Judy Mikovits

Judy Mikovits Suggests Retroviruses Play a Role in COVID-19

Posted by

0


Transcending Fear — Surgeon General of Florida Speaks Out

https://articles.mercola.com/themes/blogs/mercola/VideoPanel.aspx?PostID=994600&v=20220904&CacheVideo=1

Story at-a-glance

  • Cellular and molecular biologist Judy Mikovits, Ph.D., believes COVID-19 — the disease — is not caused by SARS-CoV-2 alone, but rather that it’s the result of a combination of SARS-CoV-2 and XMRVs (human gammaretroviruses)
  • SARS-CoV-2 also appears to have been manipulated to include components of HIV that destroys immune function along with XMRVs
  • Those already infected with XMRVs may end up getting serious COVID-19 infection and/or die from the disease. Mikovits’ research suggests more than 30 million Americans carry XMRVs and other gammaretroviruses in their bodies from contaminated vaccines and blood supply
  • Mikovits believes 40 years of data suggest Type 1 interferon at a very low dose would be an ideal treatment for COVID-19
  • RT-PCR (reverse transcription polymerase chain reaction) testing, currently used to diagnose active infection by detecting the presence of SARS-CoV-2 genetic material, overestimates infection rates. For an accurate account of COVID-19 prevalence, we need to test for antibodies

Judy Mikovits, Ph.D. is a cellular and molecular biologist,1 researcher and founding research director of the Whittemore Peterson Institute that researches and treats chronic fatigue syndrome (CFS) in Reno, Nevada.

She is likely one of the most qualified scientists in the world to comment on this disease because of her groundbreaking research in molecular biology and virology. Mikovits is absolutely brilliant but, like many gifted researchers, her complex discussions on science are quite challenging for the average lay person to follow.

For this reason, I present her interview in a different format, cutting and splicing pieces together to present a more cohesive and coherent presentation of her many important points. I would encourage you to watch the initial, very short, videos first, so you will be well-grounded, and if you are motivated, watch the entire interview at the bottom of this article.

Because there were so many surprising and important revelations in this interview I will present part 2 next week along with an interview with Bobby Kennedy Jr. which will revolve more on the vaccine issue.

Mikovits Doesn’t Believe SARS-CoV-2 Is the Cause of COVID-19

https://www.bitchute.com/embed/Ts42IGOjnxS1/ Video Link

One of the most shocking revelations Mikovits reveals is that she doesn’t believe SARS-CoV-2 is the cause of COVID-19 but merely serves to activate or wake up a dormant XMRV infection. To support her assertion, she states that COVID-19 patients have the same cytokine signature as the gammaretrovirus XMRV, which she published many years ago.

XMRV stands for “xenotropic murine leukemia virus-related virus.” Xenotropic refers to viruses that only replicate in cells other than those of the host species. So, XMRVs are viruses that infect human cells yet are not human viruses.2

The XMRV retrovirus is actually the virus that has the same cytokine storm signature as COVID-19, not coronaviruses, which are far more benign. (I delve into what retroviruses are in another section further below.)

Additionally, there may be other infections that also are contributing to the infection, such as Borrelia and Babesia or parasites, which may be why some of the antiparasite drugs like Ivermectin and hydroxychloroquine are working.

Vaccine Gammaretroviruses Have Adapted and Are Aerosolized

https://www.bitchute.com/embed/tQQWQPQtRmUn/ Video Link

Getting back to the issue of gammaretroviruses, Mikovits’ research showed that many of our vaccines are contaminated with them. How did this happen? In short, vaccine viruses were replicated and grown in animal cell cultures that were already contaminated with retroviruses. In other words, the root of the problem stems from the use of contaminated cell culture lines.

Vaccine manufacturing frequently involves the use of animal tissues and many vaccines are grown in animal culture cell lines. As noted in the 2010 paper, “Of Mice and Men: On the Origin of XMRV,” published in Frontiers in Microbiology (which Mikovits did not work on):3

“The novel human retrovirus xenotropic murine leukemia virus-related virus (XMRV) is arguably the most controversial virus of this moment. After its original discovery in prostate cancer tissue from North American patients, it was subsequently detected in individuals with chronic fatigue syndrome from the same continent …

The detection of integrated XMRV proviruses in prostate cancer tissue proves it to be a genuine virus that replicates in human cells, leaving the question: how did XMRV enter the human population?

We will discuss two possible routes: either via direct virus transmission from mouse to human … or via the use of mouse-related products by humans, including vaccines. We hypothesize that mouse cells or human cell lines used for vaccine production could have been contaminated with a replicating variant of the XMRV precursors encoded by the mouse genome.”

Mikovits goes even further, explaining that, “It became clear in 2011 that these [gammaretro]viruses had adapted to become aerosolized.” This is a rather shocking finding, and this, Mikovits says, is what allows the gammaretroviruses to spread in laboratories from one cell line to another.

This could be related to research catalyzed by Charles Lieber, the former head of Harvard’s chemistry department, who is a nanoscience expert and was arrested by federal authorities in January 2020 for working with the Wuhan Virology Institute.

