Emergence of Pathogenic Coronaviruses in Cats by Homologous Recombination between Feline and Canine Coronaviruses

Terada, Yutaka; Matsui, Nobutaka; Noguchi, Keita; Kuwata, Ryusei; Shimoda, Hiroshi; Soma, Takehisa; Mochizuki, Masahito; Maeda, Ken

doi:10.1371/journal.pone.0106534

Cited by 140 publications

(136 citation statements)

References 58 publications

Supporting

Mentioning

129

Contrasting

Unclassified

Order By: Relevance

“…There is consistent evidence from independent studies that serotype II viruses emerge via double homologous recombination between serotype I FCoV and CCoV Haijema et al, 2007;Herrewegh et al, 1998;Lin et al, 2013;Lorusso et al, 2008;Terada et al, 2014). As a consequence of the recombination, approximately one-third (10 kb) of the serotype I FCoV genome including the S gene and the neighboring regions are replaced with the equivalent parts of the CCoV genome Haijema et al, 2007;Herrewegh et al, 1998;Lin et al, 2013;Lorusso et al, 2008;Terada et al, 2014). Detailed sequence analyses of numerous serotype II FCoVs revealed that the 5 0 -recombination event occurs in the polymerase gene while the 3 0 -recombination site is located in the E or M genes.…”

Section: Fcov Serotypes and Cellular Receptor Usagementioning

confidence: 66%

“…Furthermore, serotype II FCoVs have predominantly been observed in Asia and they were reported to be responsible for up to 25% of the natural infections in those countries (Amer et al, 2012;An et al, 2011;Sharif et al, 2010). There is consistent evidence from independent studies that serotype II viruses emerge via double homologous recombination between serotype I FCoV and CCoV Haijema et al, 2007;Herrewegh et al, 1998;Lin et al, 2013;Lorusso et al, 2008;Terada et al, 2014). As a consequence of the recombination, approximately one-third (10 kb) of the serotype I FCoV genome including the S gene and the neighboring regions are replaced with the equivalent parts of the CCoV genome Haijema et al, 2007;Herrewegh et al, 1998;Lin et al, 2013;Lorusso et al, 2008;Terada et al, 2014).…”

Section: Fcov Serotypes and Cellular Receptor Usagementioning

confidence: 99%

See 1 more Smart Citation

Feline Coronaviruses

Tekes

Thiel

2016

Advances in Virus Research

124

View full text Add to dashboard Cite

Feline infectious peritonitis (FIP) belongs to the few animal virus diseases in which, in the course of a generally harmless persistent infection, a virus acquires a small number of mutations that fundamentally change its pathogenicity, invariably resulting in a fatal outcome. The causative agent of this deadly disease, feline infectious peritonitis virus (FIPV), arises from feline enteric coronavirus (FECV). The review summarizes our current knowledge of the genome and proteome of feline coronaviruses (FCoVs), focusing on the viral surface (spike) protein S and the five accessory proteins. We also review the current classification of FCoVs into distinct serotypes and biotypes, cellular receptors of FCoVs and their presumed role in viral virulence, and discuss other aspects of FIPV-induced pathogenesis. Our current knowledge of genetic differences between FECVs and FIPVs has been mainly based on comparative sequence analyses that revealed "discriminatory" mutations that are present in FIPVs but not in FECVs. Most of these mutations result in amino acid substitutions in the S protein and these may have a critical role in the switch from FECV to FIPV. In most cases, the precise roles of these mutations in the molecular pathogenesis of FIP have not been tested experimentally in the natural host, mainly due to the lack of suitable experimental tools including genetically engineered virus mutants. We discuss the recent progress in the development of FCoV reverse genetics systems suitable to generate recombinant field viruses containing appropriate mutations for in vivo studies.

show abstract

Section: Fcov Serotypes and Cellular Receptor Usagementioning

confidence: 66%

Section: Fcov Serotypes and Cellular Receptor Usagementioning

confidence: 99%

Feline Coronaviruses

Tekes

Thiel

2016

Advances in Virus Research

124

View full text Add to dashboard Cite

show abstract

“…It was suggested that type II FCoV was arisen from a double recombination between type I FCoV and type II CCoV (Herrewegh et al, 1998;Terada et al, 2014). In FCoV-II 79-1146, the genomic region from ORF1b, ORF2 (encoding S protein), and ORF3c is derived from type II CCoV and the other regions are derived from type I FCoV (Herrewegh et al, 1998), suggesting that these genes are factors leading to differences in the virological properties between the FCoV serotypes.…”

Section: Discussionmentioning

confidence: 99%

“…FCoV has been classified into types I and II according to the amino acid sequence of its S protein (Motokawa et al, 1995). Type II FCoV was previously suggested to be from recombination between type I FCoV and type II canine coronavirus (CCoV) (Herrewegh et al, 1998;Terada et al, 2014). Separate from these genotypes/serotypes, FCoV consists of two biotypes: low pathogenic feline enteric coronavirus (FECV: lowvirulent FCoV) and high pathogenic FIP virus (FIPV: virulent FCoV) (Pedersen, 2014).…”

Section: Introductionmentioning

confidence: 99%

The cholesterol transport inhibitor U18666A inhibits type I feline coronavirus infection

et al. 2017

View full text Add to dashboard Cite

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.

show abstract

“…Serotype I viruses dominate in the field and account for up to 95% of FCoV infections (Hohdatsu et al, 1992;Addie et al, 2003), whereas the prevalence of type II FCoVs is much lower. Serotype II FCoVs emerged through homologous recombination between serotype I FCoVs and CCoVs (Herrewegh et al, 1998;Terada et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Characterization of monoclonal antibodies against feline coronavirus accessory protein 7b

Lemmermeyer

Lamp

Schneider

et al. 2016

Veterinary Microbiology

View full text Add to dashboard Cite

Feline coronaviruses (FCoVs) encode five accessory proteins termed 3a, 3b, 3c, 7a and 7b of unknown function. These proteins are dispensable for viral replication in vitro but are supposed to play a role in virulence. In the current study, we produced and characterized 7b-specific monoclonal antibodies (mAbs). A recombinant form of the 7b protein was expressed as a fusion protein in Escherichia coli, purified by immobilized metal affinity chromatography and used as immunogen. Two hybridoma lines, 5B6 and 14D8, were isolated that expressed mAbs that recognized 7b proteins of both FCoV serotypes. Using an extensive set of N- and C-terminally truncated 7b proteins expressed in E. coli and a synthetic peptide, the binding sites of mAbs 5B6 and 14D8 were mapped to an 18-residue region that comprises the only potential N-glycosylation site of the FCoV 7b protein. The two mAbs were suitable to detect a 24-kDa protein, which represents the nonglycosylated form of 7b in FCoV-infected cells. We speculate that glycosylation of 7b is part of the viral evasion strategy to prevent an immune response against this antigenic site.

show abstract

Emergence of Pathogenic Coronaviruses in Cats by Homologous Recombination between Feline and Canine Coronaviruses

Cited by 140 publications

References 58 publications

Feline Coronaviruses

Feline Coronaviruses

The cholesterol transport inhibitor U18666A inhibits type I feline coronavirus infection

Characterization of monoclonal antibodies against feline coronavirus accessory protein 7b

Contact Info

Product

Resources

About