猫冠状 feline coronavirus - PubMed 文献(第 2 页)
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猫冠状 的 PubMed 搜索结果(第 2 页)
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Assembly of spikes into coronavirus particles is mediated by the carboxy-terminal domain of the spike protein. 刺突蛋白装配进入冠状病毒颗粒由刺突蛋白的羧基末端结构域介导
The type I glycoprotein S of coronavirus, trimers of which constitute the typical viral spikes, is assembled into virions through noncovalent interactions with the M protein. Here we demonstrate that incorporation is mediated by the short carboxy-terminal segment comprising the transmembrane and endodomain. To this aim, we used the virus-like particle (VLP) system that we developed earlier for the mouse hepatitis virus strain A59 (MHV-A59) and which we describe now also for the unrelated coronavirus feline infectious peritonitis virus (FIPV; strain 79-1146). Two chimeric MHV-FIPV S proteins were constructed, consisting of the ectodomain of the one virus and the transmembrane and endodomain of the other. These proteins were tested for their incorporation into VLPs of either species. They were found to assemble only into viral particles of the species from which their carboxy-terminal domain originated. Thus, the 64-terminal-residue sequence suffices to draw the 1308 (MHV)- or 1433 (FIPV)-amino-acid-long mature S protein into VLPs. Both chimeric S proteins appeared to cause cell fusion when expressed individually, suggesting that they were biologically fully active. This was indeed confirmed by incorporating one of the proteins into virions which thereby acquired a new host cell tropism, as will be reported elsewhere.
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Concurrent toxoplasmosis and feline infectious peritonitis in a cat. 一例猫同时感染弓形虫病和猫传染性腹膜炎
A 13-year-old, 4-kg, neutered male Maine coon presented with ascites. Toxoplasma gondii tachyzoites were seen within neutrophils and macrophages, and free within the abdominal fluid. At necropsy, many abdominal organs were positive for feline infectious peritonitis (FIP) antigens using immunohistochemical staining. This apparently is the first report of concurrent toxoplasmosis and FIP in a domestic cat.
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Effect of chloroquine on feline infectious peritonitis virus infection in vitro and in vivo. 氯喹对猫传染性腹膜炎病毒体外和体内感染的影响
Feline infectious peritonitis (FIP) is a feline coronavirus-induced fatal disease in domestic and wild cats. Several studies have investigated potential treatments for FIP. However, there have been no reports on agents that have exhibited a therapeutic effect. Recently, chloroquine has been reported to antiviral effect. We investigated whether chloroquine can be used to treat FIP in vitro and in vivo. It was demonstrated that chloroquine has inhibitory effect against the replication of FIPV and anti-inflammatory effect in vitro. In vivo study using cats with experimentally induced FIP, the clinical score of chloroquine-treatment groups were better than in chloroquine-untreated group. However, alanine aminotransferase levels increased in the chloroquine-treated groups. It will be necessary to further investigate the possibility of FIP treatment with a combination of chloroquine and other agents.
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Transcriptional profiling of feline infectious peritonitis virus infection in CRFK cells and in PBMCs from FIP diagnosed cats. CRFK细胞和FIP确诊猫PBMC中猫传染性腹膜炎病毒感染的转录谱分析
Feline Infectious Peritonitis (FIP) is a lethal systemic disease, caused by the FIP Virus (FIPV); a virulent mutant of Feline Enteric Coronavirus (FECV). Currently, the viruses virulence determinants and host gene expressions during FIPV infection are not fully understood. RNA sequencing of Crandell Rees Feline Kidney (CRFK) cells, infected with FIPV strain 79-1146 at 3 hours post infection (h.p.i), were sequenced using the Illumina next generation sequencing approach. Bioinformatic's analysis, based on Felis catus 2X annotated shotgun reference genome, using CLC bio Genome Workbench mapped both control and infected cell reads to 18899 genes out of 19046 annotated genes. Kal's Z test statistical analysis was used to analyse the differentially expressed genes from the infected CRFK cells. Real time RT-qPCR was developed for further transcriptional profiling of three genes (PD-1, PD-L1 and A3H) in infected CRFK cells and Peripheral Blood Mononuclear Cells (PBMCs) from healthy and FIP-diseased cats. Based on Kal's Z-test, with False Discovery Rate (FDR) <0.05 and >1.99 fold change on gene expressions, a total of 61 genes were differentially expressed by both samples, where 44 genes were up-regulated and the remainder were down-regulated. Most genes were closely clustered together, suggesting a homogeneous expression. The majority of the genes that were significantly regulated, were those associated with monocytes-macrophage and Th1 cell functions, and the regulation of apoptosis. Real time RT-qPCR developed focusing on 2 up-regulated genes (PD-L1 and A3H) together with an apoptosis associated gene PD-1 expressions in FIPV infected CRFK cells and in PBMCs from healthy and FIP diagnosed cats produced concordant results with transcriptome data. The possible roles of these genes, and their importance in feline coronaviruses infection, are discussed.