Lab workers may also be inadvertently spreading them as they are using cell lines contaminated with retroviruses in vaccine production that could result in the spread of these retroviruses via the finished vaccine. Mikovits suspects COVID-19 may in fact be a type of vaccine-derived or vaccine-induced retroviral infection.

“I don’t believe [COVID-19] is infection from without,” she says. “I believe the spread across [210] countries4 is from injection, and there’s enough evidence to support that.”

SARS-CoV-2 — A Combination of SARS, Gammaretroviruses and HIV

Another of her theories is that SARS-CoV-2 is unlikely to have had a zoonotic origin but is likely synthetically produced. She believes it originated in and escaped or leaked from a biosafety laboratory. Mikovits believes both scenarios might be at play, where a lab-created virus, SARS-CoV-2, is causing serious infection and/or death only in those who have underlying retroviruses in their bodies.

Mikovits suspects that people who do not have retroviral infections, SARS-CoV-2 causes no or only mild symptoms. Another possibility is that the SARS-CoV-2 virus is the result of growing coronaviruses in retrovirus-contaminated cell lines, producing a gammaretrovirus-carrying virus.

According to Mikovits, her 2009 through 2011 work suggested 25 million to 30 million Americans were carriers of XMRVs and other gammaretroviruses. That estimate is over a decade old now so the number is likely far higher.

“There is a family of gammaretroviruses, most likely [in] contaminated blood supply and vaccines that are still to this day, almost 10 years later, being injected,” she says.

“We don’t need an infectious virus if you inject the blueprint, if you inject the provirus. And … there are a lot of data to support COVID-19 is not SARS-CoV-2 alone, that it’s SARS-CoV-2 and XMRVs (human gammaretroviruses) and HIV.”

Might Wearing a Mask Worsen Your Odds of Illness?

https://www.bitchute.com/embed/scdYZhdaIrBI/ Video Link

Mikovits is also highly critical of the recommendation (and in some places mandate) to wear a face mask or fabric cover such as a bandana around your face. She believes:

“Wearing a mask is going to cause more secretions and give more cells a home and amplify any viruses. [Wearing a mask is] immune suppressive; it’s going to limit your body’s ability to produce Type 1 interferon.

You’re driving the infection in yourself and you’re not preventing the spread. [Instead], you’re amplifying [replication of] not just [SARS-CoV-2] but also many other [viruses], including your XMRVs, influenza or other dormant viruses.

What keeps those dormant viruses dormant? Your natural killer (NK) cells, your mast cells, your macrophages. That’s where you’re getting the inflammatory signature.

So, every virus you amplify is driving the inflammatory signature, and you’re going to get sick. [The resulting illness] doesn’t have to be SARS-CoV-2 at all. You’re making yourself sick [by bringing dormant viruses out of dormancy]. It’s insanity.”

Wearing a face mask after getting a live flu vaccine may further worsen your odds, she says. Why? Because you’re injecting three or more live flu virus strains into your body, which lowers your immune function. You’re also going to shed the viruses contained in the vaccine. If you wear a mask, Mikovits says, you’ll shed those viruses into the mask, which could encourage illness.

On the other hand, not wearing one might jeopardize the health of others. “If you’re shedding [the viruses] into the air, you’re going to make somebody else get another upper respiratory infection that’s going to allow [SARS-CoV-2] to make them sicker,” she warns.

Why PCR Testing Is a Bad Idea

https://www.bitchute.com/embed/o3EbWZ5NoNK9/ Video Link

We’re also being lied to about the prevalence of infection. At the height of the pandemic, we saw inflated case numbers for the simple reason that the Centers for Disease Control and Prevention stopped requiring doctors to do testing in order to confirm that a patient is in fact infected with SARS-CoV-2 or died from COVID-19. The numbers now include “suspected” and “assumed” cases.

Naturally, without widespread and accurate testing, there’s no way to get a clear idea of how prevalent the infection is, and how many actually get sick and die from it. The initial emphasis on PCR testing resulted in massive false positives and greatly inflated numbers of those infected.

As noted by Mikovits, confirming each case through testing matters greatly, as there are hundreds, if not thousands, of microbes that can cause upper respiratory infections, including seasonal influenza viruses. None of those should be lumped in with COVID-19 if we want to understand the true nature and danger of this disease.

What’s more, the initial decision to use RT-PCR (reverse transcription polymerase chain reaction) testing instead of antibody testing was an unwise one, as it virtually guaranteed an overestimation of the problem. RT-PCR is now being used to diagnose an active infection by detecting the presence of SARS-CoV-2 genetic material.5 However, by doing that, you end up with high rates of false positives. Mikovits explains how the RT-PCR test works:

“We’re taking a swab and scraping some epithelial cells [from the back of the sinuses or throat] because that’s what coronaviruses infect … We get a little RNA — because it’s an RNA virus — we reverse-transcribe that, meaning write it backwards with enzymes in the lab, and then we amplify it [through a] polymerase chain reaction …

We’re only taking a piece of the virus, we’re not taking the whole virus … The first thing about [the PCR] test is, it was admitted by the U.S. Food and Drug Administration and the CDC that the tests put out by the CDC were contaminated.

