猫冠状 feline coronavirus - PubMed 文献(第 5 页)
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猫冠状 的 PubMed 搜索结果(第 5 页)
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Retargeting of coronavirus by substitution of the spike glycoprotein ectodomain: crossing the host cell species barrier.
Coronaviruses generally have a narrow host range, infecting one or just a few species. Using targeted RNA recombination, we constructed a mutant of the coronavirus mouse hepatitis virus (MHV) in which the ectodomain of the spike glycoprotein (S) was replaced with the highly divergent ectodomain of the S protein of feline infectious peritonitis virus. The resulting chimeric virus, designated fMHV, acquired the ability to infect feline cells and simultaneously lost the ability to infect murine cells in tissue culture. This reciprocal switch of species specificity strongly supports the notion that coronavirus host cell range is determined primarily at the level of interactions between the S protein and the virus receptor. The isolation of fMHV allowed the localization of the region responsible for S protein incorporation into virions to the carboxy-terminal 64 of the 1,324 residues of this protein. This establishes a basis for further definition of elements involved in virion assembly. In addition, fMHV is potentially the ideal recipient virus for carrying out reverse genetics of MHV by targeted RNA recombination, since it presents the possibility of selecting recombinants, no matter how defective, that have regained the ability to replicate in murine cells.
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Genomic organization and expression of the 3' end of the canine and feline enteric coronaviruses.
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. Comparison of the latter two has previously revealed an extra open reading frame (ORF) at the 3' end of the FIPV genome, lacking in TGEV, which is currently designated ORF 6b. Both CCV and FECV possess 6b-related ORFs at the 3' ends of their genomes. The presence of ORF 6b in three of four viruses in this antigenic cluster strongly suggests that TGEV has lost this ORF by deletion. The CCV ORF 6b is collinear with that of FIPV, but the predicted amino acid sequences are only 58% identical. The FECV ORF 6b contains a large deletion compared to that of FIPV, reducing the collinear part to 60%. The sequence homologies were highest between CCV and TGEV on the one hand and between FECV and FIPV on the other. Previously, we showed that the expression product of the FIPV ORF 6b can be detected in infected cells by immunoprecipitation (Vennema et al., 1992). In the present study we have performed similar experiments with CCV and FECV. In infected cells both viruses produced proteins related to but different from the FIPV 6b protein.
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VV116 exerts potent efficacy against feline infectious peritonitis.
Feline infectious peritonitis (FIP) is a fatal disease in cats caused by feline infectious peritonitis virus (FIPV) with no officially approved antiviral therapy. In this study, we evaluated the anti-FIPV potential of VV116 and found that it potently inhibited viral replication in CRFK cells (EC = 1.57 μM). In experimental FIPV-infected cats, VV116 significantly reversed clinicopathological abnormalities, improved survival to 75%, and reduced viral loads in most organs to levels below or at the limit of detection, achieving a greater reduction compared to GS‑441524. Marked histopathological improvement was also observed in both treated groups. Together, these findings support VV116 as a promising oral candidate for the treatment of FIP and warrant further evaluation in veterinary clinical settings.
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Evaluation of the association of Bartonella species, feline herpesvirus 1, feline calicivirus, feline leukemia virus and feline immunodeficiency virus with chronic feline gingivostomatitis.
Gingivostomatitis (GS) is a significant condition in cats because of oral discomfort and associated periodontal disease. Several infectious agents have been associated with the presence of GS, but a causal relationship is unclear. The cats in this study were housed together, had a history of flea exposure, and were vaccinated with a modified live FVRCP product. There were nine cats with active GS and 36 unaffected cats at the time of sample collection. Serum was tested for feline leukemia virus (FeLV) antigen and antibodies against feline immunodeficiency virus, feline calicivirus (FCV), feline herpesvirus 1 (FHV-1), and Bartonella species (enzyme-linked immunosorbent assay and Western blot immunoassay). PCR assays for Bartonella species and FHV-1 and a reverse transcriptase PCR assay for FCV were performed on blood and throat swabs. All cats were negative for FeLV. Assay results failed to correlate to the presence of GS in the group of cats studied.
