of these B-cell differentiation/survival factors were overexpressed in antibody-dependent enhancement (ADE)-induced macrophages. We also collected macrophages from FIP cats and measured the expression levels of the viral RNA and mRNA of B-cell differentiation/survival factors: IL-6, CD40 ligand (CD40L), and Bcell-activating factor belonging to the tumor necrosis factor family (BAFF).
cord-280621-tph5n7ak	2016	Shifts in tissue or cell tropism and resulting changes in virulence have also been reported for coronaviruses; porcine respiratory coronavirus causes mild respiratory infection in pigs and presumably arose from transmissible gastroenteritis virus (TGEV), the etiologic agent of gastroenteritis in young pigs with a high fatality, by spontaneous mutations and/or deletions in its genome [9] . Effective treatment intervention for coronavirus infections with an immunopathological component, such as SARS, MERS and FIP, is speculated to involve the judicious use of immunomodulatory agents to enhance protective host immunity and decrease pathological immune responses and antiviral drugs to directly inhibit viral replication. These results on viral titers show that FIPV 3CLpro is a valid target for FIPV antiviral drugs and GC376 can effectively reduce the virus load in the macrophages from the ascites and the omentum of cats with FIP.
cord-283132-rfw8njpo	1993	
cord-283739-p7b4mtbl	2020	We investigated the potential drug-liked compounds and their inhibitory interaction on the 3CL(pro) active sites of CoVs by the structural-bases virtual screening. Evaluation of antiviral activity using cell-based assay showed that NSC629301 and NSC71097 could strongly inhibit the cytopathic effect and also reduced replication of FIPV in CRFK cells in all examined conditions with the low range of EC(50) (6.11 ± 1.90 to 7.75 ± 0.48 μM and 1.99 ± 0.30 to 4.03 ± 0.60 μM, respectively), less than those of ribavirin and lopinavir. According to the FIPV 3CL pro structurral based study, we determined if the candidate 293 compounds that could bind to the active site and inhibited the protease activity still actively 294 Cys144 and His41, the active residues of FIPV 3CL pro , formed the π-alkyl interaction 352 and hydrogen bond to the compounds, respectively.
cord-287157-6rwevq39	2004	authors: Kiss, I.; Poland, A.M.; Pedersen, N.C. title: Disease outcome and cytokine responses in cats immunized with an avirulent feline infectious peritonitis virus (FIPV)-UCD1 and challenge-exposed with virulent FIPV-UCD8 Feline infectious peritonitis (FIP) is a highly fatal disease in Felidae caused by a coronavirus and usually affects cats between 6 months and 3 years of age (reviewed by Pedersen, 1995) . Three of eight vaccinated cats (nos 522, 616, 622) developed effusive FIP within 2 weeks of challengeexposure to FIPV-UCD8, typical of classical nonenhanced disease (Pedersen and Boyle, 1980) ( Table 1) . In this study, two of eight vaccinated cats (nos 524 and 625) appeared immune to challenge-exposure with virulent FIPV-UCD8 and two (nos 623 and 624) developed non-effusive FIP (indicative of partial immunity; Pedersen, 1995) . In the presented preliminary experiment, vaccination of cats with an attenuated live strain of FIPV-UCD1 appeared to induce a degree of protection, in that two of eight cats were immune and two more developed non-effusive FIP post challenge.