And when you amplify something a million times, or 10 million times — whatever they do in the 30 cycles or so — it’s logarithmic that RNA then is way overestimated … [But] no [viral] particle was identified or isolated from your saliva or from your nasal passages. Nobody took the secretions from your nose or your mouth and isolated the [actual] viruses.

[When I isolated] HIV in 1983, I isolated it from saliva. What you do is you take the virus and grow it in any human cell, in an appropriate cell line, and you make many copies. [Viral replication] means you have [a positive test for] that virus. Then you sequence the whole virus.

A PCR [test, on the other hand] can give you a lot of false positives [by amplifying RNA fragments].

We [also] showed the people that had [HIV] infection had antibodies; that they had been fully exposed and it was not a piece of nucleic acid in a biopsy or in their throat or in their nose. [A piece of nucleic acid] is not a virus. And it’s certainly not infectious.

If RNA is there and in the tiniest amount, I’m not going to cough it on somebody, especially if I’m not coughing. I’m not going to breathe that [out and infect] somebody because there’s no evidence of an infectious virus.”

Better Testing Strategy: Antibodies

Rather than using PCR testing, “what should have been done is test for antibodies,” Mikovits says. This is what was done in South Korea. An antibody test will tell you whether you had the infection at some point, and have developed a strong immune response or immunological memory that will allow you to fight the infection should you encounter it again.

“Epidemiology is not done with PCR. In fact, Kary Mullis who invented PCR, Nobel Laureate, and others, said PCR was never intended for diagnostic testing. So that puts that to bed.

It takes nothing to develop a really good serology [i.e., antibody] test … [It takes] a few weeks. It’s pretty easy because the people who have recovered have antibodies. So, you isolate those antibodies, you take their plasma, you purify the antibodies, and then you can grow them.

Then you develop the tests… It’s usually ELISA or Western Blot [which check for] the protein and the antibody binds. You form an immune complex, and you detect it with a dye. You can do that test with a finger stick … and it takes 15 minutes to get the answer, almost like a pregnancy test.”

My belief is that the use of PCR instead of a proper antibody test was intentional, as it inflates the case numbers. Mikovits agrees, saying “I wouldn’t get any tests right now. I’d simply wash my hands and drink hot lemon water as I always do for any flu season.”

Evidence SARS-CoV-2 May Be a Lab-Created Virus

https://www.bitchute.com/embed/GbAnM24CXcH3/ Video Link

In the Epoch Times documentary, “Tracking Down the Origin of the Wuhan Coronavirus,”6 Mikovits details some of the evidence supporting the view that SARS-CoV-2 is not a naturally-evolved virus, but rather a laboratory concoction.

One piece of evidence is that the virus contains a protein envelope from the HIV virus. It’s also very similar to SARS which, according to bioweapons expert Francis Boyle, is an engineered bioweapon.

As explained by Mikovits, an Indian paper7,8 detailed the presence of Gp120, a protein envelope from the HIV virus. That paper was quickly retracted due to political pressure. However, Mikovits colleague, Luc Montagnier, made a similar discovery, finding Gp41 in the SARS-CoV-2 virus, which is the transmembrane domain of the HIV virus.

“The folks from India also had GAG. That’s structural proteins. That gives you a clue that it wasn’t a CRISPR technique or a pseudotyping where the envelope was expressed in a gene therapy-type of way. If it were CRISPR, you wouldn’t put the GAG sequences in there.

What was done is, the virus was acquired as they grew SARS-CoV-2 in Vero-E6 cells — the monkey kidney cells where you get HIV.

Simian immune deficiency virus was the origin, and we were told all the way back in the 80s that somebody forgot to cook their food in Africa and a few promiscuous men spread this [HIV] virus around the world. So, you can see again the patterns of the lies and of what people end up believing.”

The addition of this envelope protein from HIV gives SARS-CoV-2 the ability to impair the immune system. It also contributes to its pathogenicity. Mikovits continues her explanation:

“The first thing is, you must grow a virus to make a lot of it. So, you grow it in cell lines. They didn’t take [SARS-CoV-2] from the bat and it jumped into a human. It normally goes through another cell [from] a monkey or a smaller animal. The cell line that supports the growth and expansion [of viruses] are monkey kidney cells.

Maybe [SARS-CoV-2] is not engineered at all … but the end result is, now it not only infects the epithelial cells of the lungs, it infects the white blood cells, it infects the immune cells. We see the splenomegaly in large spleens, we’re seeing penias, cytopenias. We’re losing cells like HIV-killing T-cells …

So, it’s got not only an expanded host range, but also disease symptoms that make no sense for a coronavirus.

Hence, we’re killing people because they’re treating an upper respiratory infection, and you’re getting that inflammatory disease signature because you’re infecting the very innate immune response, the macrophages, the monocytes, the natural killer cells, the T cells. And it’s primarily the T-cells in the macrophages because those are the cells HIV 120 and Gp41 infect through CCR5 in the CD4 receptor.