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Treatment of non-effusive feline infectious peritonitis using oral remdesivir or GS-441524: a randomized, double-blind, non-inferiority trial. 口服瑞德西韦或GS-441524治疗非渗出性猫感染性腹膜炎：一项随机、双盲、非劣效性试验
ObjectivesFeline infectious peritonitis (FIP) is a fatal disease caused by feline coronavirus. The nucleoside analog GS-441524, the parent nucleoside of remdesivir, is the most commonly used FIP antiviral. Remdesivir is Food and Drug Administration approved to treat COVID-19 in humans and has been used primarily as an adjunctive treatment for FIP. Data on its efficacy as a first-line oral therapy, as well as its use to treat non-effusive FIP, remain limited. Therefore, this study compares the effectiveness of oral remdesivir vs GS-441524 as a first-line antiviral therapy for cats with non-effusive FIP in a prospective, randomized, double-blind, non-inferiority clinical trial. Furthermore, this study aims to bolster the literature supporting remdesivir use in these cats, anticipating potential future fluctuations in drug cost, availability and legal access.MethodsCats with non-effusive FIP were randomly assigned to receive either oral remdesivir (38-42 mg/kg, n = 10) or oral GS-441524 (18-22 mg/kg, n = 10) q24h for 84 days (12 weeks). Follow-up was conducted at 6 and 16 weeks, and response to therapy, survival and disease-free remission were assessed. Long-term follow-up was also obtained by contacting owners 1.5-2 years after conclusion of the study.ResultsAt week 16, 9/10 (90%) cats treated with remdesivir and 7/10 (70%) cats treated with GS-441524 were alive and in clinical remission. Remdesivir met the statistical criteria for non-inferiority, with a difference in disease-free survival of 20% (90% confidence interval -8.5 to +48.5). All deaths during treatment occurred within the first 11 days of the trial. Long-term follow-up revealed new onset of clinical signs and raised concerns for potential late relapse of disease in four cats (two in each group).Conclusions and relevanceThis study supports the hypothesis that oral remdesivir is non-inferior to GS-441524 for achieving survival and disease-free remission from FIP at 16 weeks. Given evolving global drug access and costs, remdesivir is a viable first-line option.
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Detection of feline coronavirus infection in southern African nondomestic felids. 南部非洲非家养猫科动物中猫冠状病毒感染的检测
Feline coronavirus (FCoV) infects members of the Felidae family with results ranging from seroconversion with no disease to fatal feline infectious peritonitis (FIP). Infection of non-domestic felids with FCoV is of concern, particularly in endangered populations such as cheetahs (Acinonyx jubatus). In this investigation, we tested 342 animals in the Republic of South Africa and Namibia, including 140 animals from wild populations, for evidence of FCoV infection by serology and/or reverse transcription/nested polymerase chain reaction (RT/nPCR) on feces from 1999 through 2001. Past or current infection was evaluated. Of these, 195 animals had evidence of infection and included 41 animals from wild populations. Serology (indirect immunofluorescence) did not always correlate with viral RNA detection, as seronegative animals were occasionally virus-positive, while many seropositive animals were not shedding virus. Serology indicated the infecting virus was most closely related to type I FCoV. Antibody levels in the majority of animals were low, even in those actively infected. Ten of 48 animals tested at more than one time point by RT/nPCR were shedding virus at multiple time points possibly indicating persistent infection. Infection in free-ranging animals was also notable, as over a quarter of the free-ranging animals tested had evidence of current or previous FCoV infection. Testing by serology and RT/nPCR is recommended for screening for FCoV infection.
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Molecular and serological investigation of cat viral infectious diseases in China from 2016 to 2019. 2016至2019年中国猫病毒性传染病的分子和血清学调查
In order to analyse the prevalence of cat viral diseases in China, including feline parvovirus (FPV), feline calicivirus (FCV), feline herpesvirus 1 (FHV-1), feline leukaemia virus (FeLV), feline immunodeficiency virus (FIV) and feline infectious peritonitis virus (FIPV), a total of 1,326 samples of cats from 16 cities were investigated from 2016 to 2019. Collectively, 1,060 (79.9%) cats were tested positive for at least one virus in nucleotide detection, and the positive rates of cat exposure to FeLV, FPV, FHV-1, FCV, FIV and FIPV were 59.6%, 19.2%, 16.3%, 14.2%, 1.5% and 0.5%, respectively. The prevalence of FHV-1 and FPV was dominant in winter and spring. Cats from north China showed a higher positive rate of viral infection than that of cats from south China. The virus infection is not highly correlated with age, except that FPV is prone to occur within the age of 12 months. In the serological survey, the seroprevalences of 267 vaccinated cats to FPV, FCV and FHV-1 were 83.9%, 58.3% and 44.0%, respectively. Meanwhile, the seroprevalences of 39 unvaccinated cats to FPV, FCV and FHV-1 were 76.9% (30/39), 82.4% (28/34) and 58.6% (17/29), respectively. This study demonstrated that a high prevalence of the six viral diseases in China and the insufficient serological potency of FCV and FHV-1 remind the urgency for more effective vaccines.