cord-290540-r0d6oaez	1999	Special attention is given to the genetic dynamics of the viruses as these now allow us to begin to understand the origin of the different phenotypes, in particular the genesis of virulence during persistent infection. The conclusion from these experiments is that feline coronaviruses may persist in the lower intestinal tract where the virus continues to replicate at low levels. Conceivably, the persisting virus confers to its host resistance against superinfection by the closely related feline coronaviruses, which were infecting the other cats. The idea was that''feline enteric coronaviruses'' are indeed restricted in tropism, while''FIP viruses'' would cross the epithelium, infect macrophages and go systemically. The result of all these studies is that generally there is no protection when an antibody response to the spike protein is induced there is rather an enhancement of the infection, with an''early death'' phenomenon. Detection of feline coronavirus RNA in feces, tissues and body fluids of naturally infected cats by reverse transcriptase PCR
cord-291707-dzmvjh7j	1987	
cord-291858-e0s3o2r4	2016	Feline infectious peritonitis (FIP) belongs to the few animal virus diseases in which, in the course of a generally harmless persistent infection, a virus acquires a small number of mutations that fundamentally change its pathogenicity, invariably resulting in a fatal outcome. We discuss the recent progress in the development of FCoV reverse genetics systems suitable to generate recombinant field viruses containing appropriate mutations for in vivo studies. Deletions of the entire FCoV ORF 3 and 7 genome regions showed that the accessory genes are dispensable for viral growth in vitro; they were suggested to be important for virus replication and virulence in vivo (Haijema et al., 2004) . According to pathogenicity, FCoVs are separated into two biotypes that are generally referred to as feline enteric coronavirus (FECV) and feline infectious peritonitis virus (FIPV). Molecular characterization of feline infectious peritonitis virus strain DF-2 and studies of the role of ORF3abc in viral cell tropism
cord-292570-618bt2vh	2015	Based on bioinformatics analysis, five deregulated genes of the apoptosis cluster were chosen for further analysis; namely, Ras association (RalGDS/AF-6) domain family member 1 (RASSF1), Basic Leucine Zipper Transcriptional Factor ATF-Like 2 (BATF2), Melanoma antigen family B 16 (MAGEB16), Programmed cell death 5 (PDCD5) and TNF receptor-associated factor 2 (TRAF2). Although TNFa did not show significant deregulation at 9 hpi using RNA-seq analysis, the number of related affected genes including significant up regulation of FADD, TRADD, TRAF2, Tumor necrosis factor induced protein 1 and 3 (TNFAIP1 and TNFAIP3) show the importance of analysis of this cytokine during apoptosis mechanism of FIPV. After investigation of the trend of apoptosis and expression change of selected genes from apoptosis cluster, the TNF receptor-associated factor 2 (TRAF2) and programmed cell death-5 (PDCD5) were the only genes that showed significant up regulation from the first hour after infection (Fig. 3) .
cord-292908-rbn3foj3	1991	title: Antigenic analysis of feline coronaviruses with monoclonal antibodies (MAbs): Preparation of MAbs which discriminate between FIPV strain 79-1146 and FECV strain 79-1683 Abstract We prepared 31 monoclonal antibodies (MAbs) against either FIPV strain 79-1146 or FECV strain 79-1683, and tested them for reactivity with various coronaviruses by indirect flourescent antibody assay (IFA). Sixteen MAbs which reacted with all of the 11 strains of feline coronaviruses, also reacted with canine coronavirus (CCV) and transmissible gastroenteritis virus (TGEV). For serological diagnosis of feline infectious peritonitis virus (FIPV) infection, detection of antibody by indirect fluorescent antibody assay (IFA) is popular (Pedersen, 1976b; Horzinek and Osterhaus, 1979; Scott, 1979) . They divided FIPV into Types I and II according to the presence or absence of the induction of FIP, ability of the viruses to proliferate in cell cultures, and the antigenic relationship with porcine and canine coronaviruses.
cord-293565-420thmsr	2012	These viruses occur as 2 pathotypes with an enigmatic, even controversial, relationship: the lowvirulence or nonvirulent feline enteric coronavirus (FECV) and the highly lethal feline infectious peritonitis virus (FIPV). To identify the distinguishing difference(s) between the FCoV pathotypes, we initiated a full genome sequencing program of FECVs found in the feces of apparently healthy cats and of FIPVs found in organs or ascites of cats with pathologically confi rmed feline infectious peritonitis. Thus, we propose that alternative mutations in the S protein of FECV give rise to a tropism change that allows the virus to escape from the intestine into body tissues, where it causes feline infectious peritonitis. Phylogenetic tree based on partial amino acid sequences (aa 1056-1069) of the spike proteins of 118 feline infectious peritonitis viruses (FIPVs) and 183 feline enteric coronaviruses (FECVs) obtained by using reverse transcription nested PCR and sequencing of the distinguishing genomic region.
cord-299342-l8ugjou9	1988	Using gut sections from pigs infected with porcine epidemic diarrhea virus (strain CV 777) and ascitic fluid from cats which had succumbed to feline infectious peritonitis (FIP), a weak cross reaction was found by immunofluorescence. No reaction was found at the nucleocapsid protein position when blots of a mock infected N L F K cell lysate had been incubated with anti-CV 777 antibodies. As shown in figure 3 , results of the RIP confirmed the cross-reaction between pig anti-CV 777 sera and the 43,000 protein of FIPV found in Western blots; the homologous reaction reveals the typical pattern of FIPV structural polypeptides with Mr of 210,000 (peplomer), 45,000 (nucleocapsid) and 25,000 to 32,000 (envelope). We have confirmed the finding of cross reactions within one group, namely between transmissible gastroenteritis virus (TGEV) of swine, FIPV and canine enteric coronavirus, and showed that common determinants are present on all three structural polypeptides [7] .
