Field strain feline coronaviruses with small deletions in ORF7b associated with both enteric infection and feline infectious peritonitis

Lin, Chao; Su, Bi Ling; Huang, Hui; Lee, J.; Hsieh, Min Wei; Chueh, Ling Ling

doi:10.1016/j.jfms.2008.09.004

Cited by 32 publications

(37 citation statements)

References 28 publications

(22 reference statements)

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“…One FIPV isolate (SFS-01) in the present study had a premature stop codon in the region overlapping 3a, b, another (SFS-11) had a mutation that resulted in an extended 3b protein and no 3c product, and two FIPV isolates had 3 nt and 27 nt deletions in the M protein. The 7a and 7b genes and their products were not studied herein, because isolates of both FECVs and FIPVs with significant mutations have been found to coexist in nature (Kennedy et al, 2001;Lin et al, 2009). Furthermore, deletion of 7b causes FIPVs to become avirulent (Herrewegh et al, 1995).…”

Section: What Is the Mutation That Causes Fecvs To Become Fipvs?mentioning

confidence: 99%

Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats

Pedersen

Liu

Scarlett³

et al. 2012

Virus Research

106

161

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Feline infectious peritonitis virus (FIPV) was presumed to arise from mutations in the 3c of a ubiquitous and largely nonpathogenic feline enteric coronavirus (FECV). However, a recent study found that one-third of FIPV isolates have an intact 3c and suggested that it is not solely involved in FIP but is essential for intestinal replication. In order to confirm these assumptions, 27 fecal and 32 FIP coronavirus isolates were obtained from resident or adopted cats from a large metropolitan shelter during 2008-2009 and their 3a-c, E, and M genes sequenced. Forty percent of coronavirus isolates from FIP tissues had an intact 3c gene, while 60% had mutations that truncated the gene product. The 3c genes of fecal isolates from healthy cats were always intact. Coronavirus from FIP diseased tissues consistently induced FIP when given either oronasally or intraperitoneally (i.p.), regardless of the functional status of their 3c genes, thus confirming them to be FIPVs. In contrast, fecal isolates from healthy cats were infectious following oronasal infection and shed at high levels in feces without causing disease, as expected for FECVs. Only one in three cats shed FECV in the feces following i.p. infection, indicating that FECVs can replicate systemically, but with difficulty. FIPVs having a mutated 3c were not shed in the feces following either oronasal or i.p. inoculation, while FIPVs with intact 3c genes were shed in the feces following oronasal but not i.p. inoculation. Therefore, an intact 3c appears to be essential for intestinal replication. Although FIPVs with an intact 3c were shed in the feces following oronasal inoculation, fecal virus from these cats was not infectious for other cats. Attempts to identify potential FIP mutations in the 3a, 3b, E, and M were negative. However, the 3c gene of FIPVs, even though appearing intact, contained many more non-synonymous amino acid changes in the 3' one-third of the 3c protein than FECVs. An attempt to trace FIPV isolates back to enteric strains existing in the shelter was only partially successful due to the large region over which shelter cats and kittens originated, housing conditions prior to acquisition, and rapid movement through the shelter. No evidence could be found to support a recent theory that FIPVs and FECVs are genetically distinct.

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Section: What Is the Mutation That Causes Fecvs To Become Fipvs?mentioning

confidence: 99%

Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats

Pedersen

Liu

Scarlett³

et al. 2012

Virus Research

106

161

View full text Add to dashboard Cite

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“…Furthermore, intact 7b genes were described in other field strains of FECV. 52,58 Testing for antibodies directed against the 7b protein was compared against the IFA in one study. The authors showed that the 7b protein assay had high sensitivity but poor specificity, with many false-positive results occurring in uninfected animals.…”

Section: Serologymentioning

confidence: 99%

“…44 The ORF 7b gene was also reported to be truncated in FECV but intact in FIPV strains. 56,57 However, such deletions may not be relevant to biotype since they also can occur with in vitro passage 53 and Lin and colleagues 58 found that small deletions in ORF7b could be found in both biotypes.…”

mentioning

confidence: 99%

Feline Coronavirus in Multicat Environments

Drechsler

Alcaraz

Bossong

et al. 2011

Veterinary Clinics of North America: Small Animal Practice

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Feline infectious peritonitis (FIP), a fatal disease in cats worldwide, is caused by FCoV infection, which commonly occurs in multicat environments. The enteric FCoV, referred to as feline enteric virus (FECV), is considered a mostly benign biotype infecting the gut, whereas the FIP virus biotype is considered the highly pathogenic etiologic agent for FIP. Current laboratory tests are unable to distinguish between virus biotypes of FCoV. FECV is highly contagious and easily spreads in multicat environments; therefore, the challenges to animal shelters are tremendous. This review summarizes interdisciplinary current knowledge in regard to virology, immunology, pathology, diagnostics, and treatment options in the context of multicat environments.

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“…These deletions may have been acquired during in vitro passaging of the virus as these genes are known to be dispensable for viral replication in cultured cells; actually, during propagation in cell culture FCoV mutants with deletions in the 7b gene are even selected for, suggesting that functional loss of the gene increases viral fitness in vitro (Herrewegh et al, 1995). Of note, avirulent field viruses with (generally small) deletions in gene 7b have been described (Desmarets et al, 2016;Lin et al, 2009a). It is also worrisome that strain 79-1683 thus far is the only serotype II enteric coronavirus isolated.…”

Section: Discussionmentioning

confidence: 99%

Differential susceptibility of macrophages to serotype II feline coronaviruses correlates with differences in the viral spike protein

2018

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The ability to infect and replicate in monocytes/macrophages is a critically distinguishing feature between the two feline coronavirus (FCoV) pathotypes: feline enteric coronavirus (FECV; low-virulent) and feline infectious peritonitis virus (FIPV; lethal). Previously, by comparing serotype II strains FIPV 79-1146 and FECV 79-1683 and recombinant chimeric forms thereof in cultured feline bone marrow macrophages, we mapped this difference to the C-terminal part of the viral spike (S) protein (S2). In view of the later identified diagnostic difference in this very part of the S protein of serotype I FCoV pathotypes, the present study aimed to further define the contribution of the earlier observed ten amino acids difference to the serotype II virus phenotype in macrophages. Using targeted RNA recombination as a reverse genetics system we introduced the mutations singly and in combinations into the S gene and evaluated their effects on the infection characteristics of the mutant viruses in macrophages. While some of the single mutations had a significant effect, none of them fully reverted the infection phenotype. Only by combining five specific mutations the infections mediated by the FIPV and FECV spike proteins could be fully blocked or potentiated, respectively. Hence, the differential macrophage infection phenotype is caused by the cooperative effect of five mutations, which occur in five functionally different domains of the spike fusion subunit S2. The significance of these observations will be discussed, taking into account also some questions related to the identity of the virus strains used.

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Field strain feline coronaviruses with small deletions in ORF7b associated with both enteric infection and feline infectious peritonitis

Cited by 32 publications

References 28 publications

Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats

Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats

Feline Coronavirus in Multicat Environments

Differential susceptibility of macrophages to serotype II feline coronaviruses correlates with differences in the viral spike protein

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