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Molecular determinants of species specificity in the coronavirus receptor aminopeptidase N (CD13): influence of N-linked glycosylation. 冠状病毒受体氨肽酶N（CD13）种属特异性的分子决定因素：N-连接糖基化的影响
Aminopeptidase N (APN), a 150-kDa metalloprotease also called CD13, serves as a receptor for serologically related coronaviruses of humans (human coronavirus 229E [HCoV-229E]), pigs, and cats. These virus-receptor interactions can be highly species specific; for example, the human coronavirus can use human APN (hAPN) but not porcine APN (pAPN) as its cellular receptor, and porcine coronaviruses can use pAPN but not hAPN. Substitution of pAPN amino acids 283 to 290 into hAPN for the corresponding amino acids 288 to 295 introduced an N-glycosylation sequon at amino acids 291 to 293 that blocked HCoV-229E receptor activity of hAPN. Substitution of two amino acids that inserted an N-glycosylation site at amino acid 291 also resulted in a mutant hAPN that lacked receptor activity because it failed to bind HCoV-229E. Single amino acid revertants that removed this sequon at amino acids 291 to 293 but had one or five pAPN amino acid substitution(s) in this region all regained HCoV-229E binding and receptor activities. To determine if other N-linked glycosylation differences between hAPN, feline APN (fAPN), and pAPN account for receptor specificity of pig and cat coronaviruses, a mutant hAPN protein that, like fAPN and pAPN, lacked a glycosylation sequon at 818 to 820 was studied. This sequon is within the region that determines receptor activity for porcine and feline coronaviruses. Mutant hAPN lacking the sequon at amino acids 818 to 820 maintained HCoV-229E receptor activity but did not gain receptor activity for porcine or feline coronaviruses. Thus, certain differences in glycosylation between coronavirus receptors from different species are critical determinants in the species specificity of infection.
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Upregulation of endothelial cell adhesion molecules characterizes veins close to granulomatous infiltrates in the renal cortex of cats with feline infectious peritonitis and is indirectly triggered by feline infectious peritonitis virus-infected monocytes in vitro. 内皮细胞黏附分子上调是猫传染性腹膜炎肾脏皮质肉芽肿性浸润附近静脉的特征，并由体外猫传染性腹膜炎病毒感染的单核细胞间接触发
One of the most characteristic pathological changes in cats that have succumbed to feline infectious peritonitis (FIP) is a multifocal granulomatous phlebitis. Although it is now well established that leukocyte extravasation elicits the inflammation typically associated with FIP lesions, relatively few studies have aimed at elucidating this key pathogenic event. The upregulation of adhesion molecules on the endothelium is a prerequisite for stable leukocyte-endothelial cell (EC) adhesion that necessarily precedes leukocyte diapedesis. Therefore, the present work focused on the expression of the EC adhesion molecules and possible triggers of EC activation during the development of FIP. Immunofluorescence analysis revealed that the endothelial expression of P-selectin, E-selectin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was elevated in veins close to granulomatous infiltrates in the renal cortex of FIP patients compared to non-infiltrated regions and specimens from healthy cats. Next, we showed that feline venous ECs become activated when exposed to supernatant from feline infectious peritonitis virus (FIPV)-infected monocytes, as indicated by increased adhesion molecule expression. Active viral replication seemed to be required to induce the EC-stimulating activity in monocytes. Finally, adhesion assays revealed an increased adhesion of naive monocytes to ECs treated with supernatant from FIPV-infected monocytes. Taken together, our results strongly indicate that FIPV activates ECs to increase monocyte adhesion by an indirect route, in which proinflammatory factors released from virus-infected monocytes act as key intermediates.
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Role of sialic acids in feline enteric coronavirus infections. 唾液酸在猫肠道冠状病毒感染中的作用
To initiate infections, many coronaviruses use sialic acids, either as receptor determinants or as attachment factors helping the virus find its receptor underneath the heavily glycosylated mucus layer. In the present study, the role of sialic acids in serotype I feline enteric coronavirus (FECV) infections was studied in feline intestinal epithelial cell cultures. Treatment of cells with neuraminidase (NA) enhanced infection efficiency, showing that terminal sialic acid residues on the cell surface were not receptor determinants and even hampered efficient virus-receptor engagement. Knowing that NA treatment of coronaviruses can unmask viral sialic acid binding activity, replication of untreated and NA-treated viruses was compared, showing that NA treatment of the virus enhanced infectivity in untreated cells, but was detrimental in NA-treated cells. By using sialylated compounds as competitive inhibitors, it was demonstrated that sialyllactose (2,6-α-linked over 2,3-α-linked) notably reduced infectivity of NA-treated viruses, whereas bovine submaxillary mucin inhibited both treated and untreated viruses. In desialylated cells, however, viruses were less prone to competitive inhibition with sialylated compounds. In conclusion, this study demonstrated that FECV had a sialic acid binding capacity, which was partially masked by virus-associated sialic acids, and that attachment to sialylated compounds could facilitate enterocyte infections. However, sialic acid binding was not a prerequisite for the initiation of infection and virus-receptor engagement was even more efficient after desialylation of cells, indicating that FECV requires sialidases for efficient enterocyte infections.