cord-299904-i5c6nf18	2009	authors: Cornelissen, E.; Dewerchin, H.L.; Van Hamme, E.; Nauwynck, H.J. title: Absence of antibody-dependent, complement-mediated lysis of feline infectious peritonitis virus-infected cells ADCML consists of virus-specific antibodies that bind to cell surface expressed viral proteins which result in complement activation and cell lysis. ADCML consists of virus-specific antibodies that bind to cell surface expressed viral proteins which result in complement activation and cell lysis. Surprisingly, no lysis was observed in the CrFK cells and the monocytes that do show surface-expressed viral proteins, while controls showed that the ADCML assay was functional. Surprisingly, no lysis was observed in the CrFK cells and the monocytes that do show surface-expressed viral proteins, while controls showed that the ADCML assay was functional. Absence of surface expression of feline infectious peritonitis virus (FIPV) antigens on infected cells isolated from cats with FIP Feline infectious peritonitis virus-infected monocytes internalize viral membrane-bound proteins upon antibody addition
cord-299976-36r794ow	2018	
cord-300489-gzcb6uqw	1993	title: Detection of feline infectious peritonitis virus infection in cell cultures and peripheral blood mononuclear leukocytes of experimentally infected cats using a biotinylated cDNA probe Abstract A dot blot hybridization assay, using a biotinylated cDNA probe, was able to detect feline infectious peritonitis virus (FIPV) RNA in Felis catus whole fetus (fcwf-4) cells infected with the FIPV isolates DF2, 79-1146, UCDI, and UCD2. In an in vivo study, the probe was used to detect FIPV RNA in peripheral blood mononuclear leukocytes (PBML) isolated at various post-infection days (PID) from cats experimentally infected with the FIP-producing coronavirus isolate FIPV-79-1146 or FIPV-DF2. In this study, we describe a dot blot hybridization procedure, using a biotinylated recombinant cDNA probe complementary to a major portion of the N protein gene, to detect FIPV in feline cell cultures and PBML isolated from cats infected experimentally with the virulent FIP virus isolate 79-1146 or DF2.
cord-309205-l8vjtrjq	2018	
cord-311625-d7iycdyh	2014	
cord-311982-wkg56xeq	2007	Comparisons of the enteric (jejunum) and non-enteric (liver) derived viral RNA sequences revealed 100% nucleotide identity, a finding that questions the well accepted ''internal mutation theory'' of FIPV pathogenicity. Comparisons of the enteric (jejunum) and non-enteric (liver) derived viral RNA sequences revealed 100% nucleotide identity, a finding that questions the well accepted ''internal mutation theory'' of FIPV pathogenicity. Furthermore, the structural and accessory gene regions of viral RNA isolated from the liver of the same cat (FCoV C1Li) were sequenced and the data derived from the enteric (jejunum) and non-enteric (liver) sources were compared. Sequence data previously generated for the laboratory strain FCoV, FIPV 79-1146, were used to design primers for conventional reverse transcriptase polymerase chain reaction (RT-PCR) amplification of short lengths (100e500 bases) of the field strain RNA. Analysis of the accessory gene 7 region of the FCoV C1Je genome identifies two ORFs, which have translation products sharing high amino acid identity with proteins 7a and 7b of FIPV 79-1146.
cord-312006-c08u4t16	2014	
cord-312247-cza4qsv5	2005	Next, we investigated whether FIPV and fMHV could be targeted to human cancer cells by constructing a bispecific single-chain antibody directed on the one hand against the feline coronavirus spike protein – responsible for receptor binding and subsequent cell entry through virus–cell membrane fusion – and on the other hand against the human epidermal growth factor receptor (EGFR). To investigate whether scFv 23F-425 could serve as an adapter molecule for FIPV and fMHV infection via human EGFR, cultures of human cancer cell lines of different tissue origin with confirmed expression of EGFR ( Figure 4 ) were inoculated with similar amounts of FIPV or fMHV in the presence or absence of the bispecific antibody. Inoculation of Targeting non-human coronaviruses to human cancer cells T Würdinger et al FIPV and fMHV onto a number of different EGFRexpressing human cancer cell lines of various tissue origins in the presence of scFv 23F-425 resulted in infection, replication, and subsequent formation of syncytia.
