Sequence Analysis of Feline Coronaviruses and the Circulating Virulent/Avirulent Theory

Chang, Hui‐Wen; Egberink, Herman; Rottier, Peter J. M.

doi:10.3201/eid1704.102027

Cited by 44 publications

(63 citation statements)

References 9 publications

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“…Brown et al (2009) reported differences at five aa positions within the M protein which allow differentiation between FCoV biotypes. Like Chang et al (2011), we were not able to confirm these aa signatures in our samples. The same group also promoted a so-called ''circulating virulent-avirulent FCoV'' hypothesis of viral pathogenesis suggesting that non-pathogenic and pathogenic strains circulate in a population based on phylogenetic analyses of the ORF7b and M genes (Brown et al, 2009).…”

Section: Discussioncontrasting

confidence: 74%

“…This conclusion was based on sequencing ORF7 and the M gene. The results which led to this hypothesis were questioned by others (Chang et al, 2011).…”

mentioning

confidence: 94%

“…Comparative sequence analyses suggest that the highly virulent FIPV arises by mutation from the low virulent FECV (Vennema et al, 1998). Point mutations and/or deletions have been identified in the accessory genes, the spike protein gene and the membrane protein gene of FIPV (Herrewegh et al, 1995a;Vennema et al, 1998;Kennedy et al, 2001;Rottier et al, 2005;Brown et al, 2009;Pedersen et al, 2009Pedersen et al, , 2012Chang et al, 2010Chang et al, , 2011Chang et al, , 2012Brown, 2011;Takano et al, 2011;Licitra et al, 2013). Special attention has been paid to the ORF3c gene which is heavily affected in the majority of FIPVs but intact in FECVs (Pedersen et al, , 2012Chang et al, 2010).…”

mentioning

confidence: 99%

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Mutations of 3c and spike protein genes correlate with the occurrence of feline infectious peritonitis

Bank-Wolf

Stallkamp

Wiese

et al. 2014

Veterinary Microbiology

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The genes encoding accessory proteins 3a, 3b, 3c, 7a and 7b, the S2 domain of the spike (S) protein gene and the membrane (M) protein gene of feline infectious peritonitis virus (FIPV) and feline enteric coronavirus (FECV) samples were amplified, cloned and sequenced. For this faeces and/or ascites samples from 19 cats suffering from feline infectious peritonitis (FIP) as well as from 20 FECV-infected healthy cats were used. Sequence comparisons revealed that 3c genes of animals with FIP were heavily affected by nucleotide deletions and point mutations compared to animals infected with FECV; these alterations resulted either in early termination or destruction of the translation initiation codon. Two ascites-derived samples of cats with FIP which displayed no alterations of ORF3c harboured mutations in the S2 domain of the S protein gene which resulted in amino acid exchanges or deletions. Moreover, changes in 3c were often accompanied by mutations in S2. In contrast, in samples obtained from faeces of healthy cats, the ORF3c was never affected by such mutations. Similarly ORF3c from faecal samples of the cats with FIP was mostly intact and showed only in a few cases the same mutations found in the respective ascites samples. The genes encoding 3a, 3b, 7a and 7b displayed no mutations linked to the feline coronavirus (FCoV) biotype. The M protein gene was found to be conserved between FECV and FIPV samples. Our findings suggest that mutations of 3c and spike protein genes correlate with the occurrence of FIP.

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Section: Discussioncontrasting

confidence: 74%

“…This conclusion was based on sequencing ORF7 and the M gene. The results which led to this hypothesis were questioned by others (Chang et al, 2011).…”

mentioning

confidence: 94%

mentioning

confidence: 99%

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Mutations of 3c and spike protein genes correlate with the occurrence of feline infectious peritonitis

Bank-Wolf

Stallkamp

Wiese

et al. 2014

Veterinary Microbiology

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“…The underlying mechanisms that allow the tissue tropism change is reported to be associated with mutations in the S and open reading frame 3c genes and the aberrant immune response of the host, but the detailed mechanism of the altered tropism has not been clearly established (Chang et al, 2012a; Chang et al, 2011; Pedersen et al, 2012; Poland et al, 1996; Vennema et al, 1998). The feline enteric coronaviruses are present ubiquitously in the environment and easily transmitted via a fecal-oral route.…”

Section: Discussionmentioning

confidence: 99%

Potent inhibition of feline coronaviruses with peptidyl compounds targeting coronavirus 3C-like protease

et al. 2013

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Feline coronavirus infection is common among domestic and exotic felid species and usually associated with mild or asymptomatic enteritis; however, feline infectious peritonitis (FIP) is a fatal disease of cats that is caused by systemic infection with a feline infectious peritonitis virus (FIPV), a variant of feline enteric coronavirus (FECV). Currently, there is no specific treatment approved for FIP despite the importance of FIP as the leading infectious cause of death in young cats. During the replication process, coronavirus produces viral polyproteins that are processed into mature proteins by viral proteases, the main protease (3C-like [3CL] protease) and the papain-like protease. Since the cleavages of viral polyproteins are an essential step for virus replication, blockage of viral protease is an attractive target for therapeutic intervention. Previously, we reported the generation of broad-spectrum peptidyl inhibitors against viruses that possess a 3C or 3CL protease. In this study, we further evaluated the antiviral effects of the peptidyl inhibitors against feline coronaviruses, and investigated the interaction between our protease inhibitor and a cathepsin B inhibitor, an entry blocker, against feline coronaviruses in cell culture. Herein we report that our compounds behave as reversible, competitive inhibitors of 3CL protease, potently inhibited the replication of feline coronaviruses (EC50 in a nanomolar range) and, furthermore, the combination of cathepsin B and 3CL protease inhibitors led to a strong synergistic interaction against feline coronaviruses in cell culture systems.

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“…The hypothesis known as the "internal mutation theory" is widely accepted (POLAND et al, 1996;HERREWEGH et al, 1997;VENNEMA et al, 1998;PEDERSEN et al, 2009;CHANG et al, 2010;ROTTIER, 2011), and it states that FIP occurs when a cat is exposed to variants of FCoV that have mutated within the host and are able to disseminate from the gut (the primary site of infection) by gaining the ability to efficiently replicate within the macrophages (POLAND et al, 1996;VENNEMA et al, 1998). However, any stable genetic differences between FECoV and FIPV that can account for their differing pathogenicities remain to be identified (DYE; SIDDELL, 2007).…”

Section: Paltrinieri; Pedersen 2004)mentioning

confidence: 99%

Diversidade gênica do coronavírus felino em populações virais entéricas e sistêmicas intra e inter-hospedeiros

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Sequence Analysis of Feline Coronaviruses and the Circulating Virulent/Avirulent Theory

Cited by 44 publications

References 9 publications

Mutations of 3c and spike protein genes correlate with the occurrence of feline infectious peritonitis

Mutations of 3c and spike protein genes correlate with the occurrence of feline infectious peritonitis

Potent inhibition of feline coronaviruses with peptidyl compounds targeting coronavirus 3C-like protease

Diversidade gênica do coronavírus felino em populações virais entéricas e sistêmicas intra e inter-hospedeiros

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