Discover more from Remnant | MD
Do viruses cause Cancer? | Virology Series
In medical training, the idea that viruses can cause cancer is taught as fact. Unfortunately, that claim is devoid of historical context, biological plausibility, as well as confirmatory evidence.
The following information is adapted from various historical accounts, including those documented by professor Peter Duesberg of UC Berkeley.
The discovery of viruses began as vectors for infectious disease, but slowly morphed into a field of unproven conjectures. For decades we have been looking for ways to blame cancer on viruses.
At first, we used viruses to account for acute illness that seem to coexist in space and time (AKA outbreaks). They clustered around a geographic location, at a specific point in time. Then, we moved unto identifying novel pathogens, then seasonal pathogens. Eventually we got to harmless skin lesions (herpes, pox). As infectious diseases became far less prevalent - in large part due to the advent of sanitation and access to clean water - there was less and less for virology to diagnose & treat.
The post-polio-era virologists were looking for a new game. Cancer was on the rise. So, they began applying their tools to find the hypothetical cancer-causing virus.
In the Beginning
In 1905, there was a reception for Robert Koch (of Koch's Postulates) who had been awarded the Nobel Prize. German Emperor Wilhelm II noted to have said to Koch:
My dear professor, now you must find the cancer-bug.
...but in german.
Virologists faced two major obstacles:
Cancer is not contagious, but viral disease is.
Viruses reproduce by entering a cell, using its resources to replicate, then break out of the cell - destroying it.
Cancer is a disease in which cells continue to live & propagate uncontrolled. These cells change their behavior to become more aggressive, less cooperative, and invasive of boundaries. As these cells consume your body, like insatiable parasites, you can die.
If a virus destroy cells in their lifecycle, how could it possibly cause them to become immortal & cancerous?
Think about this another way:
If the objective of viruses is to replicate and propagate across time...why would a virus evolve to induce a cellular state (cancer) that is so resource consumptive, that there would be none left for the viral genes that are trying to self-propagate.
In fact, you could make the case that once a cell becomes cancerous - unrestricted growth & replication - it marks the end of the virus. The cancer would deplete the resources required to propagate the virus. Thus, any virus that did cause cancer would take itself out of the evolutionary tree.
As biotechnology got more sophisticated, the virologists began experimenting with them in their hunt for cancer. This seemed to solve their problem (of irrelevance) and enabled them to seize control of the field of cancer research.
They claimed that:
If you wait long enough, the virus would progress from infection to cancer. Anywhere up to 50+ years after the initial infection.
They postulated a defective virus that was unable to multiply (keeping the cell alive), but still able to cause cancer...inventing a unique class of viruses.
To their credit, virologists made a perfectly legitimate observation of a rare event. A fluke of nature virus caused tumor growth in some extraordinarily rare instance, in a susceptible animal.
Enter Rous Sarcoma Virus
The first tumor-virus was observed in 1908.
Vilhelm Ellerman & Oluf Bang discovered that something tiny enough to pass through a bacterial filtration system - assumed to be a virus - caused leukemia in newly infected chickens. Peyton Rous isolated filtrate from a chicken with a solid tumor, and discovered that it caused rapidly growing tumors in other chickens within days of infection - named this Rous Sarcoma Virus (RSV)
RSV is a retrovirus. Retroviruses propagate through the continued existence of the host cell lineage. The more harmless they are, the more successful - because the host lives a long and healthy life. The continued survival of the host cell opens the possibility of potential carcinogenic activity, if even through random mutation.
But, RSV was mostly ignored. We could not find it in humans because human cancers are not contagious - unlike some animal cancers. These viruses would only affect special strains of mice that had been intentionally weakened by generations of inbreeding.
These conditions can cause disease & cancer spontaneously - no need for the virus.
Furthermore, these viruses could not cause cancer in mice from the wild.
Decades later, the virologists would seize upon these scattered experimental observations as precedent to claim that harmless viruses cause cancer.
Funding starts rolling in...
In the late 1930s, 24 grants were distributed by the National Cancer Institute (NCI) in its first 5 years in existence - only 2 went to virus research. Over the next several decades, the NCI kept cancer virology alive. As the virologists took senior positions at the NCI, they used the Rous Sarcoma Virus as justification for funding this line of work.
Ludwik Gross took a position at the Bronx VA, and began research on a virus that caused leukemia in mice. He stumbled upon the same problem - it caused cancer in the sick inbred lab-mice, not the healthy wild mice.
Other researchers quickly began replicating Gross' work. Sarah Stewart discovered a second virus that caused tumors throughout the body - named polyomavirus.
As others bandwagonned, the challenge became self-evident:
Find a virus that causes cancer in humans.
The Hunt Is On
By the 1970s, over a dozen viruses were isolated from mice with leukemia...all of which were as meaningless as the first. Nonetheless, the NIH kept distributing funds. This had the effect of drawing a lot of attention from virologists and grad students.
At some point, people suggested that if they could create a vaccine for the virus, they could prevent cancer!
