What I Really Think about HIV and Ebola
It’s my intention to make this the simplest chapter of the book to understand.
The downside is I’m likely to completely destroy your faith in vaccines as well as a big chunk of public health.
When this chapter is over, I don’t think you’ll ever look at vaccines in the same way. I apologize in advance for any problems this may cause among your friends and family.
I strongly encourage you to check my work to see if I’ve made any errors of fact or interpretation, but I feel as strongly about this claim as anything in my life.
(Please enjoy this excerpt from the book and consider supporting the Authors)
The first concept I want you to understand is called zoonosis, or more properly, zoonotic diseases. If you think it’s a funny word and you immediately imagined a picture of a zoo, you wouldn’t be far off. Zoonosis literally means a disease which can spread between animals and humans.
It may surprise you given my reputation as a renegade, but I believe the Centers for Disease Control (CDC) can occasionally provide good, basic information to the public. Here is what they have on their website about zoonotic diseases.
Every year, tens of thousands of Americans will get sick from diseases spread between animals and people. These are known as zoonotic diseases. Zoonotic means infectious diseases that are spread between animals and people. Because these diseases cause sickness or death in people, CDC is always tracking them.
Animals provide many benefits to people. Many people interact with animals in their daily lives, both at home and away from home. Pets offer companionship and entertainment, with millions of households having one or more pets . . .
However, some animals can carry harmful genes that can be shared with people and cause illness—these are known as zoonotic diseases or zoonoses. Zoonotic diseases are caused by harmful germs like viruses, bacteria, parasites, and fungi. These germs can cause many different types of illnesses in people and animals ranging from mild to serious illness to death. Some animals can appear healthy even when they are carrying germs that can make people sick.
Zoonotic diseases are very common, both in the United States and around the world. Scientists estimate that more than 6 out of every 10 known infectious diseases in people are spread from animals, and 3 out of every 4 new emerging infectious diseases in people are spread from animals.1
That’s good solid information from the CDC and underscores the scope of the problem. Tens of thousands of Americans at the very least will get sick every year from illnesses spread by some form of association with animals. Zoonotic diseases account for more than 60 percent of known infectious diseases and at least 75 percent of new emerging infectious diseases. This is probably one of the biggest challenges in public heath you’ve never heard about, even though you can find it prominently displayed on the CDC website.
What are some of these diseases, you might ask? This is a partial list: anthrax, bird flu, bovine tuberculosis, cat scratch fever, dengue fever, Ebola, encephalitis from ticks, enzootic abortion, hemorrhagic colitis, hepatitis E, listeria infection, Lyme disease, malaria, parrot fever, plague, rabies, rat-bite fever, ringworm, Rocky Mountain spotted fever, swine flu, toxoplasmosis, West Nile virus, and zoonotic diphtheria.2
And the biggest zoonotic disease that is not covered in that list is HIV-AIDS, which affected more than sixty million people leading to our world’s greatest modern plague. While a good deal of ink has been dedicated to the question of how prejudice against the gay lifestyle delayed efforts to properly address the disease, our job as scientists is to provide an explanation of events in the past and how problems might be avoided in the future.
Let’s make sure we understand our terms. The human immunodeficiency virus (HIV) is linked to the condition known as acquired immunodeficiency syndrome (AIDS). There was a brief time when the disease was known as gay-related immune disease (GRID), and many activists claim the name change to AIDS prompted a more balanced examination of the disease. Perhaps this is true.
But what of the genesis of the retrovirus HIV? Where did it come from?
We have a clear answer.
It came from a primate. The field agrees the precursor to HIV was the simian immunodeficiency virus or SIV.
To be more precise, the human virus came from a monkey or chimpanzee virus.
After that, any potential areas of agreement break down.
I vividly recall working as a technician at the Biological Response Modifiers Program at Fort Detrick in the early 1980s, where it was my job to isolate HIV from samples and find a cell line or tissue to grow the virus. If you can’t grow the virus outside a human body, you can’t study it.
What we were told at the time was that the disease probably jumped to humans as a result of Africans forgetting how to cook their food, in this case chimpanzees, often referred to as “bush meat,” and that the promiscuous sexual lifestyles of African peoples (with implications of possible bestiality with primates) led to the cross-species jump and spread of the virus among the human population. I am now appalled that at the time we did not more closely question these assumptions.
Since that time, there have been two competing and, in my mind, closely related theories of how a chimpanzee retrovirus made the jump to humans.
The first was popularized by the journalist Edward Hooper and expanded upon in his lengthy 1999 book, The River: A Journey to the Source of HIV and AIDS, for which he conducted more than six hundred interviews. Of the interviews conducted, Hooper was most impressed with evolutionary biologist Bill Hamilton, who, along with other independent researchers such as Louis Pascal, Tom Curtis, and Blaine Elswood, was proposing an idea that, before my work with XMRV, I would have found quite radical. They proposed that the jump from chimpanzees to humans came as a result of vaccine trials in the Belgian Congo from 1957 to 1960 in which more than five hundred common chimpanzees and bonobos (pygmy chimpanzees) were killed so that their kidney cells and sera could be used to grow the oral polio vaccine. This vaccine was subsequently administered to more than a million Africans during that time period.