So now you’re going to lose your adaptive immune response, you’re going to drive the inflammation. And it’s the fire [of inflammation] that does the tissue damage.”

Another piece that hints at SARS-CoV-2 being a manufactured virus is the construction of its spike proteins, which bind to ACE2 receptors to gain access into the cell. This appears to be an engineering feature. According to Mikovits, it’s quite clear that the spike proteins came from the original SARS virus, which also infects through ACE receptors.

There are also “single point mutations there that make it far more infectious, easier to spread,” she says, “and how those were acquired, nobody really can say.” At least not yet. Nanotechnology may also have been used to aerosolize it for ease of transmission.

“The nano[size] further increases the host range. So now you can go into every cell. Now you can go across the blood brain barrier. That’s nano. Now you don’t need a receptor. You can breathe it, it can go into every cell of the body. You don’t need the gatekeeper. You don’t need the receptor. You don’t need the lock and key.”

Contaminated Cell Line Shared With Wuhan Biolab

According to Mikovits, one contaminated cell line is the Vero monkey kidney cell line called Vero E6, which was given by Fort Detrick — a U.S. Army Medical Command installation that hosts many of our national biological defense programs and houses the National Cancer Institute laboratory where she used to work — to the biosafety 4 laboratory (BSL-4) in Wuhan, China. This cell line is what the Wuhan lab used to grow and study coronaviruses, she says.

The Vero cell line is listed in the 2015 paper,9 “A SARS-like Cluster of Circulating Bat Coronaviruses Shows Potential for Human Emergence,” co-written by University of North Carolina researchers and Dr. Shi Zhengli, a Chinese virologist at the Wuhan lab who in 2010 published a paper10 discussing the weaponization of the SARS virus.

The contaminated Vero monkey kidney cells were also used in the production of polio vaccines, Mikovits notes. The original polio vaccines were passed through mice brains, as we didn’t have cell lines in the 1930s when that vaccine was originally developed. According to Mikovits, the spread of this Vero retrovirus has occurred through laboratory workers and hospital caretakers for decades.

“That’s why the family studies we did were so important,” she says, referring to studies in which retroviral transmission was tracked to determine how it spread between family members.11

Alas, whenever patterns were detected, she was always directed to cover them up. Her refusal to hide the information from the public was what led to her firing in 2011. According to Mikovits, we’re seeing the same pattern of sweeping evidence under the rug now during the COVID-19 pandemic.

“The patterns are the same as far as the science goes, and the patterns are the same as far as the political corruption, the plague of corruption, in covering up data,” she says.

Mikovits Pioneering Research in XMRV

In 2009, Mikovits got embroiled in controversy when she wrote a paper reporting that a retrovirus known as xenotropic murine leukemia virus-related virus may play a causal role in CFS and other diseases, including autism.

Her career background and past troubles also involved Fauci who, according to Mikovits, is guilty of scientific fraud. She details this in her book, “Plague of Corruption: Restoring Faith in the Promise of Science.”

According to Mikovits, Fauci does not appear to have changed his stripes, and is still misleading the public and hiding the truth about SARS-CoV-2, just like he did with the HIV virus and retroviral-associated diseases.

“I think the way to think about the background of what’s going on right now is to go back to my first interactions with Dr. Tony Fauci when I was a 25-year-old lab technician in the National Cancer Institute. At that time, we had isolated — from blood and saliva — the lymphadenopathy virus.

[Lymphadenopathy-associated virus (LAV)] was the name given to it by Luc Montagnier, the Nobel Laureate, [who] first isolated and discovered that virus and its association with HIV/AIDS.12

In that situation, Fauci delayed the serology testing [to find out] who was exposed [to HIV]. It was politicized such that the only people that were [said to be] susceptible to getting infected with HIV was gay men [and] IV drug users.

The country was told not to worry about it. It was only spread through blood and body fluids and shouldn’t be a problem for most other people. So, the testing that could have been done wasn’t done because of political reasons, and the treatments weren’t done because Fauci had patents, and — we didn’t know this at the time — the wrong type of treatment was used. That led to the spread and [death] of millions worldwide …”

The Discovery of Human Gammaretroviruses

Ultimately, Mikovits and her colleagues discovered that the HIV virus was spread through a contaminated blood supply. After that, they proceeded to look into other “clearly retroviral-associated diseases,” such as CFS,13 certain kinds of autism, cancers, leukemias and lymphomas.

Gammaretroviruses14 are viruses that can cause cancer, leukemia and immune deficiencies in various animals. Examples include murine leukemia virus, feline leukemia virus and mink focus forming virus. As explained in a 2011 paper on gamma retroviruses:15

“Retroviruses are evolutionary optimized gene carriers that have naturally adapted to their hosts to efficiently deliver their nucleic acids into the target cell chromatin, thereby overcoming natural cellular barriers …

Retroviral vectors are fascinating and efficient delivery tools for the transfer of nucleic acids. As a hallmark, all retroviruses are capable of reverse transcribing their single stranded RNA genome into double stranded DNA, which will be stably integrated into the host cell genome.

