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Coronaviridae
1. CORONAVIRIDAE-theoretical virology
Veterinarians perspective- Haroon Rashid Chaudhry, IUB
Introduction:
Corona means crown, they have been named so because under the electron microscope
they appear like a crown. Rounded or pleomorphic in nature due to the envelope which
is about 20-30% derived from the host cell membrane which is lipid in nature. It is
theoretically close to saying the lipid solving agents like alcohol and alcohol based
sanitizer will degrade the envelope. This envelope imparts it the resistance against acid
and acid derived sanitizers it has been estimated that some coronavirus may tolerate an
acidic pH upto 3.0. Thus it wont be killed in the stomach pH. The envelope holds other
protein which are 70-80% derived from virus, meaning that the virus transcribes and
translates these proteins and lines on the surface of the cell membrane of the host from
where the virus ejects. The exact mechanism of exiting is poorly understood as the virus
replicates through the endoplasmic reticulum and golgi apparatus of the host cell then
exiting the host cell taking part of the cell membrane with it. The virus replicates in the
cytoplasm as the virus contains a single stranded positive RNA which behaves like a host
cell RNA almost immediately transcribing and replicating in the host cell without
difficulty.
Coronaviridae family is divided into two main genera
Coronavirus
Torovirus (pig, camel, horses)
Size: As most people abuse the social media and say it is the size of 100 microns absolutely not
it is a relatively large virus like influenza virus ranging in size as stated below.
140-160 nm---corona
120-140 nm---torovirus
The scientist refer to micrometer, because of its capacity to travel through droplets of
micrometer size when the carrier coughs and sneezes
Genome:
SSRNA +ve sense
Nucleocapsid
Tubular toroa
Helical corona
Enveloped virus having spikes on envelope
These spikes are called s- spikes which contain hypervariable regions which are
responsible for its mutagenicity, viral escape from host and interspecies jumping.
I would like to clarify few points here. Viruses by nature has evolved to be highly
host specific or species specific in nature and one virus does not infect other
host, they may be organ specific or site specific in nature as well like the
advanced papovaviridae and poxviridae. Few viruses like the Orthomyxoviridae ,
2. which causes influenza, Rabies viruses which causes Rabies, few Herpesviridae
and the newly discovered coronaviridae may jump species and cause disease in
other host not natural to the virus. But usually as in the case of influenza virus
the virus requires a mixing vessel which is pig, the mixing vessel tends to
increase the adaptability of the virus for species jump. This may be done by
morphologically changing the host entry receptors or by mutagenesis at the
genomic level. The Rabies virus called Rhabdoviridae also adapt to chick embryo
but in affect loses it disease causing ability, and also makes a species jump from
canines to feline and other animals also humans. The coronaviridae also does
this with the help of slight mutations which we observed in SARS, SARS-II, and
MERS, if we look closely the genomic picture relates all these human viruses to
bat coronavirus, it is still not clear whether the pig works as a mixing vessel or
the snakes do or the camel does in case of MERS, but we are sure the live food
animal markets triggered whatever genetic assortment which was essential for
the interspecies jump. One thing I would like to also theorize that an adapting
virus continue to mutate one option is it mutates such that it can no longer
cause disease or enter into the new species that means that it no more infects
and no more disease. Another mutation would be that it mutates into a perfect
virus parasite and does not cause harm to its host meaning does not kill it and
adapts well to host, it simply means less virulent strains develop which replicate
in host but no disease. Another mutation would be it becomes lethal to new host
meaning increased disease. Since the mutations in such viruses are not very
proof read and are at random during replication of viruses anything would be
possible. Coronaviridae studies in animals especially pig, cats and dogs are highly
suggestive that this virus adapts and mutates for example it causes a mild
disease in cats gastroenteritis and diarrhea and it is thought that feline
coronavirus somehow mutated in dogs and started replicating in macrophages of
peritoneum instead of enterocytes of feline intestines leading to a severe
disease called feline peritonitis. Such interorgan travel and interspecies jumps
have been found in coronavirus and I fear that the current SARS-II virus if
mutates and jumps from humans to food animals we would be at a much greater
risk as coronavirus is found in poultry, pig, horse, cattle etc.
Media:
Hard to grow in lab media, apart from the poultry coronavirus which cause a severe
disease in poultry called infectious bronchitis almost all coronaviruses have been found
to be hard to grow in laboratory media under laboratory conditions.
Replication:
Intra-cytoplasmic replication
Resistance:
pH = 3.0 tolerates this pH well due to its envelope
3. acid tolerant
heat sensitive, as much data is derived from the poultry coronavirus this virus is highly
heat labile and usually in winter we see the various gastroenteritis in mammals and
infectious bronchitis in poultry, during summer months the disease in animals and birds
are either nonexistent or very mild.
all disinfectant labile, almost all non ionic detergents and alcohol based or organic
solvents detergents are highly effective in killing the virus as they dissolve the lipid
membrane and the virus become naked and unable to enter into the host, if it cant
enter the host it cant replicate and no replication means no disease.
Formaldehyde and glutaraldehyde are highly efficacious in killing the virus as they cause
alkylation of the s protein or spike protein which is important for entry and exit of the
virus.