cord-322629-kv83ekg0	2019	title: Pathogenesis of oral type I feline infectious peritonitis virus (FIPV) infection: Antibody-dependent enhancement infection of cats with type I FIPV via the oral route Feline infectious peritonitis virus (FIPV) causes a severe, immune-mediated disease called FIP in domestic and wild cats. In this study, when cats passively immunized with anti-FIPV-I KU-2 antibodies were orally inoculated with FIPV-I KU-2, FIP was caused at a 50% probability, i.e., FIPV not causing FIP through oral infection caused FIP by inducing antibody-dependent enhancement. Based on the findings of this study, type I FIPV which orally infected cats may cause FIP depending on the condition. In this study, we investigated whether oral inoculation with FIPV-I KU-2 causes FIP in cats passively immunized with anti-FIPV-I KU-2 antibodies. Mutation of neutralizing/antibody-dependent enhancing epitope on spike protein and 7b gene of feline infectious peritonitis virus: influences of viral replication in monocytes/macrophages and virulence in cats
cord-323805-9n63ms3c	2014	The cats were from several studies conducted over the past 5 years, and as a result, some of them had prior exposure to feline enteric coronavirus (FECV) or avirulent FIPVs. The cats were housed under optimized conditions of nutrition, husbandry, and quarantine to eliminate most of the cofactors implicated in FIPV infection outcome and were uniformly challenge exposed to the same field strain of serotype 1 FIPV. The cats were from several studies conducted over the past 5 years, and as a result, some of them had prior exposure to feline enteric coronavirus (FECV) or avirulent FIPVs. The cats were housed under optimized conditions of nutrition, husbandry, and quarantine to eliminate most of the cofactors implicated in FIPV infection outcome and were uniformly challenge exposed to the same field strain of serotype 1 FIPV. Genome-wide association studies (GWAS) on 73 cats that died of FIP after one or more exposures (cases) and 34 cats that survived (controls) demonstrated four significant associations after 100k permutations.
cord-325827-492xi3ee	1988	
cord-329642-5t8yuq4v	2013	Several agents that significantly inhibit FCoV replication in vitro have been identified (Balzarini et al., 2006; Barlough and Shacklett, 1994; Hsieh et al., 2010; Kim et al., 2012; Takano et al., 2008) ; however, whether or not these agents exhibit a therapeutic effect in cats with FIP has not been investigated. The effect of chloroquine on FIPV infection in fcwf-4 cells and SPF cat-derived monocytes was investigated. In monocytes inoculated with a mixture of FIPV and MAb 6-4-2, IL-1b, TNF-a and IL-6 mRNA expression levels were significantly lower in the Pre/Post treatment group than in the None group (Fig. 3B) . The influence of chloroquine on cytokine mRNA and FCoV N gene expressions was investigated in monocytes from cats with FIP. IL-1b, TNF-a, and IL-6 mRNA expression levels of PBMC in FIPV-infected cats treated with chloroquine. In this study, chloroquine significantly inhibited inflammatory cytokine mRNA expression levels in FIPV-infected monocytes.
cord-330554-xg49foch	2012	Cyclosporin A (CsA), an immunosuppressive agent that targets the nuclear factor pathway of activated T-cells (NF-AT) to bind cellular cyclophilins (CyP), dose-dependently inhibited FIPV replication in vitro. Cyclophilin B (CyPB) is another target of CsA that promotes hepatitis C virus (HCV) replication by regulating the RNA-binding ability of the HCV NS5B protein. Here, we show that CsA inhibits intracellular replication of the FIPV genome and viral protein expression in vitro independently of the NF-AT pathway. After adsorption for 1 h at 37°C, the medium containing the virus was removed, and the cells were rinsed three times with phosphate-buffered saline [PBS (−)] and incubated with or without various concentrations of CsA (Sigma-Aldrich), cyclosporin H (CsH; Cosmobio, Tokyo, Japan) and FK506 (Sigma-Aldrich) for 20 h. Quantitative RT-PCR showed that 0.63 -10 μM CsA dose-dependently suppressed FIPV RNA replication, whereas FK506 did not exert significant inhibitory effects, except at 10 μM FK506 (approximately 30 % reduction compared to 0 μM FK506, P < 0.05; Figure 3A ).