As highly evolved parasites they act in concert with cellular host factors to deliver their nucleic acid into the nucleus, where they exploit the host cell’s machinery for their own replication and long-term expression occurs.”

The key take-home here is that retroviruses are “integrated into the host cell genome,” and infection can result in “long-term expression.” In other words, once they’re in your body, they can remain dormant, only to reactivate when conditions are favorable. In this regard, they’re quite different from your average virus that, when you’re exposed, invades your cells, replicates and causes symptoms, and is eventually eliminated from your body through your immune response.

In 2009, Mikovits and her team discovered and isolated the first human gammaretrovirus family of retroviruses, known then as XMRVs. As mentioned earlier, XMRV stands for “xenotropic murine leukemia virus-related virus.” Xenotropic refers to viruses that only replicate in cells other than those of the host species. So, XMRVs are viruses that infect human cells yet are not human viruses.16

My Entire Interview With Judy Mikovits

To reiterate some of the key take-home messages Mikovits delivers in this interview:

• She believes COVID-19 — the disease — is not caused by SARS-CoV-2 alone, but rather that it’s the result of a combination of SARS-CoV-2 (which appears to have been manipulated to include components of HIV that destroys immune function). Previous XMRV (human gammaretroviruses) infection may facilitate SARS-CoV-2 to express the COVID-19 illness.

Put another way, COVID-19 may be initiated by SARS-CoV-2 but dependent upon a preexisting infection with and awakening of other viruses such as XMRV, gamma retroviruses, possibly Lyme and other coinfections, including parasites, and this is why anti-parasitic medications like hydroxychloroquine and Ivermectin help.

• Blood products and vaccines are contaminated with XMRVs that can damage your immune system and cause CFS, cancer and other chronic diseases. The viruses spread within laboratories as they have adapted to become aerosolized, and contaminate cell lines used in vaccine production and other viral research, including research on coronaviruses.

• Flu vaccines have spread a host of dangerous viruses around the world, which can then interact with SARS COV-2.

• It is possible to develop safer oral vaccines, and interferon alpha could be a valuable treatment alternative against COVID-19. Aside from interferons, other treatment strategies discussed in our interview include hyperbaric oxygen therapy, cannabinoids (CBD), peptide T and antioxidant support.

• SARS-CoV-2 is more dangerous and virulent than typical coronaviruses because it includes sequences of HIV, SARS and another virus, which enable it to infect more than just your respiratory epithelium. It can also infect blood cells and hematopoietic organs such as the spleen.

Source: mercola.com

Virology: Fighting for a cause.

Posted by

0


When Judy Mikovits found links between chronic fatigue syndrome and a virus, the world took notice. Now, she’s caught between the patients who believe her work and the researchers who don’t.

Ewen Callaway

On a sunny January afternoon in Santa Rosa, California, a small crowd waits patiently for Judy Mikovits to arrive. She is scheduled to deliver a talk on a mysterious virus called XMRV, which she believes underlies chronic fatigue syndrome. Although she’s two hours late — held up by fog at San Francisco International Airport — not a single person has left. And when she arrives, they burst into applause.

To a rapt audience, she gives a chaotic and wide-ranging talk that explores viral sequences, cell-culture techniques and some of the criticisms that have been thrown at her since she published evidence1 of a link between XMRV and chronic fatigue in 2009. Afterwards, Mikovits is swarmed by attendees. A middle-aged woman who spent most of the talk in a motorized scooter stands up to snap pictures of her with a digital camera. Ann Cavanagh, who has chronic fatigue and has tested positive for XMRV, says that she came in part for information and in part to show her support for Mikovits. “I just wish there were a hundred of her,” Cavanagh says.

The event was “surreal”, says Mikovits, a viral immunologist at the Whittemore Peterson Institute for Neuro-Immune Disease (WPI) in Reno, Nevada. She is discomfited by the attention from patients, which at times borders on adulation. But her reception among scientists has been markedly cooler. Numerous follow-up studies have found no link between the virus and the disease; no group has published a replication of her findings; and some scientists argue that XMRV is an artefact of laboratory contamination. Now, even some of Mikovits’s former collaborators are having second thoughts.

Mikovits has dug in, however, attacking her critics’ methods and motives. She says that their distrust of her science stems from doubts about the legitimacy of chronic fatigue syndrome itself. Chronic fatigue, also known as myalgic encephalomyelitis, affects an estimated 17 million people worldwide, but it is extremely difficult to diagnose. Many with the disorder are told that their symptoms — which include exhaustion, joint and muscle pain, cognitive issues, and heart and respiratory problems — are psychosomatic. “I had no idea there was that much bias against this disease,” Mikovits says.

The stakes are high and many are taking the risks seriously. Several countries have barred people with chronic fatigue from donating blood in case the virus spreads (see ‘Something in the blood’). And the US government has launched a US$1.3-million study to investigate the link. Patients are already being tested for XMRV, and some are taking antiviral drugs on the assumption that the virus causes chronic fatigue by attacking their immune defences. Many say that such action is premature, but Mikovits is steadfast. “We’re not changing our course,” she says.

