scholarly journals Cellular Metabolic Profiling of CrFK Cells Infected with Feline Infectious Peritonitis Virus Using Phenotype Microarrays

Pathogens ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 412 ◽  
Author(s):  
Shing Wei Ng ◽  
Gayathri Thevi Selvarajah ◽  
Yoke Kqueen Cheah ◽  
Farina Mustaffa Kamal ◽  
Abdul Rahman Omar
Keyword(s):  
Metabolic Profiling ◽  
Metabolic Pathways ◽  
Nitrogen Sources ◽  
Cellular Level ◽  
Glutamine Metabolism ◽  
Phenotype Microarray ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Infected Cells

Feline infectious peritonitis (FIP) is a fatal feline immune-mediated disease caused by feline infectious peritonitis virus (FIPV). Little is known about the biological pathways associated in FIP pathogenesis. This is the first study aiming to determine the phenotypic characteristics on the cellular level in relation to specific metabolic pathways of importance to FIP pathogenesis. Methods: The internalization of type II FIPV WSU 79-1146 in Crandell-Rees Feline Kidney (CrFK) cells was visualized using a fluorescence microscope, and optimization prior to phenotype microarray (PM) study was performed. Then, four types of Biolog Phenotype MicroArray™ plates (PM-M1 to PM-M4) precoated with different carbon and nitrogen sources were used to determine the metabolic profiles in FIPV-infected cells. Results: The utilization of palatinose was significantly low in FIPV-infected cells; however, there were significant increases in utilizing melibionic acid, L-glutamine, L-glutamic acid and alanyl-glutamine (Ala-Gln) compared to non-infected cells. Conclusion: This study has provided the first insights into the metabolic profiling of a feline coronavirus infection in vitro using PMs and deduced that glutamine metabolism is one of the essential metabolic pathways for FIPV infection and replication. Further studies are necessary to develop strategies to target the glutamine metabolic pathway in FIPV infection.

scholarly journals In Vivo Antiviral Effects of U18666A Against Type I Feline Infectious Peritonitis Virus

Pathogens ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 67 ◽  
Author(s):  
Tomoyoshi Doki ◽  
Tomoyo Tarusawa ◽  
Tsutomu Hohdatsu ◽  
Tomomi Takano
Keyword(s):  
Clinical Symptoms ◽  
Treated Group ◽  
Control Group ◽  
Type I ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Amphiphilic Drug ◽  
Antiviral Effects

Background: The cationic amphiphilic drug U18666A inhibits the proliferation of type I FIPV in vitro. In this study, we evaluated the in vivo antiviral effects of U18666A by administering it to SPF cats challenged with type I FIPV. Methods: Ten SPF cats were randomly assigned to two experimental groups. FIPV KU-2 were inoculated intraperitoneally to cats. The control group was administered PBS, and the U18666A-treated group was administered U18666A subcutaneously at 2.5 mg/kg on day 0, and 1.25 mg/kg on days 2 and 4 after viral inoculation. Results: Two of the five control cats administered PBS alone developed FIP. Four of the five cats administered U18666A developed no signs of FIP. One cat that temporarily developed fever, had no other clinical symptoms, and no gross lesion was noted on an autopsy after the end of the experiment. The FIPV gene was detected intermittently in feces and saliva regardless of the development of FIP or administration of U18666A. Conclusions: When U18666A was administered to cats experimentally infected with type I FIPV, the development of FIP might be suppressed compared with the control group. However, the number of animals with FIP is too low to establish anti-viral effect of U18666A in cats.

In vitro culture of feline infectious peritonitis virus

1981 ◽  
Vol 108 (25) ◽  
pp. 535-537 ◽  
Author(s):  
L. Hitchcock ◽  
K. O'Reilly ◽  
J. Beesley
Keyword(s):  
In Vitro Culture ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis

scholarly journals Feline infectious peritonitis virus-infected monocytes internalize viral membrane-bound proteins upon antibody addition

2006 ◽  
Vol 87 (6) ◽  
pp. 1685-1690 ◽  
Author(s):  
Hannah L. Dewerchin ◽  
Els Cornelissen ◽  
Hans J. Nauwynck
Keyword(s):  
Viral Proteins ◽  
Cell Type Specificity ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Specific Antibodies ◽  
Humoral Immune ◽  
Dependent Cell ◽  
Infected Cells ◽  
Membrane Bound ◽  
In Cells

Feline infectious peritonitis virus (FIPV) may cause a highly lethal infection in cats, in spite of a usually strong humoral immune response. Antibodies seem unable to identify infected cells and mediate antibody-dependent cell lysis. In this study, the effect of antibodies on Feline coronavirus (FCoV)-infected monocytes was investigated. Upon addition of FCoV-specific antibodies, surface-expressed viral proteins were internalized through a highly efficient process, resulting in cells without visually detectable viral proteins on their plasma membrane. The internalization was also induced by mAbs against the Spike and Membrane proteins, suggesting that both proteins play a role in the process. The internalization did not occur spontaneously, as it was not observed in cells incubated with medium or non-specific antibodies. Further, the internalization could not be reproduced in feline cell lines, indicating its cell-type specificity. This study sheds new light on the immune-evasive nature of FIPV infections.

scholarly journals ORF7-encoded accessory protein 7a of feline infectious peritonitis virus as a counteragent against IFN-α-induced antiviral response

2014 ◽  
Vol 95 (2) ◽  
pp. 393-402 ◽  
Author(s):  
Annelike Dedeurwaerder ◽  
Dominique A. J. Olyslaegers ◽  
Lowiese M. B. Desmarets ◽  
Inge D. M. Roukaerts ◽  
Sebastiaan Theuns ◽  
...  
Keyword(s):  
Antiviral Response ◽  
Replication Capacity ◽  
Type I ◽  
Type I Ifn ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Efficient Replication ◽  
In Trans

The type I IFN-mediated immune response is the first line of antiviral defence. Coronaviruses, like many other viruses, have evolved mechanisms to evade this innate response, ensuring their survival. Several coronavirus accessory genes play a central role in these pathways, but for feline coronaviruses this has never to our knowledge been studied. As it has been demonstrated previously that ORF7 is essential for efficient replication in vitro and virulence in vivo of feline infectious peritonitis virus (FIPV), the role of this ORF in the evasion of the IFN-α antiviral response was investigated. Deletion of ORF7 from FIPV strain 79-1146 (FIPV-Δ7) rendered the virus more susceptible to IFN-α treatment. Given that ORF7 encodes two proteins, 7a and 7b, it was further explored which of these proteins is active in this mechanism. Providing 7a protein in trans rescued the mutant FIPV-Δ7 from IFN sensitivity, which was not achieved by addition of 7b protein. Nevertheless, addition of protein 7a to FIPV-Δ3Δ7, a FIPV mutant deleted in both ORF3 and ORF7, could no longer increase the replication capacity of this mutant in the presence of IFN. These results indicate that FIPV 7a protein is a type I IFN antagonist and protects the virus from the antiviral state induced by IFN, but it needs the presence of ORF3-encoded proteins to exert its antagonistic function.

scholarly journals Addendum: Ng, S.W. et al. Cellular Metabolic Profiling of CrFK Cells Infected with Feline Infectious Peritonitis Virus Using Phenotype Microarrays. Pathogens 2020, 9, 412

Pathogens ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 931
Author(s):  
Shing Wei Ng ◽  
Gayathri Thevi Selvarajah ◽  
Yoke Kqueen Cheah ◽  
Farina Mustaffa Kamal ◽  
Abdul Rahman Omar
Keyword(s):  
Metabolic Profiling ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Phenotype Microarrays ◽  
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