Diseases:
1. Enteric
Diarrhea
In Human (neonates, sometimes adult)
In ruminants (calf)
In horses (foals)
Same in pets
Cause diarrhea
Treatment:
ORS
Supportive treatment
Antibiotic (neomycin…)
2. Respiratory:
Signs:
Coughing, usually dry cough as it causes deep seated pneumonia in the
alveoli of lungs, post recovery may cause 20-30% lowering of lung
capacity as it interferes with flexibility of the alveoli to expand and
contract due to liquid accumulation..
Nasal discharge
Blood pressure up & down, because it is somehow related to ACE related
cells in the lungs, where it causes deep seated pneumonia and threat to
heart patients and blood pressure patients
Pneumonia, with accumulation of liquid lungs
Inability to use oxygen
4. Routes of infection:
To date direct contact from contaminated surfaces and inhalation of droplets has
been documented but a veterinarian perception is different as the virus causes diarrhea
logically stating it replicate in enterocytes also causing inflammation and diarrhea leading to a
new route of infection the feco-oral route and with that comes hand in hand with the
mechanical vector the common house hold fly and sanitation breach, it has yet to tested and
confirmed in case of humans.
Transmission:
Bats (90%) genomic traceability based on genomic similarity
These two organs are affected in mammalian coronaviruses but more acute macrophage
replication is seen in peritonitis of cats.
3. Systemic
Feline co virus
Feline peritonitis virus, in this case the theory of recombination and mutation is
expressed as the feline CoV somehow came to mutate with the Canine CoV and
instead of growing in the enterocytes of the cats intestine it started replicating in
the macrophages of the immune system and peritoneal cells causing severe
peritonitis and became a lethal FIP-CoV so furthering the theory that it can
change overtime species, host cells, and organs for its growth leading to new
signs and symptoms.
FIP
Poultry:
Infectious bronchitis
4-symptoms are involved ( systemic)
Respiratory
GIT
Reproductive
Urinary
Signs:
Cheasy white plug at syrinx
Block the trachea
Difficulty in breathing
On necropsy tracheal plug
Severe nasal discharge
Respiratory signs
GIT signs Slight diarrhea
Reproductive signs In layers misshaped/soft shell/small egg
5. Kidney failure and uric acid deposition in kidneys and ureters
Treatment options:
Interferon therapy(almost failed in this category) As its genome a positive sense RNA
behaves and starts transcribing almost immediately the host cell cant differentiate the
mRNA of host and those of viral RNA, leading to failure of the interferon activity, which
we have observed by using various interferon therapy has failed in this infection.
Another point of importance is that interferons are the main defense line against viruses
as they tend to block other viruses from infecting when one virus has already infected
the host in this case since interferon has no appreciable effect the infection by other
viruses like rhiniviruses, AIDS, orthomyxoviruses, a potential outcome could be further
mutation and increased ability of the virus.
A point to note here is that initially there is lack of interferon and if we start interferon
therapy it is helpful but at a later stage due to some unknown reasons there is a
superflood/storm of interferon activity which is usually fatal, Chloroquine has somehow
clears the interferon storm.
Antivirals ( some reports in use of antivirals like AZT used in AIDS may be helpful but
almost failed in this category also)
Vaccination (live developing avirulent viruses as a result of uncontrolled mutation may
be present and already circulating in the population but not found yet they may help get
a good live vaccine candidate, killed vaccines but you need to grow in lab which is risky
again can be killed by BEI to remove ss RNA and make an empty virus coat and envelope
or inactivated by alkylation of the s spike protein by formaline both have to be tested.,
recombinant vaccines against the s protein of spike may be helpful but again requires
time)
H120 strain vaccine for poultry, this candidate is ideal for poultry disease called
Infectious bronchitis and used in commercial poultry during almost all stages of its
growth, another lesson we have to learn from it is that it has the tendency for reversion,
if during winter we vaccinated the flock and skip vaccination in summer flocks the
residual virus found in the poultry sheds tend to show mortality and cause disease
which the veterinarian is promulgating to poultry farmers that no matter what the
vaccine should be followed true to the spirit may it be winter or summer.
Live and attenuated vaccines available for food animals
Supportive therapy usually practiced. A paper stating that Tea helps in recovery was
uploaded but then removed from the journal, Tea a general body tonic containing
optimum amounts of theophylline and poly enols and poly enols with general body
stimulants will help as a good breathing aid in case of respiratory stress, then again
going to off feed status or less food status with minimal protein intake would help aid in
less stress to lungs for breathing more oxygen, a non absorbing antibiotic like neomycin,
or a safer antibiotic of the cephalosporin group with broad spectrum would aid
unconditionally in avoiding secondary infection. An old concoction to aid in breathing
not possessing Dextromethorphan (it may increase difficulty in breathing) possessing
theophylline etc would aid clearing upper respiratory tract.
Serotherapy would be great help once you know how much blood or serum is required
6. for recovery. Keeping in view the threats of blood group, hepatitis, blood protozoan and
AIDS, blood bank screened bags from recovered patients of coronavirus would be great
help in controlling the infection, but the exact amount of sera or blood required to
complete recovery has yet to be tested but it would be safe to administer ¼ or ½ pint
blood bag blood to infected patient for recovery but I am not yet sure about that
because the efficacy is still under research
Control measure:
This the population knows much better.