Hooper suggests there was great resistance to this idea, since even in the late 1950s and early 1960s there was little public support for the idea of using chimpanzees in such medical experiments. In addition, the Belgian royal family was publicly supporting the idea of wildlife conservation, and the revelation of these actions would go against that image. Hooper believes another reason for resistance to his idea is that if his theory was accepted, it would shake public confidence in the medical establishment as well as lead to multibillion-dollar class action lawsuits for the AIDS epidemic.
This is what Edward Hooper has written on his website about the circumstances surrounding the creation of HIV-AIDS from these experiments and why it makes more sense than the competing bush-meat and “cut hunter” theory.
By contrast, the oral polio vaccine (OPV) theory proposes that an experimental OPV that had been locally prepared in chimpanzee cells and administered by mouth, or “fed,” to nearly one million Africans in vaccine trials staged in the then Belgian-ruled territories of the Belgian Congo and Ruanda-Urundi between 1957 and 1960, represents the origin of the AIDS pandemic. It provides a historically-supported background: that between 1956 and 1959 over 500 common chimpanzees (Pan troglodytes schweinfurthi and Pan troglodytes troglodytes) and bonobos or pygmy chimpanzees (Pan paniscus) were housed together at Lindi Camp (Near Stanleyville in the Belgian Congo, or DRC).3
Hooper goes on to explain that the use of chimpanzees was not technically prohibited by any conventions, but that in most countries around the world at the time, Asian macaques were used in polio virus preparation. As for the claim of other outbreaks, Hooper believes they fit comfortably within the bounds of his theory:
The OPV theory ascribes the minor outbreaks of AIDS caused by other variants of HIV-1 (Group O, Group N and the more controversial “Group P”) to other polio vaccines (both oral and injected) that were prepared in the cells of chimpanzees and administered in French Equatorial Africa (including Congo Brazzaville and Gabon) in the same late fifties period. It ascribes the outbreak of AIDS from HIV-2 (of which it maintains that only two were epidemic outbreaks) to other polio vaccines (both oral and injected) that were prepared in the cells of sooty mangabeys (or other monkeys that had been caged with sooty mangabeys) and administered in French West Africa in 1956–1960. All the other HIV-2 groups that are claimed by bush-meat theorists have infected just a single person, and some OPV theory supporters argue that dead-end, non-transmissible infections such as these are the natural fate of SIVs that infect human beings via the bushmeat route: that unless they are introduced in an artificial manner (as via a vaccine), they simply die out.4
I find myself in complete agreement with Hooper’s analysis. Yes, viruses can jump from one species to another, possibly by the eating of an infected animal. But the natural process of degradation by the digestive system, as well as cooking (even when poorly done) is likely to inactivate most pathogens.
The second plausible theory, which has come to be known as the “bush-meat” theory, is that sometime early in the twentieth century an individual became infected with SIV from handling chimpanzees or chimpanzee bush-meat. It usually involves the actions of some anonymous native hunter (often called the “cut hunter” because he cut himself shortly after having killed a chimpanzee). Added to this scenario is urbanization encroaching upon the jungle, allowing it to be spread by those newly introduced western evils of prostitution and intravenous drug usage.
This theory has recently been expanded by the science writer David Quammen in The Chimp and the River: How AIDS Emerged from an African Forest. Based on an extrapolation of some scientific data, Quammen sets the date for this viral transfer from chimp to human around 1908 in the area known as Leopoldville (later Kinshasa) in the Democratic Republic of the Congo. The description is vivid, and plausible, but I question much about it:
Let’s give him due stature: not just a cut hunter but the Cut Hunter. Assuming he lived hereabouts in the first decade of the twentieth century, he probably captured his chimpanzee with a snare made from a forest vine, or in some other form of a trap, and then killed the animal with a spear. He may have been a Baka Pygmy man, living independently with his extended family in the forest or functioning as sort of a serf under the “protection” of a Bantu village chief . . . There’s no way of establishing his identity, nor even his ethnicity, but this remote southeastern corner of what was then Germany’s Kamerun colony offered plenty of candidates . . .
The chimp too, tethered by a foot or a hand, would have been terrified as the man approached, but also angry and strong and dangerous. Maybe the man killed it without getting hurt; if so, he was lucky. Maybe there was an ugly fight; he might even have been pummeled by the chimp, or badly bitten. But he won. Then he would have butchered his prey, probably on the spot . . .
I imagine him opening a long, sudden slice across the back of his left hand, into the muscular web between thumb and forefinger, his flesh smiling out pink and raw almost before he saw the damage or felt it, because his blade was so sharp . . . His blood flowed out and mingled with the chimp’s, the chimp’s flowed in and mingled with his, so that he couldn’t quite tell which was which. He was up to his elbows in gore. He wiped his hand. Blood leaked again into his cut, dribbled again into it from the chimp, and again he wiped. He had no way of knowing, no language or words or thoughts by which to conceive, that this animal was SIV-positive. The idea didn’t exist in 1908.5
It’s a possible scenario. I can’t say something like that didn’t happen. I just wonder why it hadn’t happened many centuries earlier. Africans had been hunting chimpanzees for thousands of years and cooking them. An interesting addition Quammen makes to the theory is that subsequently the virus spreads slowly among the population. But then starting in 1917, there were vaccination campaigns against sleeping sickness by European doctors who used glass syringes that were reusable. One French colonial doctor during a two-year period treated more than five thousand cases with only six syringes.6 These campaigns peaked in the early 1950s, and by that time the precursor to the deadly strain of HIV had arisen.
When you think about it, you come to the realization there’s a battle of narratives, with science having a definite preference for one over the other.
In the first scenario, unwitting scientists release a plague of massive proportions on the population because of their use of questionable animal experiments, infecting more than sixty million people and causing the death of at least thirty-nine million.
In the second scenario, a chance event in a jungle encounter with an infected chimpanzee leads to cross-species transmission, then because it’s always a good play to blame urbanization and prostitution, as well as maybe a little inadvertent help from western medicine, and you have a new disease!
Is it any surprise that scientists far prefer scenario number two?
While I can’t come to a definitive conclusion as to which scenario is more likely, the first one, in which chimpanzees are directly harvested for their organs and the growing of polio virus, makes the most sense to me. It doesn’t have as many moving parts.
The virus is in a certain percentage of the five hundred chimpanzees sacrificed. They’re cut up, then used to grow polio vaccine, which is then given orally to nearly a million Africans. And there’s another part of the story that makes Hooper’s account sound more plausible.
After Hooper made his claim that the oral polio vaccine grown in chimpanzee tissue and given to humans was the source of the HIV-AIDS epidemic, there was an “investigation.” As I read Hooper’s account, it sounded a lot like the Ian Lipkin investigation into XMRV.
In this great investigation, they sampled stocks of polio vaccine from the 1957–1960 period for traces of chimpanzee DNA, or simian virus. Lo and behold, they found NOTHING!
There’s just one problem. All of the samples they used were from the United States.
They did not have any samples of polio vaccine from Africa. The samples of polio vaccine from the United States had never used chimpanzee tissues as a growth medium or cell line.
They DID NOT test African samples of the oral polio vaccine for that which used chimpanzee tissue.
This is what Hooper wrote about the supposed investigation into the use of chimpanzee tissue in the development of the polio vaccine that was performed by the Royal Society in September of 2000:
Instead of the open and honest debate, and the even-handed investigation of the OPV theory, which had been promised, what actually took place was a carefully-planned attempt to suppress the theory by fair means or foul. The conference became focused around the testing of samples of CHAT vaccine which the parent institute (The Wistar in Philadelphia) had finally released for independent analysis. The vaccinators and the meeting organizers insisted that the vaccine samples were representative of the batches which had been prepared for use in Africa. Since they tested negative for HIV, SIV, and chimpanzee DNA, they concluded that the OPV hypothesis had been disproved— and an acquiescent press largely concurred.
The reality, however, was very different. None of the tested samples had ever been near Africa, let alone prepared for the African trials.
As the weeks and months passed after the meeting, it became clear that a carefully-organized whitewash was being carried out, partly by the original protagonists (who had, among other things, leant on witnesses to change key parts of their stories), and partly by well-meaning research scientists who could not countenance the possibility that their work of the last ten years might be erroneous, and who secondly were unwilling or unable to imagine that their peers might not be telling the truth.7
I’ve never met Edward Hooper, but he was writing this in 2004, years before I ever pursued a similar line of inquiry. I’m sure he must have undergone a similar evolution, from hopeful questioner to disillusioned critic. Is it so difficult to imagine that members of an organization will not believe the worst about their own members? Don’t we see the same pattern among police, members of the clergy, and our political class? Isn’t it the rare member of an organization who sees the flaws of their own group?
We leave scientists alone in their research and practice, expecting somehow that they can self-police. But we do not even allow the police to self-police. There are citizen review boards, internal affairs, and oversight committees.
In a similar manner, we have learned through bitter experience that just because a person is a member of the clergy doesn’t mean they are not capable of crimes against children. We are also beginning to understand that these crimes are not just committed against the flock, but there are more nuns and sisters in the Catholic Church who are coming forward with stories of rape and sexual assault committed by the male members of the clergy. These stories sicken us, but perhaps we have simply trusted too much in unaccountable authorities.
Now, maybe Hooper is wrong about his accusation, but it sounds like a pretty serious charge to make. Given what I observed in the “official” investigation into XMRV and the way they cavalierly rewrote basic principles of virology, I’m more inclined to believe Hooper’s account. The scientific establishment tells their stories and expects we will believe them.
The simian virus gets transferred into humans, and then the question becomes one of immune activation. What happened in the gay community in the late 1970s and early 1980s?
There was a great deal of recreational drug usage, and it’s a scientific fact that anal sex, with its subsequent tearing of tissue, promotes immune activation. The sexual revolution for the heterosexual population, and the lesbian population as well, did not involve such risks.