cord-333403-imx3990a	1989	The characteristics of a temperature sensitive feline infectious peritonitis virus (TS-FIPV) were examined. Viral structural proteins and RNA were synthesized at 39 °C but some undefined maturational defect prevented the formation of infectious TS-FIPV at its nonpermissive temperature. TS-FIPV proteins in supernatants from cells infected at 31 °C and 39 °C were examined by Western blot. Immune sera from both TS-FIPV vaccinated cats and WT-FIPV challenged cats showed the same differences in the envelope protein of the two viruses as did the monoclonal antibody (data not shown). The culture supernatant from TS-FIPV infected cells was monitored for the appearance of structural proteins at both the permissive and nonpermissive temperatures. All three structural proteins of TS-FIPV were detected in the cells by IFA at both the permissive and nonpermissive temperatures ( Table 2 ). Surface expression of TS-FIPV and WT-FIPV peplomer and envelope proteins but not nucleocapsid at the optimal temperature for each virus resembles the situation in FIPV-infected macrophage-like cells [8] .
cord-336639-jaue41mv	2004	
cord-345863-j01l71dh	2020	
cord-346321-drhiqch0	1994	
cord-348204-365z3qxz	2013	
cord-349800-s9w2yr08	1991	Seven monoclonal antibodies (MAbs) with neutralizing activity against feline infectious peritonitis virus (FIPV) strain 79-1149 (type II) were prepared. The reactivity of these MAbs with 6 viruses classified as FIPV type I (UCD-1, UCD-2, UCD-3, UCD-4, NW-1, and Black), feline enteric coronavirus (FECV) type II strain 79-1683, canine coronavirus (CCV) strain 1-71, and transmissible gastroenteritis virus (TGEV) strains TO-163 and SH was examined by neutralization tests. Feline coronaviruses are divided into FIPV types I and II, and FECV types I and II, on the basis of the disease types, that is, whether it causes feline infectious peritonitis (FIP) or not, the ability of the viruses to proliferate in cell cultures, and the antigenic relationship to TGEV and CCV [17] . These MAbs did not neutralize the 6 FIPV type I viruses, but neutralized FECV strain 79-1683, TGEV strains TO-163 and SH, and CCV strain 1-71, which do not cause feline infectious peritonitis (Table 4) .
cord-349964-38rgcc5h	1978	
cord-351955-9l4786lb	2009	
cord-355051-w18ptl0n	2010	title: Characterization of T helper (Th)1‐ and Th2‐type immune responses caused by baculovirus‐expressed protein derived from the S2 domain of feline infectious peritonitis virus, and exploration of the Th1 and Th2 epitopes in a mouse model In FP-HR2 protein-immunized mice, the concentrations of IFN-γ and IL-2 in the supernatant of splenocytes cultured with or without FIPV antigen were significantly higher than in that of splenocytes derived from wild-type baculovirus-infected SF-9-or PBS-immunized mice (P < 0.05, P < 0.01, respectively). In IH proteinimmunized mice, the concentration of IL-2 in the supernatant of splenocytes cultured with or without FIPV antigen was significantly higher than in that of splenocytes derived from wild-type baculovirus-infected SF-9or PBS-immunized mice (P < 0.05, P < 0.01, respectively). However, in PC protein-immunized mice, the concentrations of IFN-γ and IL-2 in the supernatant of splenocytes cultured with or without FIPV antigen were not significantly higher than in that of splenocytes derived from wild-type baculovirus-infected SF-9-or PBS-immunized mice.
cord-356112-c32icxir	1988	Specific-pathogen-free kittens experimentally infected with feline infectious peritonitis virus (FIPV) subsequently demonstrated increased plasma levels of the arachidonic acid metabolites, leukotriene (LT) B4 and prostaglandin (PG) E2. Loss of fluid and other plasma constituents from inflamed blood vessels, immunologically damaged by complexes of virus, antiviral antibodies and complement (C) proteins (August, 1984; Barlough &Weiss, 1983; Pedersen & Boyle, 1980; Weiss & Scott, 1981~; Jacobse-Geels et al., 1982) or by cytotoxic lymphokines or other enzymatically-active factors released during cellular immune responses (Pedersen, 1985) , may occur in cases of acute FIP. Although vascular lesions, and possibly the pathologic effusions, in FIP are believed to occur via immunological (antibody-mediated) mechanisms (Pedersen, 1985; August, 1984; Weiss & Scott, 1981b; 1981c) , the occurrence of fever and increased plasma levels of LTB4 and PGE2 prior to detectable antibody responses in some FIPV-infected kittens suggest that nonimmunological factors can be involved in some disease manifestations.