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Immune mechanisms in the pathogenesis of feline infectious peritonitis in renal tissue: Focus on lymphocytes and cytokines in effusive and non-effusive forms.
Feline infectious peritonitis (FIP) is a fatal systemic disease caused by a virulent biotype of feline coronavirus, characterized by complex and heterogeneous immune responses. This study aimed to comparatively evaluate renal histopathological alterations and immune profiles in effusive and non-effusive forms of FIP, with particular emphasis on cytokine expression, lymphocyte subsets, and apoptosis. Formalin-fixed, paraffin-embedded kidney tissues from 40 cats with immunohistochemically confirmed FIP (20 effusive, 20 non-effusive) were retrospectively analyzed. Renal lesions were semi-quantitatively scored using digital pathology, and immunohistochemistry was performed to assess IL-1, IL-6, TNF-α, CD8, CD19, and Caspase-3 expression. Effusive FIP was characterized by prominent vascular and exudative lesions, accompanied by significantly increased expression of proinflammatory cytokines (IL-1, IL-6, TNF-α) and higher CD19 B-cell immunoreactivity, consistent with a cytokine-driven, humoral-dominant immune response. In contrast, non-effusive FIP exhibited more localized granulomatous inflammation, increased CD8 T-cell infiltration, more pronounced interstitial fibrosis, and significantly higher Caspase-3 immunoreactivity, indicating enhanced apoptotic activity. Correlation analysis demonstrated no consistent positive association between CD8 T-cell density and Caspase-3 expression, suggesting that apoptosis in renal tissue is not solely mediated by cytotoxic T-cell activity. Furthermore, despite elevated TNF-α expression in effusive cases, Caspase-3 immunoreactivity remained relatively low, implying that alternative, potentially caspase-independent mechanisms of cell injury may predominate in this form. Overall, these findings indicate that effusive and non-effusive FIP are associated with distinct patterns of immune polarization and tissue injury rather than representing sequential stages of a uniform pathogenic process. Recognition of these divergent immunopathological profiles may contribute to improved interpretation of FIP lesions and support the development of targeted diagnostic and therapeutic strategies.
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Anti-idiotypic antibodies: biological function and structural studies.
Under a variety of circumstances antibodies can be elicited against the variable region of other antibody molecules (anti-idotypic antibodies, anti-ids). Some of the antibodies are directed against the binding sites of the eliciting antibodies. Of particular interest are the antibodies that recognize epitopes of the original antibody that are in contact with antigen. Antibodies of this kind have been produced and used in a variety of situations including attempts at using them as therapeutic agents. In recent years structural data at the atomic level have emerged for anti-idiotypic antibodies from X-ray diffraction studies. These studies provided structural basis for molecular mimicry of anti-ids. For a large globular antigen (lysozyme), where epitope is noncontinuguous, molecular mimicry is not present at the atomic level. In this case, idiotopes are largely composed of CDR residues, but framework residues are also used. For an epitope that is sequence-specific (anti-FIPV system), molecular mimicry appears to be present as evidenced by the sequence homology between the CDR loops of the anti-id and the epitope of the original antigen. In the case of a small hormone antigen (angiotensin II), an internal image of the eliciting antigen appears to be represented in a single CDR loop of the antiiodiotypic antibody.
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Compound C inhibits the replication of feline coronavirus.
Feline Coronavirus (FCoV) is a viral pathogen of cats and a highly contagious virus. Cats in a cattery can be infected by up to 100%, and even household cats are infected by 20-60%. Some strains of FCoV are known to induce a fatal disease in cats named Feline Infectious Peritonitis (FIP). However, no effective treatments are available. We demonstrated that compound C (dorsomorphin) can potentially inhibit feline coronavirus replication. Compound C treatment decreased the FCoV-induced plaque formation and cytopathic effect in FCoV-infected cells. Compound C treatment also significantly reduced the amount of viral RNA and viral protein in the cells in a dose-dependent manner. Our findings suggest that compound C is potentially useful for feline coronavirus-related diseases.