Are dangers to the human population limited to the use of chimpanzee tissue in the development of medical products, or is it a more general question of any animal tissue? I tend to believe the latter and use as an example the controversy over Simian Virus-40 (SV-40) in the same antipolio campaign of the 1950s and 1960s. The concern is that these viruses may lie dormant in people until some form of immune stimulation, just as we saw with HIV and the gay lifestyle that included multiple partners, sexual activity that involved anal tearing, and high recreational drug usage.
In her Pulitzer Prize-nominated book, The Pentagon’s Brain, detailing the work of the Defense Advanced Research Projects Agency (DARPA), author Annie Jacobsen provides a brief overview of this controversy. One of the DARPA scientists she interviewed for the book was microbiologist Stephen Block, and this is what she wrote:
If the notion of a stealth virus, or silent load, sounded improbable, Block cited a little-known controversy involving the anti-polio vaccination campaign of the late 1950s and early 1960s. According to Block, during this effort millions of Americans risked contracting the “cryptic human infection” of monkey virus, without ever being told. “These vaccines,” writes Block, “were prepared using live African green monkey kidney cells, and batches became contaminated by low levels of a monkey virus, Simian virus 40 (SV 40), which eluded the quality control procedures of the day. As a result, large numbers of people—probably millions in fact—were inadvertently exposed to SV 40.”8
The controversy over SV 40 was whether it would ultimately lead to cancers in humans decades later. The virus would often be found in cancerous tissues, raising the question of whether it was simply a passenger or a causative agent. Again, this is the same concern raised by the finding of bovine leukemia virus in samples of breast cancer tissue and whether the use of growth hormone in the cattle was prompting the expression of this virus. It’s also worth noting that essentially zero testing is done these days of animal viruses contaminating our vaccines or other medical products. Our medical authorities simply assume we’re all tough enough to fight off these contaminating viruses. Jacobsen continues:
Block says that two outcomes of this medical disaster remain debated. One side says the 98 million people vaccinated dodged a bullet. The other side believes there is evidence the vaccine did harm. “A great deal of speculation occurs about whether [simian virus] may be responsible for some diseases” that manifests much later in the vaccinated person’s life, says Block, including cancer.9
Let’s go to the doubters who agree that at least ninety-eight million people were inoculated with a polio virus that was contaminated with SV-40. Is it reasonable to assume that if you fire ninety-eight million bullets, none will cause any harm?
And this only considers the polio vaccine. Every vaccine has been grown in animal tissue, usually of several different species, including monkey, mouse, bird, and cow. Each one of these cross-species events has the potential to transfer a pathogen to humans, or to create some new strain that can cause harm. We have fired several billion bullets of biological ammunition at the human species, and it is the height of arrogance to believe we have caused zero damage.
In my discussion of Ebola, I want to highlight an idea many others have been discussing in recent years in one form or another, but that is likely to reconfigure how we go about promoting health.
For more than a century, we’ve been promoting two different concepts, which when you think about it are fundamentally at odds with each other. The first concept is that we need to ensure our food, air, and water is as free of pollutants and pathogens as possible. I have no problem saying I’m in favor of this effort a hundred percent.
The second concept involves the belief that we need to prime our immune system with weakened or dead pathogens in order to deal with any challenges that might come our way over the course of a lifetime. This is the fundamental idea behind vaccinations.
I think we’re committing overkill of a good idea, and it is leading to tragic unintended consequences.
If we are living in a relatively clean environment, and we have proper nutrition, then our immune system is going to develop naturally. I’ve heard many activists make the claim that vaccinations create “fake” immunity, whereas a robust immune system is more likely to be able to respond to any pathogens that might be encountered in the course of our regular lives in a relatively clean environment. I have a great deal of sympathy for this position.
Here’s one of the things that concerns me as an unintended outcome of vaccinations. If we are taking all the possible pathogens, serious and mild, that we might conceivably encounter over the course of a lifetime, we are being exposed to more pathogens than might otherwise be expected. That exposure is in most cases bypassing critical immunity, such as the skin and gut. Each challenge to the immune system by a vaccination has the potential to dysregulate the immune system. We have no idea what happens when multiple different pathogens are injected at the same time.
The paper that most catalyzed my thinking in this area was published in November of 2009, just around the same time I published my XMRV findings in Science. That paper was published by some of my former colleagues at the National Institutes of Health. The title of it was “War and Peace Between Microbes: HIV-1 Interactions with Co-infecting Viruses,” and it may be one of the most important papers of the last twenty-five years.
From the introduction:
The development of immunology in the last century led to the concept of a healthy “germ-free” human body that repulses and eliminates invading microbes by generating effective immune reactions. Through the years, it became clear that a healthy host is not germ free and does not always fight “germs” but may, rather, live in symbiotic relationships with some of them . . .
