SARS-CoV-2 AND ITS RELATION TO FELINE INFECTIOUS PERITONITIS
LINING OF ABDOMEN (PERITONITIS) vs LINING OF BLOOD VESSELS (VASCULITIS)
Feline Coronavirus (FECV) is a pathogen of minor significance; however, a spontaneous mutation of this virus yields FIPV, which is capable of replicating in peritoneal macrophages and producing peritonitis and occasionally FIP, a fatal Arthus-like pyogranulomatous disease in kittens and cats.
This is an extremely significant fact. In chess, you can begin a game in one opening, and by MOVE ORDER, TRANSPOSE into another opening. I believe looking at COVID and its relation to FIP in a similar way yields critical insight.
Whilst FIP invades MACROPHAGES in cats, SARS-CoV-2 invades MONOCYTES in humans. The only critical difference between macrophages and monocytes is where they are located. They both perform virtually the same functions. Macrophages are found in tissue. Monocytes are found in blood.
In cats, the virus invades MACROPHAGES in the PERITONEUM. Peritonitis is a redness and swelling (inflammation) of the tissue that lines your belly or abdomen. This tissue is called the peritoneum. It can be a serious, deadly disease.
In humans, the Spike Protein invades MONOCYTES in the BLOOD STREAM. I believe you can now logically follow the progression of disease. And, perhaps like FIP, this vasculitis only occurs in a fraction of those infected. Or, is it multiphasic in all those exposed to SARS-CoV-2?
I do not know. We need to examine monocytes of a very large segment of the population and study based upon known exposures to the Spike Protein.
What would be the mechanism of this? The hypothetical pathogenetic process for covid-19 could occur in three phases: a) Viral phase, asymptomatic or weakly symptomatic, with an a-specific innate immune response; b) Immunological phase, intermediately symptomatic, with an anomalous specific immune response (delayed, slow and/or low synthesis of IgM and IgG) in antigen excess conditions, immune complex formation and complement activation with tissue damages; c) Hemo-vascular phase, severely symptomatic, where complement-mediated tissue damages would induce vascular inflammation and systemic alteration of the coagulation homeostasis.
An Arthus-like reaction.
What is most interesting is that the markers for FIP in FECV cats, are also present in all COVID patients, and are markedly elevated in those with severe disease or those who die.
We may be dealing with another HIV – Human Infectious Vasculitis.
Thanks Walter for all the COVID dots that you connect. It's hard to believe that you aren't a medical research professional. I actually once bought a kitten that had FIP. He had a swollen belly, like really swollen like it had a watermelon growing in there, after only 2 weeks of having him, I took him to the vet and they that is when I found out was FIP was. The vet put him to sleep right there and then. It was so sad, I never thought for a moment that I wouldn't come back home with him.
I do some research (sometimes it's many topics at the same time) just for my own interest in everything. So, for my research, I needed to find the missing link which could connect snakes and SARS. My search stopped at Civet cats. Following ''civet cats'' I found some interesting papers. I thought maybe you want to see this cos you have been thinking about ''SARS-CoV-2 AND ITS RELATION TO FELINE INFECTIOUS PERITONITIS''
Quote: ''A personal journey through coronavirus evolution
The Sir Arnold Theiler Memorial Lecture
In Utrecht, it all started with a disease: Feline Infectious Peritonitis (FIP)
which is fatal in most (clinical) cases
its biology was poorly understood
prevention (still) is difficult
It is an enigmatic disease:
a sporadic fatal viral condition is a contradiction in terms
antibodies are of no benefit for the cat
they may even precipitate disease, causing the
'early death' phenomenon
undulating, unresponsive fever
ocular/neurologic symptoms, icterus
wet form: polyserositis with effusions
dry form: disseminated pyogranulomas
The discovery (1977): FIP is caused by a coronavirus''
(picture of 2 papers, found them)
Interesting that the second paper also is there but not accessible:
''The result of this discovery was threefold:
1.we started to work on feline viruses
2.we focused on coronaviruses
3.we became fascinated by viral evolution
“...nothing in biology makes sense except in the light of evolution...”
Theodosius Dobzhansky (1900-1975)
I should like to entertain you about coronavirus evolution as it leads to new* diseases
in individual animals: pathogenesis (FIP)
in the field: epidemiology (TGEV/PEDV;SARS; MERS)
*new in the sense: hitherto unknown to science
Because they are the largest enveloped, positive-stranded RNA viruses with the largest viral RNA known to science, and thus: the highest probability of making genetic mistakes (errors -mutations)
without a proof-reading mechanism to correct them.
Evolutionary “behaviour” of coronaviruses
Occupation of new ecological niches through change in tropism (deletions; point mutations;
TGEV – gut to lung
FIPV – enterocyte to macrophage
SARS-CoV: “species jumping” civet to human
MERV-CoV: “species jumping” bat to camel to human
Transmissible Gastroenteritis Virus (TGEV) of swine is found in feces of pigs ≤ 8 wk after recovery
but has been isolated from lungs > 3 mo p.i. - meaning virus persistence
1984: a “new” respiratory coronavirus was identified in pigs in Belgium, with ≈700nt deletions in the S gene, but conservation of neutralisation-relevant epitopes
The respiratory variant has displaced the enteropathogenic parent virus in all pig populations
thereby acting as a “natural vaccine”.
Peritonitis-causing feline coronaviruses are in vivo mutants occurring in individual, persistently infected cats e.g. when cell-mediated immunity is suppressed (such as under “crowding” stress, after FeLV- or FIV- infections) arise stochastically, under conditions that allow expansion of the so-called “quasispecies cloud''
Crucial for the FECV –FIPV transition:
The A at nucleotide 23531 was 100% conserved in all 183 FECVs in our collection.
Of the 118 FIPVs, 96 (81.4%) had a T and 12(10.2%) a C at this position; in both cases, this changes
the methionine (M) occurring at position 1058 in the FECV S protein into a leucine (L) in FIPV (i.e.,
Viruses have crossed the host species barrier
time and again,
and will forever...
severe acute respiratory syndrome(SARS): palm civet – to man
middle East respiratory syndrome (MERS): African bats, camelids –to man
bat coronavirus: Leschenault's rousettes (Rousettus leschenaulti, fruit bats Megachiroptera) - to
Pomona leaf-nosed bats (Hipposideros pomona, insectivorous, Microchiroptera)
SARS – the first human ‘killer’ coronavirus'' Quote ends.
And a picture from CDC
''Notice of embargo of civets. Embargo is effective on January 13, 2004 and will remain in effect until further notice''