Feline coronavirus

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Feline Coronavirus (FCoV) is an RNA virus that is infectious for cats. It has two different forms; the FECV (Feline Enteric Coronavirus) that infects the intestines and the FIPV (Feline Infectious Peritonitis Virus) that causes the disease Feline infectious peritonitis. This virus is part of the coronavirus group 1, which includes the porcine gastroenteritis swine coronavirus (TGEV), the canine coronavirus (CCOV) and some human coronavirus.

Contents

Feline Coronavirosis

The digestive form of FECV

FECV virus is responsible for an infection of the gastrointestinal epithelial cells (see also enterocytes, brush border, microvilli, villi). This intestinal infection has few outward signs, and is usually chronic. The virus is excreted in the feces of the healthy carrier, and can be detected by Polymerase Chain Reaction or "PCR" of feces or by PCR testing of rectal samples.

Cats living in groups can contaminate each other during visits to a communal litter tray. Some cats are resistant to the virus and can avoid infection or even becoming carriers, while others may become FECV carriers. Carriers may heal spontaneously, but acquired immunity may be short and they may go on to reinfect, usually within a few weeks, if they are living in a group with healthy, but persistent excretory carriers. Some cats never heal and the excretory phase remains permanently.

Mutation from the FECV form to FIPV

Random errors can occur in the virus infecting an enterocyte causing the virus to mutate from FECV to FIPV.

In a large group of cats (n) the epidemiological risk of mutation (E) is higher:

E = (n ²)-n

A house hosting 2 cats therefore has a mutation risk = 2. when 4 kittens born into this house, the risk goes up from 2 to 30.

Cats visiting communal litter trays can be permanently infected with a larger number of different strains of virus.

In their pre-domestication natural state cats were solitary animals and didn't share their areas (hunting areas, rest areas, defecation sites, etc.). Domestic cats living in a group create a much higher epidemiological risk situation.

After this mutation, the FCoV acquires a tropism for macrophages [1] (see also: Immune cells, leucocyte, monocyte, dendritic cells, mononuclear cell, antigen-presenting cell) while losing intestinal tropism.

Feline infectious peritonitis and the FIPV virus

See also the special article about feline infectious peritonitis

In a cat group, overcrowding increases the risk of mutation and conversion (from FECV to FIPV) and constitutes a major risk factor for the development of feline infectious peritonitis(FIP) cases. FIP will mainly develop in cats whose immunity is low; such as younger kittens, old cats, immunosuppression due to viral — FIV (Feline immunodeficiency virus) and / or FeLV Feline leukemia virus and stress, including the stress of separation and adoption.

Infection of macrophages by FIPV is responsible for development of a fatal granulomatous vasculitis, or FIP (see granuloma).

Therefore, FIP occurs when 2 factors are present: (virus mutation) AND (cat health status)

2 different clinical forms of FIP '(feline infectious peritonitis )':

  1. An effusive form with effusion peritoneal fluid (= ascites), pleural and pericardial,
  2. And a dry form.

The outcome is usually fatal, but a few cases of healing, with feline omega interferon treatment, have been reported.

Molecular aspects of virus fusion to the host cell

The 2 different forms of FCoV, enteric (FECV) and FIP (FIPV), get 2 different serotypes along with different antigens resulting in production of different antibodies: serotype.

The FCoV serotype I (also called Type I) is most frequent; 80% of infections are due to type I FECV that could mutate to FIPV type I. Serotype I FCoV cultures are difficult to perform, with few resulting studies.

The FCoV serotype II (also called type II) is less frequent: FECV type II that can mutate to FIPV type II. FCoV type II is a recombinant virus type I with spike genes (S protein) replacement from FCoV by the canine enteric coronavirus (CCOV) spikes.[2] The type II cultures are easier to perform, so we have got many studies about type II (though it is less common form).

Model: "data about FCoV type II"

Virus fusion

FCoV is an RNA viruses that is included in the coronaviruses group 1. Coronaviruses are covered with several types of proteins "S proteins" (or E2) forming a crown of protein spikes to the virus surface. Coronaviruses take their name from the observation of this crown by electron microscopy

These spikes of Cov (group 1 and serotype II) are responsible for the infection power of the virus by binding the virus particle to a membrane receptor of the host cell: the Feline Amino peptidase N (fAPN).[3][4][5]

The viral receptor: aminopeptidase N (APN )

fAPN (feline), hAPN (human) and pAPN (porcine) differ in some areas of N-glycosylation, therefore:

At the cellular level this explains why the glycosylation level of enterocytes APN is important for the binding of virus to the receptor. [6][7]

About viral spikes

The FECV spikes have a high affinity for enterocytes fAPN, while the mutant FIPV spikes have a high affinity for the macrophages fAPN.

