Rabies, snakes and the ghost virus

Plus, are there traditional herbal rabies cures?

Dr Sam Bailey is one of a growing cohort of doctors and scientists who do not believe in the existence of viruses. Other leading advocates of this movement include Dr Tom Cowan, Dr Stefan Lanka, Dr David Rasnick and Dr Andrew Kaufman. Some of these discuss the fraudulent nature of virology in a zoom presentation which I have embedded at the end of my earlier article Do Viruses Exist?

I found Sam Bailey when I was trying to test this theory by looking up what the virus sceptics have to say about rabies. Her presentation was very interesting (see video below). Basically she says, yes, rabies exists, and it is deadly. But just because it exists does not mean it is a virus. No rabies virus has been identified. A toxin would be an equally plausible explanation for the symptoms of rabies and subsequent death.

This makes sense. As we know from stories of surreptitious ricin poisoning, people can die from pinpricks that inject very small amounts of nerve toxin. If Sam Bailey is right, this would not be the first time a disease caused by a toxin has been blamed on a "virus". Dr Suzanne Humphries’ book Dissolving Illusions, suggests there is far more evidence that polio is caused by DDT poisoning than by a virus. Just because a set of symptoms exists does not mean that a virus has to exist.

Rabies kills more than 50,000 people a year. It is termed an infection because it begins with a bite from a rabid animal, usually a dog, fox, raccoon or bat. The first symptoms of rabies may be similar to flu, including weakness or malaise, fever, headache. There also may be discomfort or itching around the bite. The incubation period may last for weeks or months, depending how far away the site of the bite is from the brain. Symptoms then progress to brain dysfunction, anxiety, confusion and agitation. In later stages the person may experience delirium, abnormal behaviour, hallucinations, hydrophobia (inability to swallow water), and insomnia. Sometimes there is gradual paralysis followed by coma.

The rabies vaccine must be administered before clinical signs of rabies appear, otherwise the disease is nearly always fatal. Once the acute phase has begun, death from encephalitis will usually occur within 2 to 10 days.

The big question

IF rabies is not due to a virus, the next obvious question has to be, "How does the rabies vaccine work?"

When I found the answer, it was mind-blowing.

The "post-exposure vaccine" that is administered after a suspected rabies infection has occurred is not the so-called prophylactic vaccine that you or your pets might receive. Prophylactic rabies vaccines consist of:

• Inactivated rabies virus* administered by injection, OR

• Modified live viruses* administered orally (by mouth): Live rabies virus from attenuated strains. Attenuated means strains that have developed mutations that cause them to be weaker and do not cause disease.
  Wikipedia
  (*As usual, no rabies "virus" has been isolated, so this can only be some kind of fluid extracted from affected animals, as described in this article.)

The post-exposure vaccine, given after a suspected rabies infection, is nothing like the above. It is an anti-toxin, prepared in a similar way to a snake-bite anti-venom preparation. It is nothing to do with killing or inactivating viruses. Interesting!

About anti-toxins

The human and animal body can create antibodies to toxins as well as to infections. The world's first snakebite anti-venom serum was invented by French biologist and immunologist Dr Léon Charles Albert Calmette (1863-1933). Calmette injected a number of animals with small amounts of cobra venom. The animals' natural immune systems created antibodies to fight the injected substance. From their blood, Calmette extracted a serum containing these toxin-fighting proteins, which would become the world's first snake anti-venom products.

The method was very similar to that used by Pasteur to create the rabies vaccine. Antibodies to the rabies toxin are purified, and that's what you inject into a post-exposure rabies victim. More information.

What? The actual rabies pathogen is a toxin?

It seems that rabies symptoms are well known to be caused by a neurotoxin (nerve toxin). This neurotoxin is a type of nicotinic acetylcholine receptor (nAChR) antagonist - which means that it inhibits the body's ability to use acetylcholine in the central nervous system. This profoundly affects the function of muscles, nerves and brain. The scientists explain it like this.

The rabies virus has a glycoprotein on its surface. In rabies victims this glycoprotein is found to be concentrated in synaptic regions and neuromuscular junctions. It contains a portion which appears very similar to snake venom neurotoxins that target and inhibit nicotinic acetylcholine receptors (nAChR). This inhibition of receptors in the nervous system could play an important role in rabies pathogenesis including behavioural changes.
www.alliedacademies.org/articles/rabies-virus-snaketoxin-like-glycoprotein-creates-changes-in-host-behavior-9442.html

More about the snake venoms and nAChR:
Bekbossynova, A.; Zharylgap, A.; Filchakova, O. Venom-Derived Neurotoxins Targeting Nicotinic Acetylcholine Receptors. Molecules 2021, 26, 3373.
Summary: Acetylcholine is an important neurotransmitter. Many snake venoms are rich in proteins and peptides that target nicotinic acetylcholine receptors (nAChRs).

So, what about the virus?

If the actual rabies pathogen is a glycoprotein containing a highly toxic portion - a glycoprotein which is already found in nature, not associated with any virus - why are we even talking about viruses? No rabies virus has been successfully isolated, so no matter how many scientists write about it, this virus is a ghost - you either believe in it or you don’t! Just like ghost stories, a whole myth has built up describing this virus. But no-one has ever seen an actual rabies pathogen that self-replicates using our DNA.

Put simply, perhaps we should be saying, "If it looks like snake venom and attacks the nervous system in a similar way to snake venom, maybe it IS snake venom, or something similar?"

That is a very interesting question. Is it outside the realms of possibility that a dog in the wilds of Asia, Africa or South America, where most rabies cases occur, could get in a fight with a snake, become bitten by the snake and perhaps eat the snake, resulting in traces of venom being left in its mouth and fur that could make its bite poisonous? Snake venom when eaten is usually not toxic, but could it perhaps cause frothing at the mouth, as seen in rabid dogs?

Other potential candidates

Leaving the snake venom theory aside for a while, are there any other toxins that could have a similar pathogenic effect?

There are two criteria to bear in mind. The toxin has to be an inhibitor of human nAChR. It must also be a toxin that has been around for at least 200 years, because rabies has been around for at least that long. So the toxin is unlikely to be a modern pesticide. Any theory about bats eating pesticided insects and then biting humans would not be valid. Nevertheless, many insecticides do target nAChR. Here is an interesting study: