The Experts below are selected from a list of 1968 Experts worldwide ranked by ideXlab platform
Stuart G Siddell - One of the best experts on this subject based on the ideXlab platform.
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Amino acid changes in the spike protein of Feline Coronavirus correlate with systemic spread of virus from the intestine and not with Feline infectious peritonitis
Veterinary Research, 2014Co-Authors: Emily Porter, Anja Kipar, Stuart G Siddell, Séverine Tasker, Michael J Day, Ross Harley, Christopher R HelpsAbstract:Recent evidence suggests that a mutation in the spike protein gene of Feline Coronavirus (FCoV), which results in an amino acid change from methionine to leucine at position 1058, may be associated with Feline infectious peritonitis (FIP). Tissue and faecal samples collected post mortem from cats diagnosed with or without FIP were subjected to RNA extraction and quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) to detect FCoV RNA. In cats with FIP, 95% of tissue, and 81% of faecal samples were PCR-positive, as opposed to 22% of tissue, and 60% of faecal samples in cats without FIP. Relative FCoV copy numbers were significantly higher in the cats with FIP, both in tissues ( P
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Genomic RNA sequence of Feline Coronavirus strain FCoV C1Je.
Journal of feline medicine and surgery, 2007Co-Authors: Charlotte Dye, Stuart G SiddellAbstract:This paper reports the first genomic RNA sequence of a field strain Feline Coronavirus (FCoV). Viral RNA was isolated at post mortem from the jejunum and liver of a cat with Feline infectious peritonitis (FIP). A consensus sequence of the jejunum-derived genomic RNA (FCoV C1Je) was determined from overlapping cDNA fragments produced by reverse transcriptase polymerase chain reaction (RT-PCR) amplification. RT-PCR products were sequenced by a reiterative sequencing strategy and the genomic RNA termini were determined using a rapid amplification of cDNA ends PCR strategy. The FCoV C1Je genome was found to be 29,255 nucleotides in length, excluding the poly(A) tail. Comparison of the FCoV C1Je genomic RNA sequence with that of the laboratory strain FCoV FIP virus (FIPV) 79-1146 showed that both viruses have a similar genome organisation and predictions made for the open reading frames and cis-acting elements of the FIPV 79-1146 genome hold true for FCoV C1Je. In addition, the sequence of the 3′-proximal third of the liver derived genomic RNA (FCoV C1Li), which encompasses the structural and accessory protein genes of the virus, was also determined. 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.
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genomic rna sequence of Feline Coronavirus strain fipv wsu 79 1146
Journal of General Virology, 2005Co-Authors: Charlotte Dye, Stuart G SiddellAbstract:A consensus sequence of the Feline Coronavirus (FCoV) (strain FIPV WSU-79/1146) genome was determined from overlapping cDNA fragments produced by RT-PCR amplification of viral RNA. The genome was found to be 29 125 nt in length, excluding the poly(A) tail. Analysis of the sequence identified conserved open reading frames and revealed an overall genome organization similar to that of other Coronaviruses. The genomic RNA was analysed for putative cis-acting elements and the pattern of subgenomic mRNA synthesis was analysed by Northern blotting. Comparative sequence analysis of the predicted FCoV proteins identified 16 replicase proteins (nsp1-nsp16) and four structural proteins (spike, membrane, envelope and nucleocapsid). Two mRNAs encoding putative accessory proteins were also detected. Phylogenetic analyses confirmed that FIPV WSU-79/1146 belongs to the Coronavirus subgroup G1-1. These results confirm and extend previous findings from partial sequence analysis of FCoV genomes.
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Genomic RNA sequence of Feline Coronavirus strain FIPV WSU-79/1146.
The Journal of general virology, 2005Co-Authors: Charlotte Dye, Stuart G SiddellAbstract:A consensus sequence of the Feline Coronavirus (FCoV) (strain FIPV WSU-79/1146) genome was determined from overlapping cDNA fragments produced by RT-PCR amplification of viral RNA. The genome was found to be 29 125 nt in length, excluding the poly(A) tail. Analysis of the sequence identified conserved open reading frames and revealed an overall genome organization similar to that of other Coronaviruses. The genomic RNA was analysed for putative cis-acting elements and the pattern of subgenomic mRNA synthesis was analysed by Northern blotting. Comparative sequence analysis of the predicted FCoV proteins identified 16 replicase proteins (nsp1-nsp16) and four structural proteins (spike, membrane, envelope and nucleocapsid). Two mRNAs encoding putative accessory proteins were also detected. Phylogenetic analyses confirmed that FIPV WSU-79/1146 belongs to the Coronavirus subgroup G1-1. These results confirm and extend previous findings from partial sequence analysis of FCoV genomes.
