scholarly journals Establishment of a Virulent Full-Length cDNA Clone for Type I Feline Coronavirus Strain C3663

2019 ◽  
Vol 93 (21) ◽  
Author(s):  
Yutaka Terada ◽  
Yudai Kuroda ◽  
Shigeru Morikawa ◽  
Yoshiharu Matsuura ◽  
Ken Maeda ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Cell Line ◽  
Reverse Genetics ◽  
Viral Gene ◽  
Cdna Clones ◽  
Type I ◽  
Specific Pathogen Free ◽  
Feline Infectious Peritonitis ◽  
Specific Pathogen ◽  
Feline Coronavirus

ABSTRACT Feline infectious peritonitis (FIP) is one of the most important infectious diseases in cats and is caused by feline coronavirus (FCoV). Tissue culture-adapted type I FCoV shows reduced FIP induction in experimental infections, which complicates the understanding of FIP pathogenesis caused by type I FCoV. We previously found that the type I FCoV strain C3663 efficiently induces FIP in specific-pathogen-free cats through the naturally infectious route. In this study, we employed a bacterial artificial chromosome-based reverse genetics system to gain more insights into FIP caused by the C3633 strain. We successfully generated recombinant virus (rC3663) from Fcwf-4 cells transfected with infectious cDNA that showed growth kinetics similar to those shown by the parental virus. Next, we constructed a reporter C3663 virus carrying the nanoluciferase (Nluc) gene to measure viral replication with high sensitivity. The inhibitory effects of different compounds against rC3663-Nluc could be measured within 24 h postinfection. Furthermore, we found that A72 cells derived from canine fibroblasts permitted FCoV replication without apparent cytopathic effects. Thus, our reporter virus is useful for uncovering the infectivity of type I FCoV in different cell lines, including canine-derived cells. Surprisingly, we uncovered aberrant viral RNA transcription of rC3663 in A72 cells. Overall, we succeeded in obtaining infectious cDNA clones derived from type I FCoV that retained its virulence. Our recombinant FCoVs are powerful tools for increasing our understanding of the viral life cycle and pathogenesis of FIP-inducing type I FCoV. IMPORTANCE Feline coronavirus (FCoV) is one of the most significant coronaviruses, because this virus induces feline infectious peritonitis (FIP), which is a lethal disease in cats. Tissue culture-adapted type I FCoV often loses pathogenicity, which complicates research on type I FCoV-induced feline infectious peritonitis (FIP). Since we previously found that type I FCoV strain C3663 efficiently induces FIP in specific-pathogen-free cats, we established a reverse genetics system for the C3663 strain to obtain recombinant viruses in the present study. By using a reporter C3663 virus, we were able to examine the inhibitory effect of 68 compounds on C3663 replication in Fcwf-4 cells and infectivity in a canine-derived cell line. Interestingly, one canine cell line, A72, permitted FCoV replication but with low efficiency and aberrant viral gene expression.

scholarly journals Antiviral Effects of Hydroxychloroquine and Type I Interferon on In Vitro Fatal Feline Coronavirus Infection

Viruses ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 576 ◽  
Author(s):  
Tomomi Takano ◽  
Kumi Satoh ◽  
Tomoyoshi Doki ◽  
Taishi Tanabe ◽  
Tsutomu Hohdatsu
Keyword(s):  
Viral Infections ◽  
Viral Disease ◽  
High Morbidity ◽  
Type I ◽  
Feline Infectious Peritonitis ◽  
Antiviral Effects ◽  
Immune Mediated ◽  
Coronavirus Infection ◽  
Feline Coronavirus

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.

scholarly journals Genetic diversity and correlation with feline infectious peritonitis of feline coronavirus type I and II: A 5-year study in Taiwan

2009 ◽  
Vol 136 (3-4) ◽  
pp. 233-239 ◽  
Author(s):  
Chao-Nan Lin ◽  
Bi-Ling Su ◽  
Ching-Ho Wang ◽  
Ming-Wei Hsieh ◽  
Ti-Jen Chueh ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Type I ◽  
Feline Infectious Peritonitis ◽  
Feline Coronavirus

A Deletion in the Gene for Transforming Growth Factor β Type I Receptor Abolishes Growth Regulation by Transforming Growth Factor β in a Cutaneous T-Cell Lymphoma

Blood ◽  
1999 ◽  
Vol 94 (8) ◽  
pp. 2854-2861 ◽  
Author(s):  
William P. Schiemann ◽  
Walther M. Pfeifer ◽  
Edi Levi ◽  
Marshall E. Kadin ◽  
Harvey F. Lodish
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Transforming Growth Factor ◽  
Cell Lymphoma ◽  
Transforming Growth Factor Β ◽  
Skin Lesions ◽  
Cdna Clones ◽  
Type I ◽  
Exon 1 ◽  
I Gene