First findings

In October 2007, Mikovits attended a prostate-cancer meeting near Lake Tahoe, Nevada, where she met Robert Silverman, a virologist at the Cleveland Clinic in Ohio. Silverman co-discovered XMRV, which stands for xenotropic murine leukaemia virus-related virus2. While examining human prostate tumours, he and his collaborators found genetic sequences that resemble retroviruses found in the mouse genome. Like all retroviruses, XMRV rewrites its RNA genome into DNA on infection, then slips the DNA into the genomes of host cells. Ancient remnants of such viruses litter animal genomes. But the only active retroviruses conclusively linked to human disease are HTLV-1, which causes leukaemia, and HIV.

At the meeting, Silverman was presenting research linking XMRV to deficiencies in a virus-defence pathway. Mikovits recalled that the same pathway was weakened in some patients with chronic fatigue. She wondered whether the prostate-tumour virus could also be behind chronic fatigue. After the meeting, Silverman sent Mikovits reagents to test for XMRV.

The idea excited Mikovits, but she had other priorities. After stints in industry and at the US National Cancer Institute (NCI) in Maryland, she had recently joined the WPI to lead its research programme. The WPI was founded in 2006 by physician Daniel Peterson, an expert on chronic fatigue, and by Annette Whittemore, the wife of a well-connected Nevada businessman, whose daughter Andrea has had chronic fatigue for more than 20 years. The Whittemores spent $5 million establishing the WPI, and several million more to support Mikovits’s research, which has attracted few other grants.

At the WPI, Mikovits established a sample collection from Peterson’s patients and began screening it for signs of an infection. A litany of pathogens has been linked to chronic fatigue over the years, including Epstein-Barr virus, Borna disease virus, human herpes virus 6 and HTLV-2. None panned out. Still, the disorder bears some hallmarks of an infection. Many patients report acute illness before chronic symptoms appear, and their bodies often show signs of an immune system at war. The disease can also crop up in apparent outbreaks, including one characterized by Peterson near Lake Tahoe in the 1980s.

Just before Christmas 2008, Mikovits turned her attention to Silverman’s reagents. She and her postdoc, Vincent Lombardi, known as Vinny, asked a graduate student to test for XMRV DNA in white blood cells from some of the most seriously ill people being studied at the WPI.

The first try turned up just two positives out of 20. But by tweaking the conditions of the test, Mikovits says her team found XMRV in all 20. “Vinny and I looked at each other and said, ‘Well, that’s interesting’,” she says. They spent the next few weeks convincing themselves that they were onto something, and soon conscripted Silverman and Mikovits’s former mentor at the NCI, Frank Ruscetti, to help prove that XMRV infection was behind chronic fatigue.

“We really retooled our entire programme and did nothing but focus on that,” she says. They kept the effort under wraps, dubbing it ‘Project X’. Even Peterson and the Whittemores weren’t clued in. Mikovits says that the secrecy was necessary because her team also found XMRV in the blood of some healthy people, raising concerns about blood products. She hoped to build an airtight case because she worried that sceptical public-health officials would undermine her work.

In May 2009, the team submitted a paper to Science reporting the identification of XMRV genetic material in two-thirds of the 101 patients with chronic fatigue they had tested and in 3.7% of 218 healthy people. They also included data suggesting that infected white blood cells could pass the virus on to uninfected cells.

“They call me every single day. I spend so much time trying to understand the patients, to understand this disease.”

Reviewers wanted more evidence: a clear electron micrograph of virus-infected cells, proof that patients mounted an immune response to the virus, an evolutionary tree showing XMRV’s relationship to other viruses and the locations where viral DNA was integrating into patient genomes. Mikovits’s team went to work. “None of us took any time off, not even a weekend,” she says. They resubmitted the paper in early July with everything the reviewers had asked for, except the DNA integration sites, which many scientists consider a gold standard in proving a retroviral infection.

Later that month, NCI officials who had learned about the work invited Mikovits to give a talk at a closed-door meeting with other XMRV researchers and government scientists. “When I finished speaking you could’ve heard a pin drop,” she says. Mikovits says she thinks at least one of her manuscript’s reviewers was at the meeting, because soon after, she got a call from a Science editor. Their paper had been accepted.

Jonathan Stoye, a retrovirologist at the MRC National Institute for Medical Research in London, wrote a commentary about the paper for Science3. He had never heard of Mikovits, but Frank Ruscetti’s name on the paper gave him confidence, he says, and “if it were true, it was clearly very important”. Stoye’s co-author John Coffin, a retrovirologist at Tufts University in Boston, Massachusetts, says he was satisfied with the data and thought it was time to “let the field and public chew on them”.

The BBC, US National Public Radio, The New York Times, The Wall Street Journal and dozens of other news outlets covered the research. “Prostate cancer pathogen may be behind the disease once dubbed ‘yuppie flu’,” Nature announced on its news website the day the paper came out. Phoenix Rising, a forum for patients with chronic fatigue that has become a hub for all things XMRV, called the work a “game changer”, and patients flocked to learn more about a virus that they hoped would explain their condition. But others, including Britain’s leading chronic fatigue patient group, urged caution until more research buttressed the link.