During the viral replication cycle, spikes proteins mature in the host cell Golgi complex with a high mannose glycosylation.

This spike manno-glycosylation stage is indispensable for the acquisition of coronavirus virility. [1][8]

Data about FCoV type I

The receptor?

In 2007, it was well established that serotype I did not work with the FCoV fapn receptor. The FCoV type I receptor still is unknown.[9]

News about CoV receptor

ACE and DC-SIGN are two trans-membrane receptors (mannose receptors) which can bind 'the plant lectins C-type mannose binding'. DC-SIGN and ACE serve as retrovirus receptors.[10]

Role of mucus and glycocalix — Interactions between viruses and sialic acid

Sialic acid is a component of the complex sugar glycocalix, i.e. mucus protecting the gastrointestinal and respiratory mucosa. Sialic acid is an important facilitating fusion factor of any viruses to its host cell. This has been very well studied for flu.

Extensive data also shows that processes using sialic acid are directly involved in the interaction with receptor's lectins.[12]

It has been demonstrated that swine enteric coronavirus (group 1) fusion to the enterocyte was through binding to the APN in the presence of sialic acid, 2 elements are necessary.[7][13][14]

About Felin coronavirus infections, it seems that the infection is sialic acid dependent.[15][16]

Inhibition of the fusion: some studies (in vitro)

To inhibit the fusion of the virus to the cell, several solutions are possible:

  1. modify glycosylation level of the viral spikes,
  2. Change the level of glycosylation of fAPN,
  3. Compete with the spikes, with molecules that will bind to fapn (occupation of the binding site),
  4. Inhibit the binding depends on the sialic acid mucus.

- Mannan binding Lectin:

  1. Allium agglutinins
  2. Urtica dioica agglutinins
  3. Pradamycine A .../...
  1. Ficoline
  2. Collectine .../...

-Manno-Oligosaccharides (MOS) : source: yeast

- sialic acid :

Experimental sialic acid inhibition can decrease the avian and human coronavirus infectivity.[18]

Protecting kittens through breastmilk

Kittens born from mothers carrying FECV are protected from infection during their first weeks of life until weaned by maternal antibodies. Diane D. Addie advocates early weaning and segregation of kittens from their mother before they contaminate each other (at about 5 to 6 weeks). Kittens with no outside contamination and that are deprived of contact with their mother during their first 2 months of life (an important immunological period) may be protected.[19]

The initial protection of the kittens is very effective. We have to reflect about the different possible ways to do it.

Antibodies

It is widely accepted that passive protection is passed on to kittens by immunoglobulins nursery (antibodies) provided by colostrum and milk from the mother.

Several questions arise:

  1. If this protection is only supported by maternal antibodies, why don't these antibodies protect the mother herself?
  2. If the kittens born to a mother's blood group B are removed from their mother for 24 hours (to avoid Hemolytic disease of the newborn) and thus have no systemic passage of maternal antibodies, why don't we see FCoV infection in these kittens more often than others?

Colostrum

Other molecules from colostrum and cat milk, could also bear this coverage:

Lactoferrin has many properties that make it a very good candidate for this anti-coronavirus activity:

  1. As CoV group I, it binds to APN [20]
  2. As the SARS CoV, it binds to enzymes convert angiotensin[21]
  3. It binds to DC-SIGN of macrophage,[22]
  4. The Lactoferrin anti-viral activity is sialic acid dependent.

The structures of the polypeptide chain and carbohydrate moieties of bovine lactoferrin (bLF) are well established. bLF consists of a 689-amino acid polypeptide chain to which complex and high-mannose-type glycans are linked (Pierce et al., 1991)

Other components

The colostrum and breast milk also contains:

  1. Many oligosaccharides (glycan) responsible for anti-viral,[23]
  2. Many maternal immune cells,
  3. Many cytokines (interferon ...); whose role by oro-mucosal route seems very important.[24][25][26]
  4. sialic acid: during lactation, it appears that neutralizing oligo-saccharides binding sialic acid decreases when it binds increasingly to glycoproteins.[27] (The APN is a glycoprotein). The anti-viral effect of lactoferrin is increased by the removal of sialic acid.[28]
  5. Mannan binding lectins.[29]

Other protective factors

Other assumptions may help to explain this resistance to FCoV infections by kittens.

References

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