Spontaneous regression of skin lesions is characteristic of lymphomatoid papulosis (LyP), a clonal cutaneous lymphoproliferative disorder. A minority of LyP patients progress to anaplastic large cell lymphoma (ALCL) in which skin lesions no longer regress and extracutaneous dissemination often occurs. In 1 such case, we developed a tumor cell line, JK cells, and show that these cells are resistant to the growth inhibitory effects of transforming growth factor β (TGF-β) due to the loss of cell surface expression of the TGF-β type I receptor (TβR-I). Reverse transcriptase-polymerase chain reaction (RT-PCR) and sequencing of JK cell TβR-I cDNA clones identified a deletion that spanned the last 178 bp of exon 1, including the initiating methionine. Hybridization of a radiolabeled fragment internal to the deletion was detected in the genomes of TGF-β–responsive cells, but not in JK cells, indicating that they contain no wild-type TβR-I gene. PCR primers that flanked the deleted TβR-I region amplified a single band from JK cell genomic DNA that lacked the last 178 bp of exon 1 and all of the ≈ 5 kb of intron 1. This JK cell-specific genomic TβR-I PCR product was distinct from products amplified from TGF-β–responsive cells and was also readily detected in tumor biopsies obtained before the establishment of the JK cell line. Our results identify the first inactivating mutation in TβR-I gene in a human lymphoma that renders it insensitive to growth inhibition by TGF-β.

scholarly journals Feline Coronaviruses Identified in Feline Effusions in Suspected Cases of Feline Infectious Peritonitis

2021 ◽  
Vol 9 (9) ◽  
pp. 1801
Author(s):  
Shih-Jung Yen ◽  
Hui-Wen Chen
Keyword(s):  
Single Infection ◽  
Type I ◽  
Type Ii ◽  
Rt Pcr ◽  
Feline Infectious Peritonitis ◽  
Internal Sequence ◽  
G Ratio ◽  
Feline Coronavirus ◽  
Northern Taiwan ◽  
High Diversity

Ninety-five effusion samples were collected from cats with suspected feline infectious peritonitis in northern Taiwan; these samples showed a 47.4% (45/95) feline coronavirus (FCoV) positivity rate on immunofluorescence staining and RT-PCR. Young cats (≤24 months old) were found to have a significantly higher risk than cats >24 months old (odds ratio (OR) = 6.19, 95% confidence interval (CI) 2.54–16.00). No significant association was found between the positive rates and sex or breed. The A/G ratio in positive cases was significantly lower than the A/G ratio in negative cases. Genotyping and sequencing of the positive cases revealed 71.9% single infection with type I strains and 28.1% coinfection with types I and II. No single infections with type II strains were noted. The type I sequences had high diversity, while the type II sequences had high internal sequence identity and were more similar to CoVs from other species, such as dogs, pigs, and various small mammals. This study demonstrates the latest analysis of FCoV infection cases in northern Taiwan.

scholarly journals Functional Genomics and Immunologic Tools: The Impact of Viral and Host Genetic Variations on the Outcome of Zika Virus Infection

Viruses ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 422 ◽  
Author(s):  
Sang-Im Yun ◽  
Byung-Hak Song ◽  
Jordan Frank ◽  
Justin Julander ◽  
Aaron Olsen ◽  
...  
Keyword(s):  
Cell Line ◽  
Zika Virus ◽  
Genetic Variations ◽  
Productive Infection ◽  
Cdna Clones ◽  
Type I ◽  
Gene Products ◽  
Artificial Chromosomes ◽  
Host Genetic ◽  
The Impact

Zika virus (ZIKV) causes no-to-mild symptoms or severe neurological disorders. To investigate the importance of viral and host genetic variations in determining ZIKV infection outcomes, we created three full-length infectious cDNA clones as bacterial artificial chromosomes for each of three spatiotemporally distinct and genetically divergent ZIKVs: MR-766 (Uganda, 1947), P6-740 (Malaysia, 1966), and PRVABC-59 (Puerto Rico, 2015). Using the three molecularly cloned ZIKVs, together with 13 ZIKV region-specific polyclonal antibodies covering nearly the entire viral protein-coding region, we made three conceptual advances: (i) We created a comprehensive genome-wide portrait of ZIKV gene products and their related species, with several previously undescribed gene products identified in the case of all three molecularly cloned ZIKVs. (ii) We found that ZIKV has a broad cell tropism in vitro, being capable of establishing productive infection in 16 of 17 animal cell lines from 12 different species, although its growth kinetics varied depending on both the specific virus strain and host cell line. More importantly, we identified one ZIKV-non-susceptible bovine cell line that has a block in viral entry but fully supports the subsequent post-entry steps. (iii) We showed that in mice, the three molecularly cloned ZIKVs differ in their neuropathogenicity, depending on the particular combination of viral and host genetic backgrounds, as well as in the presence or absence of type I/II interferon signaling. Overall, our findings demonstrate the impact of viral and host genetic variations on the replication kinetics and neuropathogenicity of ZIKV and provide multiple avenues for developing and testing medical countermeasures against ZIKV.

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