The first negative findings started to arrive in January 2010 — failing to find XMRV in 186 people with chronic fatigue from the United Kingdom4. A month later, a team including Stoye published a paper5showing no evidence of XMRV in more than 500 blood samples from patients with chronic fatigue and healthy people. One day later, theBritish Medical Journal accepted a paper reporting more negative results in Dutch patients6. Studies began piling up so fast that Coffin made a scorecard to show at talks. “I’ve lost count now,” he says.

Mikovits says that the discrepancies can be explained by differences in the geographical distribution of XMRV or in the methods used.

Judy Mikovits says that she will not abandon the hypothesis that XMRV and related viruses cause chronic fatigue syndrome, despite a growing chorus of critics.

The most common way to detect XMRV is PCR, or polymerase chain reaction, which amplifies viral DNA sequences to a level at which they can be identified. Mikovits and her team used this method to detect XMRV in some of their patients, but she contends that the most sensitive way to detect the virus is to culture patients’ blood cells with a cell line in which the virus replicates more quickly. This should create more copies of the virus, making it easier to detect with PCR and other techniques. She says that none of the negative studies applied this method exactly, a fact that annoys her. “Nobody’s tried to rep-li-cate it,” she says, sounding out each syllable for emphasis.

In summer 2010, some evidence emerged in Mikovits’s corner. Harvey Alter, a hepatitis expert at the NIH’s Clinical Center, and his team identified viruses similar to XMRV in 32 of 37 people with chronic fatigue and in 3 of 44 healthy people. They were preparing to publish their results in the Proceedings of the National Academy of Sciences. But scientists at the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, were about to publish a negative report. The authors delayed publication of both papers7,8for several weeks to assess discrepancies. The move agitated Mikovits as well as the chronic-fatigue community, who suspected that important data were being suppressed.

When Alter’s work came out in late August7, Mikovits was ecstatic, and the WPI released a YouTube video of her touting it. For other researchers, however, the new paper had shortcomings. The viral sequences from Alter’s paper differed from XMRV, says Greg Towers, a retrovirologist at University College London. “He doesn’t get variation, he gets a totally different virus.” Towers says that mouse DNA, which is chock-full of virus sequences like those Alter’s team found, probably contaminated their samples, which were collected in the 1990s. But Alter says that his team found no contamination from mouse DNA and recovered the same viral sequences from the same patients sampled a decade later.

Contamination became a dirty word for Mikovits. Just before Christmas 2010, Retrovirology published four papers9,10,11,12 that highlighted laboratory contamination as a possible explanation for her findings. One showed, for example, that mouse DNA contaminates an enzyme from a commercial kit commonly used for PCR. Coffin, an author on two of the Retrovirology papers, urges caution against over-extrapolating. These papers do not say that contamination explains Mikovits’s results, he says, just that extreme care is required to avoid it.

Towers and his colleague Paul Kellam, a virologist at the Wellcome Trust Sanger Institute near Cambridge, UK, are less charitable, however. Their study12 showed that the XMRV sequences that Mikovits and Silverman had extracted from patients lacked the diversity expected of a retrovirus that accumulates mutations as it passes between patients. “This doesn’t look like an onwardly transmittable infectious virus,” says Kellam. A press release for the paper issued by the Sanger Institute put it more bluntly: “Chronic fatigue syndrome is not caused by XMRV.”

Mikovits is riled when the topic turns to Towers’s paper over dinner one night in Reno — “Christmas garbage”, she calls it. Contamination cannot explain why her team can reproduce its results both in her lab in Reno and at Ruscetti’s at the NCI, she says. Her team checks for contamination in reagents and in the cells it grows the patients’ samples with. She says that her team has also collected viral sequences that will address Towers’s and Kellam’s criticism but that it hasn’t yet been able to publish them. Meanwhile, an unpublished study of patients in Britain with chronic fatigue bears out the link to XMRV, she says. “I haven’t for one second seen a piece of data that convinced me they’re not infected.”

Jay Levy, a virologist at the Univer­sity of California, San Francisco, has a window in his closet-sized office that looks out into the laboratory where, in the 1980s, he became one of the first scientists to isolate HIV. After his discovery was scooped by other researchers, Levy turned his attention to chronic fatigue and started a long but fruitless search for an infectious cause.

Now, Levy is putting the finishing touches on what could be the most thorough response yet to Mikovits’s Science paper, adopting the same cell-culture techniques to detect the virus and using samples from the same patients. He’s done this with the help of Daniel Peterson, who left the WPI in 2010 for what Peterson says are “personal reasons”. Peterson has questioned the institute’s singular pursuit of XMRV, a research direction that was pursued without his consultation.