Takashi Sasaki - One of the best experts on this subject based on the ideXlab platform.
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Feline Coronavirus replication is affected by both cyclophilin a and cyclophilin b
Journal of General Virology, 2017Co-Authors: Yoshikazu Tanaka, Yuka Sato, Takashi SasakiAbstract:Feline Coronavirus (FCoV) causes the fatal disease Feline infectious peritonitis, which is currently incurable by drug treatment, and no effective vaccines are available. Cyclosporin A (CsA), a cyclophilin (Cyp) inhibitor, inhibits the replication of FCoV in vitro and in vivo as well as the replication of human and animal Coronaviruses. However, the mechanism underlying the regulation of Coronavirus replication by CsA is unknown. In this study, we analysed the role of Cyps in FCoV replication using knockdown and knockout cells specific to Cyps. Inhibition of CypA and CypB reduced FCoV replication, with replication in knockout cells being much less than that in knockdown cells. Furthermore, the proteins expressed by CypA and CypB harbouring mutations in their respective predicted peptidyl-prolyl cis–transisomerase active sites, which also alter the affinities between Cyps and CsA, inhibited FCoV replication. These findings indicate that the peptidyl-prolyl cis–transisomerase active sites of Cyps might be required for FCoV replication.
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cellular peptidyl prolyl cis trans isomerase pin1 facilitates replication of Feline Coronavirus
Antiviral Research, 2016Co-Authors: Yoshikazu Tanaka, Arisa Amano, Masateru Morisaki, Yuka Sato, Takashi SasakiAbstract:Although Feline Coronavirus (FCoV) causes Feline infectious peritonitis (FIP), which is a fatal infectious disease, there are no effective therapeutic medicines or vaccines. Previously, in vitro studies have shown that cyclosporin (CsA) and FK506 inhibit virus replication in diverse Coronaviruses. CsA and FK506 are targets of clinically relevant immunosuppressive drugs and bind to cellular cyclophilins (Cyps) or FK506 binding proteins (FKBPs), respectively. Both Cyp and FKBP have peptidyl-prolyl cis-trans isomerase (PPIase) activity. However, protein interacting with NIMA (Pin1), a member of the parvulin subfamily of PPIases that differs from Cyps and FKBPs, is essential for various signaling pathways. Here we demonstrated that genetic silencing or knockout of Pin1 resulted in decreased FCoV replication in vitro. Dipentamethylene thiuram monosulfide, a specific inhibitor of Pin1, inhibited FCoV replication. These data indicate that Pin1 modulates FCoV propagation.
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Cellular peptidyl-prolyl cis/trans isomerase Pin1 facilitates replication of Feline Coronavirus.
Antiviral Research, 2015Co-Authors: Yoshikazu Tanaka, Arisa Amano, Masateru Morisaki, Yuka Sato, Takashi SasakiAbstract:Abstract Although Feline Coronavirus (FCoV) causes Feline infectious peritonitis (FIP), which is a fatal infectious disease, there are no effective therapeutic medicines or vaccines. Previously, in vitro studies have shown that cyclosporin (CsA) and FK506 inhibit virus replication in diverse Coronaviruses. CsA and FK506 are targets of clinically relevant immunosuppressive drugs and bind to cellular cyclophilins (Cyps) or FK506 binding proteins (FKBPs), respectively. Both Cyp and FKBP have peptidyl-prolyl cis-trans isomerase (PPIase) activity. However, protein interacting with NIMA (Pin1), a member of the parvulin subfamily of PPIases that differs from Cyps and FKBPs, is essential for various signaling pathways. Here we demonstrated that genetic silencing or knockout of Pin1 resulted in decreased FCoV replication in vitro . Dipentamethylene thiuram monosulfide, a specific inhibitor of Pin1, inhibited FCoV replication. These data indicate that Pin1 modulates FCoV propagation.