Simian immunodeficiency virus (SIV), which has circulated in sooty mangabeys (SIVsm) and African green monkeys (SIVagm) for a long time, does not cause AIDS, despite high replication and lack of immune control (Paiardini et al., 2009). SIV began to infect chimpanzees (SIVcpz) more recently than sooty mangabeys or African green monkeys, and it causes a disease, which is apparently less severe than the one that human immunodeficiency virus type 1 (HIV-1) causes (Keele et al. 2009) . . . Its invasion greatly imbalances the body’s equilibrium with other microbes . . .
The uncontrolled replication of the symbiotic and newly invading microbes contributes to the imbalance of the immune system by perpetuating its uncoordinated activation, which, in turn, further accelerates progression toward AIDS (Figure 1B). Thus, like an orchestra that after a sudden disappearance of the conductor continues to play fragments of the scored melodies, in HIV-1-infected individuals, the immune system continues to play out a chaotic and ineffective attack against microbes.10
There’s a good deal to unpack in all of this, but it’s pretty straightforward.
We’ve come to understand that it’s not enough to simply keep us away from germs, but that our immune system should be strong enough to either defeat those germs to which we’re exposed or reach a state of equilibrium with them. We are finding that natural exposures, such as having the measles, not only provides lifelong immunity, but also tunes the system to make it less likely you’ll have certain cancers when you’re older.
I’ve already talked about the simian immunodeficiency virus (SIV) and the fact that it can be found in chimpanzees, sooty mangabeys, and African green monkeys. Viruses and microbes have the capacity to unbalance the immune system. This can lead to activation of previously dormant viruses, or infection by others that have now turned virulent due to decreased immune function.
The image of an orchestra that has suddenly lost its conductor is one of the best metaphors I’ve ever read for understanding this issue. Without the conductor, the orchestra can continue playing music, but it’s likely to be the wrong song.
And what’s at stake is our health.
And now I come to the recent emergence of Ebola and Zika.
I want you to continue to hold onto that image of an immune system orchestra without a conductor.
It may terrify you to know that I worked with the Ebola virus from 1992 to 1994 at Fort Detrick in a biosafety level 4 lab, the highest level of containment. The Zaire strain was being studied at the US Army Medical Research Institute of Infectious Diseases (USAMRIID), and it was my job to teach it how to infect human monocytes/macrophages without killing them. Because if you can’t grow the virus, you can’t study it.
It may surprise you to know that Ebola was never observed by Western medicine until 1976. Yes, that’s right, hundreds of years of African exploration and development, and we never saw Ebola. But it must have been there, right? Yes, I’m sure it was, either in the bats or certain primates, but it never made that great leap from animals and into humans until after that time.
Again, I go to the CDC’s own website for a brief history of Ebola:
Ebola virus disease (EVD), one of the deadliest viral diseases, was discovered in 1976 when two consecutive outbreaks of fatal hemorrhagic fever occurred in different parts of Central Africa. The first outbreaks occurred in the Democratic Republic of Congo (formerly Zaire) in a village near the Ebola River, which gave the virus its name. The second outbreak occurred in what is now South Sudan, approximately 500 miles (850 km) away.
Initially, public health officials assumed these outbreaks were a single event associated with an infected person who travelled between the two locations. However, scientists later discovered that the two outbreaks were caused by two genetically distinct viruses: Zaire ebolavirus and Sudan ebola-virus . . .
Viral and epidemiological data suggest that Ebola virus existed long before these recorded outbreaks occurred. Factors like population growth, encroachment into forested areas, and direct interaction with wildlife (such as bush-meat consumption) may have contributed to the spread of the Ebola virus . . .
African fruit bats are likely involved in the spread of Ebola virus and may even be the source animal (reservoir host).11
Are we really to believe that in thousands of years of hunting, that Africans did not contract Ebola? It really seems comical to even suggest such a scenario. I believe these pathogens have likely been living in Africans for thousands of years until we did something to disturb the immune system balance of the people of that continent. The recent emergence of pathogenic Zika in Brazil and Columbia is also supported by that hypothesis.
What you do with a vaccination is you temporarily cripple a part of the immune system, as resources are diverted from protecting against other viruses to target the virus from the vaccine.
With multiple vaccinations, you cripple several parts of the immune system at the same time and do nothing to restore the balance of the system.
We don’t know what diseases we are spreading by rendering compromised immune systems susceptible. It makes me angry because some of the best people in the world, like Christian missionaries and medical aid workers, are going to these countries and creating the conditions for terrible outbreaks. They are sending our very best people to unwittingly do the very worst things for the health of humanity.
Let’s return to the CDC’s own website for a listing of outbreaks and numbers of deaths to see if you can’t discern a troubling pattern.
The Sudan outbreak of 1976 had 284 reported cases with 151 fatalities. The CDC website reports, “The outbreak is believed to have started with workers in a cotton factory where 37% of workers in the cloth room were infected.”12 Are we really to believe that workers at a cloth factory, of all the places in Africa, were the most likely to have been out in the bush hunting for monkeys and contracted this virus? Or is it more likely that just prior to coming down with Ebola, there was a workplace vaccination campaign? The other outbreak that year in Zaire had 318 reported cases with 280 deaths, although not much information is provided about the circumstances of that first appearance.
In 1977, there was only one person who contracted Ebola in Zaire and died.
We jump next to 1979, when there was another outbreak in the same area of the Sudan as the 1976 outbreak. The numbers, though, were much smaller this time. There were thirty-four reported cases with only twenty-two fatalities.
A full ten years pass until we see Ebola again, this time in 1989 and in two locations, one in the Philippines and one in the United States.
Both were . . . wait for it . . . facilities that housed monkeys.
Of the Philippine situation, the CDC wrote, “High mortality among Cynomolgus macaques was discovered in a primate facility responsible for exporting animals to the United States. Three workers in the animal facility developed antibodies, but never experienced symptoms of Ebola Virus Disease . . . Ebola-Reston virus was introduced into quarantine facilities in Virginia and Pennsylvania by monkeys imported from the Philippines.”13
In 1990, this same Ebola-Reston virus was introduced to other quarantine facilities in Virginia and Texas by monkeys imported from the Philippines.
In 1992, Ebola-Reston virus was introduced into quarantine facilities in Siena, Italy, by monkeys from the Philippines.
In 1994, there was high mortality reported among chimpanzees in a forest in the Ivory Coast, and a scientist became ill after conducting an autopsy on a wild chimpanzee but later recovered. During that same year, an outbreak occurred in several gold-mining villages in the rainforest around Makakou, Gabon. There were fifty-two reported cases and thirty-one deaths.
In 1995, there was an outbreak associated with a charcoal maker in the forested area around Kikwit, Democratic Republic of the Congo (formerly Zaire). There were 315 reported cases and 250 deaths.
In 1996, there were several small outbreaks. There was one reported case from Russia, where a Russian laboratory worker was infected while working on an experimental treatment for Ebola. There were two outbreaks in monkey facilities in the Philippines and in Texas, with monkeys imported from the Philippines.
All was calm for the next four years until 2000, when in Uganda there was an outbreak of 425 reported cases and 224 deaths.
In 2001, there was an outbreak in the Republic of the Congo with fifty-nine cases and forty-three deaths and one in Gabon with sixty-five cases and fifty-three deaths.
In 2002, there was another outbreak in the Republic of the Congo with 143 reported cases and 128 deaths.
In 2003, an outbreak in the Republic of the Congo had thirty-five reported cases and twenty-nine deaths.
In 2004, a Russian laboratory worker who was working on an Ebola vaccine was accidentally injected with the virus and died. In the Sudan, there were seventeen reported cases and seven deaths.
In 2005, a small outbreak occurred starting with two hunters in the Republic of the Congo. Twelve people were affected and there were ten deaths.
No cases were reported in 2006, but in 2007 a new strain appeared in Uganda, which was significantly less lethal. There were 131 cases, but only forty-two deaths. In the Republic of the Congo there were 264 cases and 187 deaths.
In 2008, there was another small outbreak in the Republic of the Congo, with thirty-two cases and fifteen deaths. In the Philippines, the Ebola virus jumped to pigs and infected six workers at a pig farm, but they did not develop symptoms.
Nothing was reported for three more years until 2011, when a single person was infected with Ebola in Uganda and died.
In 2012, there was an outbreak in Uganda that affected six people and caused three deaths. In the Republic of the Congo, there was an outbreak with thirty-six cases and thirteen deaths.
Nothing happened in 2013, but 2014 saw the largest number of Ebola cases ever. In the Republic of the Congo, there were sixty-nine cases and forty-nine deaths. In the West African countries of Guinea, Liberia, and Sierra Leone, there were 28,610 and 11,308. In Italy, there was one case of an Italian healthcare worker who’d volunteered during the epidemic, but he survived. In Mali, an infected traveler brought the disease, resulting in eight cases and six deaths. In Nigeria, an infected traveler was responsible for twenty cases and eight deaths. In Senegal, an infected traveler was responsible for one case, but no deaths. In Spain, a healthcare worker became infected while treating a patient evacuated from Sierra Leone, but he recovered. In the United States, there were four confirmed cases, with two being nurses who were treating an Ebola patient on American soil. One person died in the United States outbreak.
Next, we jump forward three years to 2017, when there were eight cases and four deaths in the Republic of the Congo.
In 2018, there was another outbreak in the Republic of the Congo with fifty-four cases and thirty-three deaths. The World Health Organization declared the outbreak over on July 24, 2018. This was the ninth recorded outbreak of Ebola in the Republic of the Congo.
In just a little over two pages, I’ve provided the approximately twenty known outbreaks of Ebola and a brief description of the circumstances of each outbreak. Now, let’s really try to consider what’s happening.
Let’s leave aside for a moment the question of why this disease suddenly appeared in 1976. Instead let’s focus on the ten instances of Ebola appearing in animal or scientific facilities.
In 1989, there was an outbreak of Ebola at a primate facility in the Philippines.
In 1989, there was an outbreak of Ebola at primate facilities in Virginia and Pennsylvania.
In 1990, there was an Ebola outbreak at monkey quarantine facilities in Virginia and Texas.
In 1996, a Russian lab worker was infected with Ebola while working on an experimental treatment.
In 1996, there was an Ebola outbreak in monkey facilities in the Philippines.
In 1996, there was an outbreak of Ebola at monkey facilities in Texas with monkeys imported from the Philippines.
In 2004, there was another laboratory worker in Russia who was accidentally injected with the virus and died.
In 2008, the Ebola virus somehow made a jump into pigs and from there infected six workers, but none of them developed symptoms.
Is it just my imagination, or are some of the most likely places on Earth to contract Ebola a scientific lab or hanging around with monkeys in cages, presumably in unhealthy conditions? Not monkeys in the wild.
Let’s move onto the West African outbreak.
In a little bit of research, we came across an interesting account written by Hong Kong-based journalist and former editor of The Japan Times in Tokyo, science writer Yoichi Shimatsu.
The mystery at the heart of the Ebola outbreak is how the 1995 Zaire (ZEBOV) strain, which originated in Central Africa some 4,000 km to the east in Congolese (Zairean) provinces of Central Africa, managed to suddenly resurface now a decade later in Guinea, West Africa. Since no evidence of Ebola infections in transit has been detected at airports, ports or highways, the initial infections must have come from either one of either two alternative routes . . .
The reason for suspecting a vaccine campaign rather than an individual carrier is due to the fact that the Ebola contagion did not start at a single geographic center and then spread outward along the roads. Instead, simultaneous outbreaks of multiple cases occurred in widely separated parts of rural Guinea, indicating a highly organized effort to infect residents in different locations in the same time frame.
The Ebola outbreak in Early March coincided with three separate vaccination campaigns countrywide: a cholera oral vaccine effort by Medicins Sans Frontieres under the WHO; and UNICEF-funded prevention programs against meningitis and polio.14
Let’s just say that these claims might not be able to be substantiated.
However, it seems clear to me that there were three separate vaccination campaigns PRIOR to the West African Ebola outbreak. You simply have to consult news accounts to learn about all of these vaccination campaigns.
Maybe that was a coincidence. I don’t believe in coincidences.
I’ve talked about how one of the major problems with multiple vaccinations is the so-called “war and Peace of the viruses” in which each virus preoccupies a different part of the immune system, leading to a compromised immune system. I give you this publication from the CDC titled “Emergence of Vaccine-Derived Polioviruses during Ebola Virus Disease Outbreak, Guinea, 2014–2015.” Did you catch that term “Vaccine-Derived Polioviruses”? And it happened during an Ebola outbreak. Not among those who came down with the disease, but simply in the community. The abstract reads:
During the 2014–2015 outbreak of Ebola virus disease in Guinea, 13 type 2 circulating vaccine-derived polioviruses (cVDPVs) were isolated from 6 polio patients and 7 healthy contact. To clarify the genetic properties of cVDPVs and their emergence, we combined epidemiologic and virologic data for polio cases in Guinea. Deviation of public health resources to the Ebola outbreak disrupted polio vaccination programs and surveillance activities, which fueled the spread of neurovirulent VDPVs in an area of low vaccination coverage and immunity.15
There are times when my dear colleagues in science make me want to bang my head against a wall. Let’s take that final sentence from the abstract: “Deviation of public health resources to the Ebola outbreak disrupted polio vaccination programs and surveillance activities, which fueled the spread of neurovirulent VDPVs in an area of low vaccination coverage and immunity.”
Let’s translate that mumbo-jumbo into something understandable. Then you’ll realize how that sentence makes no sense.
It should read something like this: “Because of the Ebola outbreak we couldn’t give our polio vaccines, and that promoted the spread of polio viruses from our vaccines.” Really, I encourage you to come up with any other translation.
Here’s what it really means to me. Our vaccines are generating new viruses, and in areas with low immune function, think poor and impoverished (or they’re getting so many vaccinations that their immune system is going haywire trying to keep up), we’re making sure these people will get some type of serious viral diseases like HIV, Ebola, or Zika.
Probably no name is more associated with the West African outbreak of Ebola than Dr. Kent Brantley, the US doctor who was working in Liberia during the outbreak, contracted Ebola, and was flown back to the United States for treatment and recovered. I have a great deal of respect for Dr. Brantley, a strong Christian who believes his ministry is healing people, and I found the account of his ordeal in the book Called for Life to mirror many of my own beliefs.
In the prologue to the book, Brantley wrote, “For the thirty-eight years since Ebola Virus Disease had been identified, every outbreak had been limited to small rural communities. This time, however, was different. This time, Ebola had found the perfect storm of factors, quickly spreading through three countries and into major urban centers.”16 Farther on, his account of the number of outbreaks is in accord with what I understand: “There had been fewer than twenty Ebola episodes since the virus was first identified in 1976. . . . The most deaths from an Ebola outbreak had been 280 in Zaire in 1976.”17
As to what caused the outbreak to be so severe in West Africa, Brantley writes about the main city of Monrovia in Liberia: “In the city, there was limited access to clean water, so many people could not practice proper hygiene.”18 I would also add that West Africa has been through years of instability with various wars, leaving the people in a nutritionally depleted state and vulnerable to pathogens that might be activated.
