Deletions in the 7a ORF of feline coronavirus associated with an epidemic of feline infectious peritonitis

Kennedy, Melissa; Boedeker, Nancy C.; Gibbs, Pam; Kania, Stephen A.

doi:10.1016/s0378-1135(01)00354-6

Cited by 74 publications

(74 citation statements)

References 8 publications

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“…Several genes, including the spike gene and the so-called group-specific genes 3c, 7a and 7b, have been suggested to be associated with the pathotypic switch (Kennedy et al, 2001;Rottier et al, 2005;Vennema et al, 1998). In particular, it has been noted that FIPV strains frequently carry mutations that inactivate the gene for 3c (Pedersen, 2009;Vennema et al, 1998), an accessory triple-spanning membrane protein with a predicted topology similar to that of SARS coronavirus 3a (Oostra et al, 2006).…”

mentioning

confidence: 99%

Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene

Chang

Groot

Egberink

et al. 2009

Journal of General Virology

136

188

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Feline infectious peritonitis (FIP) is a lethal systemic disease caused by FIP virus (FIPV), a virulent mutant of apathogenic feline enteric coronavirus (FECV). We analysed the 3c gene -a proposed virulence marker -in 27 FECV-and 28 FIPV-infected cats. Our findings suggest that functional 3c protein expression is crucial for FECV replication in the gut, but dispensable for systemic FIPV replication. Whilst intact in all FECVs, the 3c gene was mutated in the majority (71.4 %) of FIPVs, but not in all, implying that mutation in 3c is not the (single) cause of FIP. Most cats with FIP had no detectable intestinal feline coronaviruses (FCoVs) and had seemingly cleared the primary FECV infection. In those with detectable intestinal FCoV, the virus always had an intact 3c and seemed to have been acquired by FECV superinfection. Apparently, 3c-inactivated viruses replicate not at all -or only poorly -in the gut, explaining the rare incidence of FIP outbreaks.Feline coronaviruses (FCoVs; family Coronaviridae, order Nidovirales), important pathogens of cats, occur as two distinctly different pathotypes. Feline enteric coronavirus (FECV), the pathotype most common in the field, seems to be confined mainly to the intestinal tract and causes mild, often unapparent enteritis. The virus spreads efficiently via the faecal-oral route and, as infections may persist subclinically for up to a year and perhaps even longer (Herrewegh et al., 1997;Pedersen et al., 2008), FECV prevalence is high, reaching up to 90 % seropositivity in multi-cat environments. The other pathotype, designated feline infectious peritonitis virus (FIPV), occurs only sporadically. In sharp contrast to FECVs, FIPVs do not seem to be well-transmitted and they are highly virulent. By efficiently infecting macrophages and monocytes, FIPVs can escape from the gut and cause a lethal systemic disease with multi-organ involvement, in classical cases accompanied by accumulation of abdominal exudate (ascites; reviewed by de Groot & Horzinek,1995;Haijema et al., 2007;Pedersen, 2009).There is genetic and animal experimental evidence to indicate that the virulent pathotype evolves time and time again from the avirulent one by mutation in individual infected cats. Comparative sequence analysis of FCoV laboratory strains and field variants revealed that FECVs and FIPVs come in genetically closely related pairs, more identical to each other than to other FCoVs (Herrewegh et al., 1995b;Pedersen et al., 1981;Poland et al., 1996;Vennema et al., 1998). Direct support for the 'internal mutation' hypothesis comes from an experiment in which cats with an immunosuppressive feline immunodeficiency virus infection were superinfected with FECV. A number of these animals developed FIP in response. The (systemic) virus variants isolated from the diseased cats were isogenic to the original FECV strain yet, unlike the parental virus, induced FIP readily when inoculated into specific-pathogen-free cats (Poland et al., 1996;Vennema et al., 1998); virulence thus appears to be an acquired gene...

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mentioning

confidence: 99%

Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene

Chang

Groot

Egberink

et al. 2009

Journal of General Virology

136

188

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“…Its function, however, is not clear. In FIPV, several studies have reported that deletion of ORF 7 correlates with the virulence of the virus [5,7].…”

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confidence: 99%

Sequence Comparison of the ORF 7 Region of Transmissible Gastroenteritis Viruses Isolated in Japan

Taniguchi

Takahashi

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. The 3' end region nucleotide sequence, including ORF7, of nine Japanese and two U.S.A. isolates of transmissible gastroenteritis virus (TGEV) were determined and compared. Nine Japanese TGEV strains have been isolated over the past 40 years . From the comparison of determined nucleotide sequences, we could divide the TGEV Japanese isolates into two groups and d istinguish them from TGEV U.S.A. isolates. KEY WORDS: open reading frame 7, sequencing analysis, transmissible gastroenteritis virus.

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“…Further molecular studies are thus worth undertaking to disclose these molecular characteristics because viral molecular changes associated with FIP disease remains a very challenging question. 19,32 Our results showed that in the 15 cats presenting the typical clinical and pathologic picture of the dry form of FIP, CCV2-2 positivity in macrophages was always detected in lesions with MAC 387-positive cells. Thus, 46 of 49 samples stained positive with the CCV2-2 mAb, yielding a sensitivity of 94% for this mAb.…”

Section: Discussionmentioning

confidence: 59%

Detection of Antigenic Heterogeneity in Feline Coronavirus Nucleocapsid in Feline Pyogranulomatous Meningoencephalitis

Poncelet¹,

Coppens²,

Peeters

et al. 2008

Vet Pathol

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Abstract.A new monoclonal antibody (mAb), CCV2-2, was compared with the widely used FIPV3-70 mAb, both directed against canine coronavirus (CCoV), as a diagnostic and research tool. Western blot showed that both anti-CCoV mAbs only reacted with a protein of 50 kD, a weight consistent with the feline coronavirus (FCoV) viral nucleocapsid. A competitive inhibition enzyme-linked immunosorbent assay showed that the 2 recognized epitopes are distinct. Preincubation of CCV2-2 mAb with FCoV antigen suppressed the immunostaining. Formalin-fixed, paraffin-embedded sections from brains of 15 cats with the dry form of feline infectious peritonitis (FIP) were examined by immunohistochemistry. Immunohistochemistry was performed with both anti-CCoV mAbs, either on consecutive or on the same sections. A myeloid-histiocytic marker, MAC 387, was also used to identify FIP virus-infected cells. In all regions where MAC 387-positive cells were present, positive staining with the CCV2-2 mAb was systematically detected, except at some levels in 1 cat. In contrast, none or only a few cells were positive for the FIPV3-70 mAb. Double immunostaining showed macrophages that were immunopositive for either CCV2-2 alone or alternatively for CCV2-2 and FIPV3-70 mAbs. This reveals the coexistence of 2 cohorts of phagocytes whose FIP viral contents differed by the presence or absence of the FIPV3-70-recognized epitope. These findings provide evidence for antigenic heterogeneity in coronavirus nucleocapsid protein in FIP lesions, a result that is in line with molecular observations. In addition, we provide for the first time morphologic depiction of viral variants distribution in these lesions.

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Deletions in the 7a ORF of feline coronavirus associated with an epidemic of feline infectious peritonitis

Cited by 74 publications

References 8 publications

Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene

Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene

Sequence Comparison of the ORF 7 Region of Transmissible Gastroenteritis Viruses Isolated in Japan

Detection of Antigenic Heterogeneity in Feline Coronavirus Nucleocapsid in Feline Pyogranulomatous Meningoencephalitis

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