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Molecular epidemiological study of Feline Coronavirus strains in Japan using RT-PCR targeting nsp14 gene
BMC veterinary research, 2015Co-Authors: Yoshikazu Tanaka, Takashi Sasaki, Ryo Matsuda, Yosuke Uematsu, Tomohiro YamaguchiAbstract:Background Feline infectious peritonitis is a fatal disease of cats caused by infection with Feline Coronavirus (FCoV). For detecting or genotyping of FCoV, some RT-PCR plus nested PCR techniques have been reported previously. However, referring to the whole genome sequences (WGSs) registered at NCBI, there are no detection methods that can tolerate the genetic diversity among FCoV population. In addition, the quasispecies nature of FCoV, which consists of heterogeneous variants, has been also demonstrated; thus, a universal method for heteropopulations of FCoV variants in clinical specimens is desirable.
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Suppression of Feline Coronavirus replication in vitro by cyclosporin A
Veterinary research, 2012Co-Authors: Yoshikazu Tanaka, Yuka Sato, Shuichi Osawa, Mai Inoue, Satoka Tanaka, Takashi SasakiAbstract:The Feline infectious peritonitis virus (FIPV) is a member of the Feline Coronavirus family that causes FIP, which is incurable and fatal in cats. 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. FK506 (an immunosuppressor of the pathway that binds cellular FK506-binding protein (FKBP) but not CyP) did not affect FIPV replication. Neither cell growth nor viability changed in the presence of either CsA or FK506, and these factors did not affect the NF-AT pathway in fcwf-4 cells. Therefore, CsA does not seem to exert inhibitory effects via the NF-AT pathway. In conclusion, CsA inhibited FIPV replication in vitro and further studies are needed to verify the practical value of CsA as an anti-FIPV treatment in vivo.
Tsutomu Hohdatsu - One of the best experts on this subject based on the ideXlab platform.
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Antiviral Effects of Hydroxychloroquine and Type I Interferon on In Vitro Fatal Feline Coronavirus Infection.
Viruses, 2020Co-Authors: Tomomi Takano, Tomoyoshi Doki, Kumi Satoh, Taishi Tanabe, Tsutomu HohdatsuAbstract:Feline infectious peritonitis (FIP) is a viral disease with a high morbidity and mortality by the FIP virus (FIPV, virulent Feline Coronavirus). Several antiviral drugs for FIP have been identified, but many of these are expensive and not available in veterinary medicine. 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. We investigated whether HCQ in association with interferon-ω (IFN-ω) is effective for FIPV in vitro. A total of 100 μM of HCQ significantly inhibited the replication of types I and II FIPV. Interestingly, the combination of 100 μM of HCQ and 104 U/mL of recombinant Feline IFN-ω (rfIFN-ω, veterinary registered drug) increased its antiviral activity against type I FIPV infection. Our study suggested that HCQ and rfIFN-ω are applicable for treatment of FIP. Further clinical studies are needed to verify the combination of HCQ and rIFN-ω will be effective and safe treatment for cats with FIP.
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Nanoparticulate vacuolar ATPase blocker exhibits potent host-targeted antiviral activity against Feline Coronavirus
Scientific Reports, 2017Co-Authors: Che-ming Jack Hu, You-ting Chen, Hsiao-han Tsai, Wei-shan Chang, Zih-syun Fang, Tomomi Takano, Tsutomu Hohdatsu, Ling-ling Chueh, Wen-lin Wang, Hui-wen ChenAbstract:Feline infectious peritonitis (FIP), caused by a mutated Feline Coronavirus, is one of the most serious and fatal viral diseases in cats. The disease remains incurable, and there is no effective vaccine available. In light of the pathogenic mechanism of Feline Coronavirus that relies on endosomal acidification for cytoplasmic entry, a novel vacuolar ATPase blocker, diphyllin, and its nanoformulation are herein investigated for their antiviral activity against the type II Feline infectious peritonitis virus (FIPV). Experimental results show that diphyllin dose-dependently inhibits endosomal acidification in fcwf-4 cells, alters the cellular susceptibility to FIPV, and inhibits the downstream virus replication. In addition, diphyllin delivered by polymeric nanoparticles consisting of poly(ethylene glycol)-block-poly(lactide-co-glycolide) (PEG-PLGA) further demonstrates an improved safety profile and enhanced inhibitory activity against FIPV. In an in vitro model of antibody-dependent enhancement of FIPV infection, diphyllin nanoparticles showed a prominent antiviral effect against the Feline Coronavirus. In addition, the diphyllin nanoparticles were well tolerated in mice following high-dose intravenous administration. This study highlights the therapeutic potential of diphyllin and its nanoformulation for the treatment of FIP.
