Polio the virus and the vaccine janine roberts

Such sentiments are widespread among those opposed to vaccines. Those who emphasize the value and importance of vaccination programs espouse their own ideas about nature.

Beyond the cultural construction of unnatural versus natural immunity lie material dimensions to the history of vaccines. Vaccines are a technology? Vaccines are, after all, made from pathogens themselves. The attention in anti-vaccination writings often focuses on the unnatural additives: the mercury thimerosal used as a preservative, the formaldehyde used to inactivate viruses and toxins, and the aluminum that is used as an adjuvant.

Yet, as an environmental historian, I find the use of the viruses themselves just as remarkable. The process of polio vaccine production, for example, is a process of domestication as much as a process of fabrication. Wild polioviruses are taken and transformed into viruses under human control, which can then be deployed in large-scale vaccination programs.

Sometimes, new viruses literally evolve out of the research process leading up to vaccine production, as with a neural-adapted, virulent strain of polio called the MV strain.

Our only medical weapons against them are said to be vaccination and powerful chemotherapy-type antiviral medicines designed to stop the cell from making viruses, rather than to attack the virus itself, for apparently it has proved too elusive a target. But, why do cells make pathogenic viruses? Surely the reason for this has been established in numerous laboratory experiments? It is a doctrine in virology that cells make malignant viruses only after a disease virus arrives and infects them.

I had long presumed this must be so, but when I tried to analyse it, I had problems. I found myself asking, since a virus cannot make a virus, surely the first viruses to cause an illness must have been made by an uninfected cell? I had earlier learnt how viruses did their damage. I was now surprised to discover that this is not so; that viruses are far too small, at one-billionth of the mass of a cell, to have this effect.

Current courses on Medical Microbiology now teach, as mentioned briefly above, that viruses kill or damage cells indirectly, by triggering cellular processes that do this damage. Professor Tritz blames allergic reactions. These are often cytotoxic at relatively high concentrations. From what they say, cell deaths are not directly due to viral infection.

This perhaps makes sense. The virus is so minute compared to the cell — and our protective systems will destroy a very sick cell that does not self-destruct. Our cells often seem altruistically to decide to die when not needed, poisoned or otherwise diseased.

How can we be sure that a damaged cell is so solely because it is infected? It may be naturally dying or poisoned. It may even produce viral-like particles for waste disposal, or to attempt a cure or help protect other cells.

Also, if cell deaths in viral illnesses are mostly caused by our immune system, why do we have such deaths when the immune system is down, as surely it often is in such circumstances? But nevertheless, viruses are encoded information, and since cells can make errors, I must conclude that they may sometimes wrongly encode the viruses they send out.

These in theory could misinform other cells, perhaps sometimes encouraging them to take courses of action that they would not take otherwise. But as to how often the codes thus transported could lead to such effects, I had no idea. Dimmock and S.

Primrose, published by Blackwell Scientific Publications. Lastly it is by no means clear what advantage accrues to the virus in killing its host cell. For example: it is reported that deficiency in selenium, a metal our cells use as an antioxidant, can precede the symptoms of colds, flu and even AIDS.

There is also a strong co-relation between selenium levels in soils in African countries and the prevalence of AIDS symptoms. Dr Melinda Beck reported that selenium-deficient mouse cells show symptoms of illness and emit viruses.

She and her co-authors deduced from this that a lack of selenium made viruses dangerous — and consequently that these viruses made the cells ill. But was this deduction soundly based?

Selenium is a component of glutathione peroxidase GPX , an enzyme that protects cells from oxidative stress. Selenium-deficiency thus makes cells ill with oxidative stress without any need for a viral illness. They consequently could produce viral-like particles as waste or for repair purposes. Again, what comes first? The authors presume the virus must cause the illness — but surely the illness started with the earlier oxidative stress.

The first observation of retroviruses is credited to Peyton Rous. If retroviruses were indeed also present, might they have appeared as a defence against this toxin?

In earlier chapters we found that toxins, rather than viruses, are likely to be the primary causes of polio and AIDS — but what then about measles, mumps, flu and colds?

I had long presumed the evidence for these illnesses being due solely to viral infection must be overwhelming — but I have found to my surprise that scientists have long known that the guaranteed way to make cells produce viruses in the laboratory, including flu and measles virus, is not primarily by getting them infected, but by exposing them to stress and toxins!

Then in the s Robert Gallo reported that, when he added certain chemicals to cell cultures, these cells produced retroviruses. If retroviruses were indeed thus produced, then surely this can be explained as a cellular response to stress from toxins? Tryspin is destructive to proteins, and Phytohemagglutinin PHA is mitogenic.

It seemed that a cellular illness was all the proof he needed to conclude that unseen viruses were present — no matter how artificial the laboratory circumstances or what chemicals were added. So — viruses may not be the primary causes of illnesses — they might instead be caused by a cell being poisoned.

Why do our cells make them? Could they be possibly a protective reacition? Burcher, Sam. Selenium conquers AIDS? Institute of Science in Society. Melinda A. Fabio Farinati et al. Free Radical Biology and Medicine, December Pages Boycott AE. The transition form life to death; the nature of filterable viruses. Royal Soc. January The hunt for a virus that causes polio began in the first years of the 20th Century as an emergency response to the horrifying onset of major epidemics of paralytic polio in Sweden and the United States.

It was guided by a new scientific hypothesis then gathering strength that we now know of as the Germ Theory of Disease. These polio epidemics were new — and yet poliomyelitis, to give it its full name, was not a new disease. It had been around for centuries and was long associated with metalworking.

But the virus we now blame for polio is a common human gut virus with no obvious connection to metalworking. This virus is produced solely by human cells, and spreads from us to be common in soil. Human infants acquire lifelong immunity to it as soon as they go into the garden and put a grubby hand in their mouth, as stated in a paper published on the website of the Centers for Disease Control CDC in the US.

So — how did this virus come to cause these crippling and deadly epidemics? Sit back comfortably and read on, for this is also the story of the birth of modern virology and much of modern medicine. It took me some time to untangle it — but I think I can now explain it quite straightforwardly. We presume today that everyone knows that viruses cause major illnesses, but back in , when the polio epidemics were starting to terrorise, viruses were not yet proved to cause illnesses; in fact they had not even been proved to exist!

Initially it was speculated that viruses were smaller invisible versions of the barely visible single-celled bacteria that were already known to be able to reproduce and spread illnesses. Many medical theorists thought that epidemics were caused by minute filterable particles, like bacteria but so small that they could scarcely be seen. These were called viruses and an unknown one was suspected to cause polio…..

The scientists on the hunt conceived of viruses a priori as dangerous parasitic rivals to humans in the competition for life. In , a VDPV was found in the stool of a child in Minnesota who was not vaccinated and had a weakened immune system. The child most likely caught the virus through contact in the community with someone who had received live oral vaccine OPV in another country two months before.

Subsequently, seven other unvaccinated children in the Minnesota community were found to have poliovirus infection. None of the infected children had paralysis. Also in , a healthy, unimmunized young adult from the United States acquired vaccine-associated paralytic polio VAPP in Central America, most likely from an infant grandchild of the host family who recently had been immunized with OPV.

In , an adult with a weakened immune system developed VAPP and died of polio-associated complications. In , a fatal case was reported in an infant who received OPV in India and was severely immunocompromised. VDPVs can cause outbreaks in countries where vaccine coverage is low. Long-term excretion can also occur in people with certain immunodeficiency disorders. Also, polio vaccination protects people against naturally occurring polioviruses and vaccine-derived polioviruses.