Wendell Stanley was the first Nobel Prize winner for the study of viruses. In the 1956 National Cancer Conference he stated:
...we should assume that viruses are responsible for most, if not all, kinds of cancer...design and execute our experiments accordingly...no reason to shy away from giving consideration to viruses as causative agents in cancer...
Oncologists knew all too well that tumors rarely contained detectable virus. Why would it? It's not expressing anything other than what the cell needs to replicate & grow without restriction. That's what cancer does.
Carleton Gajdusek became popular in the 1960s because the cancer-virus crowd found his unproven concept of an 'unconventional' slow virus quite attractive. It really helped their virus-cancer case. They needed to rationalize the absence of detectable virus.
Andrew Lwoff suggested the possibility of a 'dormant' virus. He too received a grant from the NCI and got to work.
Despite all of the efforts described above, scientists could find no active virus in tumors.
The fundamental problem remained that, even in the lab setting of viruses inserting themselves into specific cells - by the very nature of resource competition - these viruses would shortly cease to exist.
So, how could one ever prove this hypothesis?
First Human Cancer-Virus (?)
Virologists used the animal models above to study the link between human viruses and cancer. Unfortunately, they could not find such cancer-causing viruses.
So, they developed yet another leap in logic.
According to their new framework, the virus could cause a tumor long after the initial infection...and without ever reactivating → the latent virus.
The last remaining rules of infectious disease and rationality had disappeared.
Over the decades & millions spent on this fruitless effort, viruses had been attributed with the following superpower:
infect a new host
remain latent for any length of time
then, cause cancer without ever being reactviated
Virologists could now claim that any cancer is infectious by blaming any virus that they could find a trace of...either fragments or antibodies (a classical sign of immunity). How would you disprove this?
Akin to proving God does not exist.
Enter Burkitt Lymphoma
In the 1950s, the surgeon Dennis Burkitt was working in Uganada. He noted large numbers of children with lymphoma. Lymphoma seemed to afflict people in central Africa. Noticing a correlation of disease with climate, he proposed that it was contagious.
In London, M. A. Epstein had tissue samples flown back for study. Epstein began the hunt for the virus. He and his lab associate, Yvonne Barr, grew the tumor cells in lab conditions, and searched with electron miscroscopy.
They found one previously unknown herpes virus - now known as the Epstein-Barr Virus (EBV). Initially thought to be the causative agent of lymphoma…and believed to cause mononucleosis (the kissing disease).
But, EBV causes mono before the immune system has mounted a response against it. In the case of Burkitt's Lymphoma, it is claimed to occur over 10 years after EBV has been neutralized.
Epstein could only find EBV in lymphoma cells cultured outside of the body, under laboratory conditions.
In other words, the virus would reactivate only in the absence of an immune system.
Molecular Sleight of Hand
Since patients with lymphoma rarely had detectable EBV, the virus-hunters had to perform another magic trick to convince people of their hypotheses.
When your immune system encounters a novel pathogen, it generates long-lasting immunity in several fashions. One component of this is to generate immunoglobulins (antibodies) - some of which act acutely and others remain for longer periods of time. In either case, the presence of IgG antibodies is indicative of robust long-term immunity.
Since they could not detect the virus itself in patients with EBV - they decided that a test for the antibody against EBV would be sufficient to diagnose EBV-related cancer. It is completely consistent with their fictitious claims:
virus remains dormant after initial infection
so dormant in fact, it is not detectable
latent viruses need not reactivate to cause cancer
thus, they used any indicator of prior infection to confirm that the virus causes cancer decades later...
A New Hope?
This proved to be rather promising for the virologists, because they soon found that almost everyone with Burkitt's Lymphoma had antibodies to EBV.
Unfortunately, they slowly realized that the entirety of the central African population, with or without cancer, also had antibodies to EBV. In the USA, roughly half of the population has been exposed to EBV - but an exceedingly small number of people have Burkitt's Lymphoma.
Thus, virologists generated more problems than they solved:
Why did the vast majority of EBV+ people never get lymphoma?
Why is the lymphoma less common than mono?
Why is a central African that is EBV+ almost 100x more likely to get lymphoma compared to an American who is EBV+?
Epstein and his colleagues then decided that there was a cofactor in Africa, that made it more likely for EBV to lead to lymphoma - malaria.
Since once infection was insufficient to explain the occurrence of cancer, they thought two infections would certainly plug the holes in their story.
As the years progressed, several scientists began suggesting that EBV also caused another cancer: this time nasopharyngeal carcinoma - though only in some eastern countries with high EBV antibodies.
Just as with Burkitt's Lymphoma, many of the patients with nasopharyngeal cancer had never been infected by the virus...
The EBV-cancer hypothesis accelerated grant-funding for cancer-causing viruses. It is worth noting that EBV as a causative agent of Burkitt's Lymphoma and Nasopharyngceal Carcinoma are taught as fact in college & medical school.
However, you would struggle to find a single doctor who knows the history of these assertions.
The real question is rather simple:
If the bedrock of virus-cancer research is as shakey as has been outlined above...then what else is wrong?
What else did a bunch of nerds in a lab lie about to garner attention and funding?
Remnant | MD is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.