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The cholesterol transport inhibitor U18666A inhibits type I Feline Coronavirus infection.
Antiviral research, 2017Co-Authors: Tomomi Takano, Misaki Endoh, Hiroaki Fukatsu, Haruko Sakurada, Tomoyoshi Doki, Tsutomu HohdatsuAbstract:Feline infectious peritonitis (FIP) is a Feline Coronavirus (FCoV)-induced fatal disease in wild and domestic cats. FCoV exists in two serotypes. Type I FCoV is the dominant serotype worldwide. Therefore, it is necessary to develop antiviral drugs against type I FCoV infection. We previously reported that type I FCoV is closely associated with cholesterol throughout the viral life cycle. In this study, we investigated whether U18666A, the cholesterol synthesis and transport inhibitor, shows antiviral effects against type I FCoV. U18666A induced cholesterol accumulation in cells and inhibited type I FCoV replication. Surprisingly, the antiviral activity of U18666A was suppressed by the histone deacetylase inhibitor (HDACi), Vorinostat. HDACi has been reported to revert U18666A-induced dysfunction of Niemann-Pick C1 (NPC1). In conclusion, these findings demonstrate that NPC1 plays an important role in type I FCoV infection. U18666A or other cholesterol transport inhibitor may be considered as the antiviral drug for the treatment of cats with FIP.
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Differential effect of cholesterol on type I and II Feline Coronavirus infection
Archives of Virology, 2016Co-Authors: Tomomi Takano, Tomoyoshi Doki, Yui Satomi, Yuu Oyama, Tsutomu HohdatsuAbstract:Feline infectious peritonitis (FIP) is a fatal disease of domestic and wild felidae that is caused by Feline Coronavirus (FCoV). FCoV has been classified into types I and II. Since type I FCoV infection is dominant in the field, it is necessary to develop antiviral agents and vaccines against type I FCoV infection. However, few studies have been conducted on type I FCoV. Here, we compare the effects of cholesterol on types I and II FCoV infections. When cells were treated methyl-β-cyclodextrin (MβCD) and inoculated with type I FCoV, the infection rate decreased significantly, and the addition of exogenous cholesterol to MβCD-treated cells resulted in the recovery of the infectivity of type I FCoV. Furthermore, exogenous cholesterol increased the infectivity of type I FCoV. In contrast, the addition of MβCD and exogenous cholesterol had little effect on the efficiency of type II FCoV infection. These results strongly suggest that the dependence of infection by types I and II FCoV on cholesterol differs.
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Serological diagnosis of Feline Coronavirus infection by immunochromatographic test.
Methods in molecular biology (Clifton N.J.), 2015Co-Authors: Tomomi Takano, Tsutomu HohdatsuAbstract:The immunochromatographic assay (ICA) is a simple antibody-antigen detection method, the results of which can be rapidly obtained at a low cost. We designed an ICA to detect anti-Feline Coronavirus (FCoV) antibodies. A colloidal gold-labeled recombinant FCoV nucleocapsid protein (rNP) is used as a conjugate. The Protein A and affinity-purified cat anti-FCoV IgG are blotted on the test line and the control line, respectively, of the nitrocellulose membrane. The specific detection of anti-FCoV antibodies was possible in all heparin-anticoagulated plasma, serum, whole blood, and ascitic fluid samples from anti-FCoV antibody positive cats, and nonspecific reaction was not noted in samples from anti-FCoV antibody negative cats.
Yoshikazu Tanaka - One of the best experts on this subject based on the ideXlab platform.
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Feline Coronavirus replication is affected by both cyclophilin a and cyclophilin b
Journal of General Virology, 2017Co-Authors: Yoshikazu Tanaka, Yuka Sato, Takashi SasakiAbstract:Feline Coronavirus (FCoV) causes the fatal disease Feline infectious peritonitis, which is currently incurable by drug treatment, and no effective vaccines are available. Cyclosporin A (CsA), a cyclophilin (Cyp) inhibitor, inhibits the replication of FCoV in vitro and in vivo as well as the replication of human and animal Coronaviruses. However, the mechanism underlying the regulation of Coronavirus replication by CsA is unknown. In this study, we analysed the role of Cyps in FCoV replication using knockdown and knockout cells specific to Cyps. Inhibition of CypA and CypB reduced FCoV replication, with replication in knockout cells being much less than that in knockdown cells. Furthermore, the proteins expressed by CypA and CypB harbouring mutations in their respective predicted peptidyl-prolyl cis–transisomerase active sites, which also alter the affinities between Cyps and CsA, inhibited FCoV replication. These findings indicate that the peptidyl-prolyl cis–transisomerase active sites of Cyps might be required for FCoV replication.
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cellular peptidyl prolyl cis trans isomerase pin1 facilitates replication of Feline Coronavirus
Antiviral Research, 2016Co-Authors: Yoshikazu Tanaka, Arisa Amano, Masateru Morisaki, Yuka Sato, Takashi SasakiAbstract:Although Feline Coronavirus (FCoV) causes Feline infectious peritonitis (FIP), which is a fatal infectious disease, there are no effective therapeutic medicines or vaccines. Previously, in vitro studies have shown that cyclosporin (CsA) and FK506 inhibit virus replication in diverse Coronaviruses. CsA and FK506 are targets of clinically relevant immunosuppressive drugs and bind to cellular cyclophilins (Cyps) or FK506 binding proteins (FKBPs), respectively. Both Cyp and FKBP have peptidyl-prolyl cis-trans isomerase (PPIase) activity. However, protein interacting with NIMA (Pin1), a member of the parvulin subfamily of PPIases that differs from Cyps and FKBPs, is essential for various signaling pathways. Here we demonstrated that genetic silencing or knockout of Pin1 resulted in decreased FCoV replication in vitro. Dipentamethylene thiuram monosulfide, a specific inhibitor of Pin1, inhibited FCoV replication. These data indicate that Pin1 modulates FCoV propagation.
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Cellular peptidyl-prolyl cis/trans isomerase Pin1 facilitates replication of Feline Coronavirus.
Antiviral Research, 2015Co-Authors: Yoshikazu Tanaka, Arisa Amano, Masateru Morisaki, Yuka Sato, Takashi SasakiAbstract:Abstract Although Feline Coronavirus (FCoV) causes Feline infectious peritonitis (FIP), which is a fatal infectious disease, there are no effective therapeutic medicines or vaccines. Previously, in vitro studies have shown that cyclosporin (CsA) and FK506 inhibit virus replication in diverse Coronaviruses. CsA and FK506 are targets of clinically relevant immunosuppressive drugs and bind to cellular cyclophilins (Cyps) or FK506 binding proteins (FKBPs), respectively. Both Cyp and FKBP have peptidyl-prolyl cis-trans isomerase (PPIase) activity. However, protein interacting with NIMA (Pin1), a member of the parvulin subfamily of PPIases that differs from Cyps and FKBPs, is essential for various signaling pathways. Here we demonstrated that genetic silencing or knockout of Pin1 resulted in decreased FCoV replication in vitro . Dipentamethylene thiuram monosulfide, a specific inhibitor of Pin1, inhibited FCoV replication. These data indicate that Pin1 modulates FCoV propagation.
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Molecular epidemiological study of Feline Coronavirus strains in Japan using RT-PCR targeting nsp14 gene
BMC veterinary research, 2015Co-Authors: Yoshikazu Tanaka, Takashi Sasaki, Ryo Matsuda, Yosuke Uematsu, Tomohiro YamaguchiAbstract:Background Feline infectious peritonitis is a fatal disease of cats caused by infection with Feline Coronavirus (FCoV). For detecting or genotyping of FCoV, some RT-PCR plus nested PCR techniques have been reported previously. However, referring to the whole genome sequences (WGSs) registered at NCBI, there are no detection methods that can tolerate the genetic diversity among FCoV population. In addition, the quasispecies nature of FCoV, which consists of heterogeneous variants, has been also demonstrated; thus, a universal method for heteropopulations of FCoV variants in clinical specimens is desirable.
