A macskák fertözö hashártyagyulla-dása (FIP) és az azt okozó virus biológíája: Irodalmi osszefoglaló

F. Olasz, Eniko Kádár-Hürkecz, A. Bálint, Béla Lakatos, Z. Zádori

Research output: Review article

1 Citation (Scopus)

Abstract

Feline infectious peritonitis (FIP) is a fatal infectious disease that prominently develops In younger cats. The disease is caused by the feline Coronavirus (FeCoV) that has two different pathotypes: The feline enteric Coronavirus (FECV) Is more common and It causes mild or unapparent enteritis, while feline infectious peritonitis virus (FIPV) is responsible for the deadly systemic Immune-mediated granulomatous disease. FECV and FIPV show functional differences, the FECV replicates mainly In intestinal epithelium and are shed In faeces, while FIPV replicates in monocytes and cause systemic disease. The key event In the pathogenesis of FIP is the effective and sustainable viral replication in monocytes of the FIPV. It can take weeks to months for FIP to develop after the Initial infection with FeCoV. Cats persistently infected with FECV remain mostly healthy despite their systemic Infection, and they can play important role to spread the virus among the healthy naive cats. Only 5-12% of FeCoV Infected animals develop the FIP syndrome. The development of the disease is unpredictable, and once FIP develops, the confirmation of diagnosis Is challenging In particular in the dry form. The process of FECV-FIPV conversion and its genetic background is not yet completely understood, though significant progress was made in the topic In the recent years. The macrophage troplsm of FIPV seems to be primary determined by mutations In the S protein. FeCoVs must have an intact 3c gene to be able to replicate In the Intestinal epithelium and deletions of the 3c gene may play a role In the transformation from FECV to FIPV. The newer results not only facilitated the better understanding of the disease but also Improved the potential toolkits for prevention, diagnostic and cure. In this paper the authors shortly summarize the history of the disease and review the latest scientific advances in FIP research.

Original languageHungarian
Pages (from-to)361-376
Number of pages16
JournalMagyar Allatorvosok Lapja
Volume139
Issue number6
Publication statusPublished - jún. 1 2017

Fingerprint

Feline Coronavirus
Feline coronavirus
Biological Sciences
Feline Infectious Peritonitis
feline infectious peritonitis
Cats
cats
Intestinal Mucosa
intestinal mucosa
monocytes
Monocytes

ASJC Scopus subject areas

  • veterinary(all)

Cite this

A macskák fertözö hashártyagyulla-dása (FIP) és az azt okozó virus biológíája : Irodalmi osszefoglaló. / Olasz, F.; Kádár-Hürkecz, Eniko; Bálint, A.; Lakatos, Béla; Zádori, Z.

In: Magyar Allatorvosok Lapja, Vol. 139, No. 6, 01.06.2017, p. 361-376.

Research output: Review article

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title = "A macsk{\'a}k fert{\"o}z{\"o} hash{\'a}rtyagyulla-d{\'a}sa (FIP) {\'e}s az azt okoz{\'o} virus biol{\'o}g{\'i}{\'a}ja: Irodalmi osszefoglal{\'o}",
abstract = "Feline infectious peritonitis (FIP) is a fatal infectious disease that prominently develops In younger cats. The disease is caused by the feline Coronavirus (FeCoV) that has two different pathotypes: The feline enteric Coronavirus (FECV) Is more common and It causes mild or unapparent enteritis, while feline infectious peritonitis virus (FIPV) is responsible for the deadly systemic Immune-mediated granulomatous disease. FECV and FIPV show functional differences, the FECV replicates mainly In intestinal epithelium and are shed In faeces, while FIPV replicates in monocytes and cause systemic disease. The key event In the pathogenesis of FIP is the effective and sustainable viral replication in monocytes of the FIPV. It can take weeks to months for FIP to develop after the Initial infection with FeCoV. Cats persistently infected with FECV remain mostly healthy despite their systemic Infection, and they can play important role to spread the virus among the healthy naive cats. Only 5-12{\%} of FeCoV Infected animals develop the FIP syndrome. The development of the disease is unpredictable, and once FIP develops, the confirmation of diagnosis Is challenging In particular in the dry form. The process of FECV-FIPV conversion and its genetic background is not yet completely understood, though significant progress was made in the topic In the recent years. The macrophage troplsm of FIPV seems to be primary determined by mutations In the S protein. FeCoVs must have an intact 3c gene to be able to replicate In the Intestinal epithelium and deletions of the 3c gene may play a role In the transformation from FECV to FIPV. The newer results not only facilitated the better understanding of the disease but also Improved the potential toolkits for prevention, diagnostic and cure. In this paper the authors shortly summarize the history of the disease and review the latest scientific advances in FIP research.",
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AU - Kádár-Hürkecz, Eniko

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AU - Lakatos, Béla

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