Genetic diversity and phylogenetic analysis of Feline Coronavirus sequences from Portugal

Duarte, Ana M.; Veiga, Inês Berenguer; Tavares, Luís

doi:10.1016/j.vetmic.2009.03.009

Cited by 19 publications

(19 citation statements)

References 14 publications

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“…These viral sequences were further analyzed using a heteroduplex mobility assay, which detected quasi-species in 17% of samples. Phylogenetic analysis of type I sequences revealed high genetic diversity among Portuguese and previously characterized strains, while the tree for type II strains had higher genetic homogeneity than the tree for type I strains (Duarte et al, 2009).…”

Section: Viral Replicationmentioning

confidence: 80%

“…The proportion of types I and II FECVs, and therefore types I and II FIPVs, varies across the world, although type I strains predominate. Duarte et al (2009) studied the distribution of types I and II FIPVs in a Portuguese cat population using a reverse transcriptase (RT)-PCR assay that amplified the 3' end of the genome encompassing the region of feline/canine coronavirus S gene recombination. In cats with FIP, type I coronavirus was present in 79% and type II coronavirus in 3.5%, whereas the remaining 17.5% could not be typed.…”

Section: Viral Replicationmentioning

confidence: 99%

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An update on feline infectious peritonitis: Virology and immunopathogenesis

Pedersen

2014

The Veterinary Journal

185

264

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Feline infectious peritonitis (FIP) continues to be one of the most researched infectious diseases of cats. The relatively high mortality of FIP, especially for younger cats from catteries and shelters, should be reason enough to stimulate such intense interest. However, it is the complexity of the disease and the grudging manner in which it yields its secrets that most fascinate researchers. Feline leukemia virus infection was conquered in less than two decades and the mysteries of feline immunodeficiency virus were largely unraveled in several years. After a half century, FIP remains one of the last important infections of cats for which we have no single diagnostic test, no vaccine and no definitive explanations for how virus and host interact to cause disease. How can a ubiquitous and largely non-pathogenic enteric coronavirus transform into a highly lethal pathogen? What are the interactions between host and virus that determine both disease form (wet or dry) and outcome (death or resistance)? Why is it so difficult, and perhaps impossible, to develop a vaccine for FIP? What role do genetics play in disease susceptibility? This review will explore research conducted over the last 5 years that attempts to answer these and other questions. Although much has been learned about FIP in the last 5 years, the ultimate answers remain for yet more studies.

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Section: Viral Replicationmentioning

confidence: 80%

Section: Viral Replicationmentioning

confidence: 99%

An update on feline infectious peritonitis: Virology and immunopathogenesis

Pedersen

2014

The Veterinary Journal

185

264

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“…In previous epidemiological studies, nested PCR techniques targeting 3′-UTR and spike sequences have been widely used for viral detection and discrimination between type I and II serotypes, respectively [3,12,[30][31][32][33][34][35][36]. However, previous methods are time-consuming, and nonspecific amplification often occurs in the course of nested PCR.…”

Section: Discussionmentioning

confidence: 99%

Molecular epidemiological study of feline coronavirus strains in Japan using RT-PCR targeting nsp14 gene

et al. 2015

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BackgroundFeline 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.ResultsTo develop an RT-PCR method for detection and genotyping of FCoV, we performed comparative genome analysis using WGSs of 32 FCoV, 7 CCoV and 5 TGEV strains obtained from NCBI. As the PCR target, we focused on the nsp14 coding region, which is highly conserved and phylogenetically informative, and developed a PCR method targeting nsp14 partial sequences. Among 103 ascites, 45 pleural effusion and 214 blood specimens from clinically ill cats, we could detect FCoV in 55 (53.4%), 14 (31.1%) and 19 (8.9%) specimens using the present method. Direct sequencing of PCR products and phylogenetic analysis allowed discrimination between type I- and II-FCoV serotypes. Our nsp14 amino acid sequence typing (nsp14 aa ST) showed that the FCoV clone with sequence type (ST) 42, which was the most predominant genotype of WGS strains, was prevalent in domestic cats in Japan.ConclusionsOur nsp14 PCR scheme will contribute to virus detection, epidemiology and ecology of FCoV strains.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-015-0372-2) contains supplementary material, which is available to authorized users.

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“…158 Genome sequences and subsequent phylogenetic analysis showed that FCoV isolates form geographical clusters. [10][11][12]42,102,132 FCoV from cats of the same household exhibit over 95% genetic identity, suggesting infection from a common virus. 5,102,162 Focussing on the S gene, one study specifically examined the evolution of virus strains in cohorts of naturally infected cats over several years.…”

Section: Historymentioning

confidence: 99%

Feline Infectious Peritonitis

2014

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Feline infectious peritonitis (FIP) is one of the most important fatal infectious diseases of cats, the pathogenesis of which has not yet been fully revealed. The present review focuses on the biology of feline coronavirus (FCoV) infection and the pathogenesis and pathological features of FIP. Recent studies have revealed functions of many viral proteins, differing receptor specificity for type I and type II FCoV, and genomic differences between feline enteric coronaviruses (FECVs) and FIP viruses (FIPVs). FECV and FIP also exhibit functional differences, since FECVs replicate mainly in intestinal epithelium and are shed in feces, and FIPVs replicate efficiently in monocytes and induce systemic disease. Thus, key events in the pathogenesis of FIP are systemic infection with FIPV, effective and sustainable viral replication in monocytes, and activation of infected monocytes. The host's genetics and immune system also play important roles. It is the activation of monocytes and macrophages that directly leads to the pathologic features of FIP, including vasculitis, body cavity effusions, and fibrinous and granulomatous inflammatory lesions. Advances have been made in the clinical diagnosis of FIP, based on the clinical pathologic findings, serologic testing, and detection of virus using molecular (polymerase chain reaction) or antibody-based methods. Nevertheless, the clinical diagnosis remains challenging in particular in the dry form of FIP, which is partly due to the incomplete understanding of infection biology and pathogenesis in FIP. So, while much progress has been made, many aspects of FIP pathogenesis still remain an enigma.

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Genetic diversity and phylogenetic analysis of Feline Coronavirus sequences from Portugal

Abstract: 24The distribution of FCoV Type I and II in a Portuguese cat population was studied by a RT-PCR assay

Cited by 19 publications

References 14 publications

An update on feline infectious peritonitis: Virology and immunopathogenesis

An update on feline infectious peritonitis: Virology and immunopathogenesis

Molecular epidemiological study of feline coronavirus strains in Japan using RT-PCR targeting nsp14 gene

Feline Infectious Peritonitis

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