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Suppression of Feline Coronavirus replication in vitro by cyclosporin A
Veterinary research, 2012Co-Authors: Yoshikazu Tanaka, Yuka Sato, Shuichi Osawa, Mai Inoue, Satoka Tanaka, Takashi SasakiAbstract:The Feline infectious peritonitis virus (FIPV) is a member of the Feline Coronavirus family that causes FIP, which is incurable and fatal in cats. 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. FK506 (an immunosuppressor of the pathway that binds cellular FK506-binding protein (FKBP) but not CyP) did not affect FIPV replication. Neither cell growth nor viability changed in the presence of either CsA or FK506, and these factors did not affect the NF-AT pathway in fcwf-4 cells. Therefore, CsA does not seem to exert inhibitory effects via the NF-AT pathway. In conclusion, CsA inhibited FIPV replication in vitro and further studies are needed to verify the practical value of CsA as an anti-FIPV treatment in vivo.
Charlotte Dye - One of the best experts on this subject based on the ideXlab platform.
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Genomic RNA sequence of Feline Coronavirus strain FCoV C1Je.
Journal of feline medicine and surgery, 2007Co-Authors: Charlotte Dye, Stuart G SiddellAbstract:This paper reports the first genomic RNA sequence of a field strain Feline Coronavirus (FCoV). Viral RNA was isolated at post mortem from the jejunum and liver of a cat with Feline infectious peritonitis (FIP). A consensus sequence of the jejunum-derived genomic RNA (FCoV C1Je) was determined from overlapping cDNA fragments produced by reverse transcriptase polymerase chain reaction (RT-PCR) amplification. RT-PCR products were sequenced by a reiterative sequencing strategy and the genomic RNA termini were determined using a rapid amplification of cDNA ends PCR strategy. The FCoV C1Je genome was found to be 29,255 nucleotides in length, excluding the poly(A) tail. Comparison of the FCoV C1Je genomic RNA sequence with that of the laboratory strain FCoV FIP virus (FIPV) 79-1146 showed that both viruses have a similar genome organisation and predictions made for the open reading frames and cis-acting elements of the FIPV 79-1146 genome hold true for FCoV C1Je. In addition, the sequence of the 3′-proximal third of the liver derived genomic RNA (FCoV C1Li), which encompasses the structural and accessory protein genes of the virus, was also determined. 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.
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genomic rna sequence of Feline Coronavirus strain fipv wsu 79 1146
Journal of General Virology, 2005Co-Authors: Charlotte Dye, Stuart G SiddellAbstract:A consensus sequence of the Feline Coronavirus (FCoV) (strain FIPV WSU-79/1146) genome was determined from overlapping cDNA fragments produced by RT-PCR amplification of viral RNA. The genome was found to be 29 125 nt in length, excluding the poly(A) tail. Analysis of the sequence identified conserved open reading frames and revealed an overall genome organization similar to that of other Coronaviruses. The genomic RNA was analysed for putative cis-acting elements and the pattern of subgenomic mRNA synthesis was analysed by Northern blotting. Comparative sequence analysis of the predicted FCoV proteins identified 16 replicase proteins (nsp1-nsp16) and four structural proteins (spike, membrane, envelope and nucleocapsid). Two mRNAs encoding putative accessory proteins were also detected. Phylogenetic analyses confirmed that FIPV WSU-79/1146 belongs to the Coronavirus subgroup G1-1. These results confirm and extend previous findings from partial sequence analysis of FCoV genomes.
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Genomic RNA sequence of Feline Coronavirus strain FIPV WSU-79/1146.
The Journal of general virology, 2005Co-Authors: Charlotte Dye, Stuart G SiddellAbstract:A consensus sequence of the Feline Coronavirus (FCoV) (strain FIPV WSU-79/1146) genome was determined from overlapping cDNA fragments produced by RT-PCR amplification of viral RNA. The genome was found to be 29 125 nt in length, excluding the poly(A) tail. Analysis of the sequence identified conserved open reading frames and revealed an overall genome organization similar to that of other Coronaviruses. The genomic RNA was analysed for putative cis-acting elements and the pattern of subgenomic mRNA synthesis was analysed by Northern blotting. Comparative sequence analysis of the predicted FCoV proteins identified 16 replicase proteins (nsp1-nsp16) and four structural proteins (spike, membrane, envelope and nucleocapsid). Two mRNAs encoding putative accessory proteins were also detected. Phylogenetic analyses confirmed that FIPV WSU-79/1146 belongs to the Coronavirus subgroup G1-1. These results confirm and extend previous findings from partial sequence analysis of FCoV genomes.