When Dr. Brantley was diagnosed with Ebola, he contacted somebody he had recently met, Dr. Randy Schoepp, chief of diagnostics with USAMRIID. You’ll forgive me, but after what I’ve learned over the years about what military infectious medical researchers do from my experiences at Fort Detrick, I’m a little wary of any individuals in that kind of a position.
Schoepp went through the options with Brantley, eventually settling on a cocktail of antibodies that were believed to target the Ebola virus. This is what Brantley wrote, and I’m sure you’ll understand immediately what concerns me so much:
Because the drug had not been administered to a human, there was no way of knowing whether it was safe. The serum was derived from a mouse antibody and grown in tobacco plants. It is a type of monoclonal antibody. I knew that monoclonal antibodies were engineered in laboratories to imitate antibodies naturally produced as part of the body’s immune system. That type of treatment had been employed to treat other conditions, and as far as I knew they were generally considered to be safe.19
Yes, we’ve got our lovely little mouse again, and we don’t know what viruses are sleeping in that little rodent, ready to wake up and wreak havoc on the human immune system. And all of that faith in biological products that are “engineered in laboratories” and “generally considered to be safe” is just a little out of my comfort zone. Still, if I’m looking at likely death from Ebola, I’ll take the option that gives me the best chance for survival.
But we need to know how the whole disaster got started. We owe that to humanity.
I think the heart of this darkness lies not in the African jungles, but in our own research labs. We play God without telling the truth about our failures.
But there is little appetite for doing good science about vaccines. Instead, the scientific media simply wants to shout down anybody who asks questions. What happened to persuasion as the appropriate method of civil discourse in our society? When did we suddenly become authoritarian? When did dialogue and listening to one another become a sign of weakness?
Consider this recent article from Scientific American on March 21, 2019. The title is “Opting Out of Vaccines Should Opt You Out of American Society.”20 The subheading reads, “People who are able to take vaccines but refuse to do so are the moral equivalent of drunk drivers.” Wow, that’s an amazing moral comparison. I guess all my years of scientific study and research have made me drunk with curiosity!
Here’s a sad sample of what passes for discussion in what used to be one of the premier magazines for discussion of scientific progress:
There is no moral difference between a drunk driver and a willfully unvaccinated person. Both are selfishly, recklessly and knowingly putting the lives of everyone they encounter at risk. Their behavior endangers the health, safety and livelihood of the innocent bystanders who happen to have the misfortune of being in their path.
The reasons why are simple and straightforward. Vaccines aren’t perfect (e.g., they can wear off over time) and not everyone can be vaccinated. There is one and only one reason to skip a vaccine: being immunocompromised. Some individuals, because of genetic deficiencies or diseases like cancer, cannot receive vaccines. Other people are too young. Vaccines such as MMR (measles, mumps, rubella) cannot be administered before 12 months of age.21
As a person trained in the skill of scientific argumentation, the two quoted paragraphs are almost painful to read. The first paragraph has nothing substantial in it, just fearmongering. Let’s move onto the second paragraph.
Vaccines aren’t perfect. Big understatement.
But what do they discuss as the only problem? They wear off over time. That’s kind of like saying the only thing wrong with chocolate is that when you finish eating it, there’s nothing left. I’d like a little more discussion.
Color me a curious scientist.
Just to be brief about the issue, I think one of the major problems with vaccines is that they’re grown in animal tissues and we don’t know what viruses and pathogens are coming back in the needle. A recent inquiry in December 2018 by the Italian lab, Corvela, on the GlaxoSmithKline vaccine Priorix Terta highlights troubling problems that our technology can now uncover but that few seem to have the courage to investigate. Translated from the Italian, the report finds:
We have continued the investigation, both chemical and biological, on the Priox Tetra, quadrivalent against measles, rubella, mumps, and varicella. We have found . . . proteobacteria and nematoda worms, 10 other viruses through ssRNA, Microviridae (bacterial or phage viruses) and numerous retroviruses including endogenous human and avian retroviruses, avian viruses, human immunodeficiency and immunodeficiency virus of monkeys (fragments that if inserted into the database detect fragments of HIV and SIV), murine virus, horse infectious anemia virus, lymphoproliferative disease virus, Rous sarcoma virus, alphaendornavirus, hepatitis B virus, and yeast virus.22
The technology exists to answer the question of how many different viruses are contaminating our typical vaccines. Look at the problems with this single vaccine. There are indications of viruses from humans, birds, monkeys, mice, and horses, all animals that we use in one way or another in vaccine production. And what about the worms, yeast, and other microorganisms that naturally occur in animal tissue?
If you eliminate the animal tissue, that leaves aborted human fetal tissue, and I think there are significant moral and scientific issues with what happens on a genetic level when you inject human tissue into the bloodstream. Then you get to the issue of chemicals in the vaccines, like mercury, aluminum, formaldehyde, polysorbate 80, and a host of others, and it begins to look like a witch’s brew that would only be given to children in some demented fairy tale.
Personally, I feel like I’m one of the few sober drivers on the road when it comes to the question of vaccines and human health.