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[Feline infectious peritonitis - a current overview]. [猫感染性腹膜炎——当前概述]
Coronaviruses (CoVs) are positive, single-stranded RNA viruses that can infect various animal species as well as humans. Particularly relevant for cats is the feline coronavirus (FCoV), which is widespread in cat populations worldwide. Infection with FCoV is usually asymptomatic. However, in multi-cat households, approximately 5-12% of FCoV-infected cats develop feline infectious peritonitis (FIP) due to mutations in the spike gene. FIP is an immune-mediated disease that previously was always fatal. These mutations result in a tropism shift from enterocytes to monocytes and macrophages. The associated change in the virulence of FCoV leads to the characteristic granulomatous vasculitis and perivasculitis observed in FIP. Recently, significant advancements have been made in understanding FIP. Studies show that antiviral drugs used in human medicine, such as the nucleoside analog GS-441524, are effective against FIP and can provide affected cats with a survival chance of up to 100%. Additionally, a novel FCoV variant, FCoV-23, has been identified in cats from Cyprus. According to newest research, this virus arose through a recombination between FCoV and the highly virulent pantropic canine coronavirus; it can be directly transmitted from cat to cat and lead to FIP. Furthermore, increasing evidence suggests that FIP is frequently associated with myocarditis. This article provides an overview of the current knowledge on FIP, including its pathology, clinical signs, effective treatment options, and preventive measures.
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FELINE CORONAVIRUS AND FELINE INFECTIOUS PERITONITIS IN NONDOMESTIC FELID SPECIES. 非家养猫科动物中的猫冠状病毒和猫传染性腹膜炎
Feline coronavirus (FCoV) is reported worldwide and known to cause disease in domestic and nondomestic felid species. Although FCoV often results in mild to inapparent disease, a small subset of cats succumb to the fatal, systemic disease feline infectious peritonitis (FIP). An outbreak of FIP in Cheetahs () in a zoological collection demonstrated the devastating effect of FCoV introduction into a naïve group of animals. In addition to cheetahs, FIP has been described in European wildcats (), a tiger (), a mountain lion (), and lion (). This paper reviews the reported cases of FIP in nondomestic felid species and highlights the surveys of FCoV in populations of nondomestic felids.
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Short Treatment of 42 Days with Oral GS-441524 Results in Equal Efficacy as the Recommended 84-Day Treatment in Cats Suffering from Feline Infectious Peritonitis with Effusion-A Prospective Randomized Controlled Study. 一项前瞻性随机对照研究显示，口服GS-441524 42天的短期治疗与建议的84天治疗猫感染性渗出性腹膜炎的疗效相同
In the past, feline infectious peritonitis (FIP) caused by feline coronavirus (FCoV) was considered fatal. Today, highly efficient drugs, such as GS-441524, can lead to complete remission. The currently recommended treatment duration in the veterinary literature is 84 days. This prospective randomized controlled treatment study aimed to evaluate whether a shorter treatment duration of 42 days with oral GS-441524 obtained from a licensed pharmacy is equally effective compared to the 84-day regimen. Forty cats with FIP with effusion were prospectively included and randomized to receive 15 mg/kg of GS-441524 orally every 24h (q24h), for either 42 or 84 days. Cats were followed for 168 days after treatment initiation. With the exception of two cats that died during the treatment, 38 cats (19 in short, 19 in long treatment group) recovered with rapid improvement of clinical and laboratory parameters as well as a remarkable reduction in viral loads in blood and effusion. Orally administered GS-441524 given as a short treatment was highly effective in curing FIP without causing serious adverse effects. All cats that completed the short treatment course successfully were still in complete remission on day 168. Therefore, a shorter treatment duration of 42 days GS-441524 15 mg/kg can be considered equally effective.