Mikovits says that she kept the XMRV work secret from Peterson over fears he would tell his patients, and left his name off the original Science manuscript until a reviewer questioned the omission. When asked whether that episode contributed to his departure, he says, “I was surprised at the secrecy and lack of collaboration.” As for his motivation to team up with Levy: “I’m just trying to get to the truth. It’s my only motive, because this is such a deserving group of patients who need to know what’s going on.”

Others, too, are rallying for a definitive answer. Ian Lipkin, a microbial epidemiologist at Columbia University in New York, has a reputation for getting to the bottom of mysterious disease–pathogen links. His team debunked the association between Borna disease virus and chronic fatigue, for example. Now he is spearheading the $1.3-million effort funded by the US government. He is leaving the testing to three labs: Mikovits’s at the WPI, Alter’s at the NIH and the CDC. Each will receive coded samples of white blood cells and plasma from 150 patients with chronic fatigue and from 150 healthy controls. The labs will test for XMRV using their method of choice. Lipkin will crunch the data and unblind the samples.

But even if a study confirms the link to chronic fatigue, it won’t be able to determine whether the virus is the cause. XMRV could, for example, be an opportunistic infection affecting those whose immune systems are already dampened by chronic fatigue. Even Mikovits can only hypothesize as to how it might cause disease.

The virus might not even exist as a natural infection. At a retrovirus conference this month in Boston, Massachusetts, Coffin and his colleague Vinay Pathak at the NCI in Frederick, Maryland, presented data showing that XMRV emerged in the 1990s, during the development of a prostate-tumour cell line called 22Rv1. Developing the line involved implanting a prostate-tumour sample into mice, retrieving cells that might divide indefinitely and repeating the process. But looking back at DNA samples taken throughout the cell-line’s development showed that human cells became infected only after passing through several different mice. Importantly, XMRV’s sequence seems to have come from two different mouse strains. “They just sort of snapped together like two puzzle pieces,” says Coffin, an event extremely unlikely to have happened twice.

Bumper stickers are just one of the supportive gifts given to the WPI.D. 

XMRV sequences retrieved from patients with prostate cancer and chronic fatigue — including some who have had chronic fatigue since the mid-1980s — are nearly identical to the virus from 22Rv1 cells. The implication, says Coffin, is that this virus, born in a laboratory, has probably been infecting samples for more than a decade, but not people. “Although people on the blogs aren’t going to believe me, I’m afraid this is by far the most reasonable explanation for how XMRV came to be,” says Coffin, who hoped that the association with chronic fatigue would pan out and still thinks some pathogen other than XMRV could explain the disease.

Silverman, who no longer works with Mikovits, says that he wasn’t using 22Rv1 cells when XMRV was discovered. Nonetheless, the work has rattled his confidence in XMRV’s link to both prostate cancer and chronic fatigue.

Mikovits, however, is undeterred. The WPI owns a company that charges patients up to $549 to be tested for XMRV, and Mikovits believes that patients who test positive should consult their doctors about getting antiretroviral drugs normally prescribed to those with HIV. Levy and others worry that she is overreaching. “That’s scary for me. These antiretroviral drugs are not just like taking an aspirin,” he says. Mikovits argues that they might be some patients’ only hope. “The people who we know they’re infected should have a right to get therapy,” she says, “They have nothing. They have no other choice.”

Context and debate

Back in her Reno laboratory two days after the talk in Santa Rosa, Mikovits examines a stack of small plastic flasks under a microscope. Some contain patient cells that she hopes will turn into cell lines and churn out XMRV. “On Wednesdays I get to take care of my cells, and that’s where I’m the happiest,” she says.

She has just come off the phone from a sobbing patient infected with XMRV whose symptoms had worsened. “They call me every single day,” Mikovits says. “I don’t do science any more. I spend so much time trying to understand the patients, to understand this disease. People have moved to Reno to be here,” she says. They’ve left gifts: stuffed animals, and stacks of bumper stickers that say “Today’s Discoveries, Tomorrow’s Cures” and, more boldly, “It’s the virus XMRV”.

Mikovits clearly shares in the frustration of those with chronic fatigue who have been marginalized over the years and told that their disease is not real. She says that this disbelief in the disorder drives the criticism of her work. Kellam and the others say that this isn’t true. They don’t deny the existence of the syndrome or even the possibility of an infectious origin. “What we’re trying to understand is the aetiology,” Kellam says. “It’s a scientific debate.”

ADVERTISEMENT

Mikovits says that she’s analysed all the papers critical of her work and found flaws in each of them. Nevertheless, she’s quick to endorse findings that support her work. She claims that Coffin and Pathak’s study, for example, “says nothing about human infection”. Yet new work presented at a different meeting that found XMRV using next-generation DNA sequencing offers “no doubt it’s not contamination — that the whole story’s real”, she says.

Despite the growing choir of sceptics, Mikovits says that she has simply seen too many data implicating XMRV and other related viruses in chronic fatigue to change her mind. For her supporters, that steadfastness offers legitimacy and hope. “The scientists are moving forward,” she announced at her talk in Santa Rosa, “and I think the politics will go away shortly.” The crowd responded with vigorous applause. 

Ewen Callaway writes for Nature from London.

  • References

    1. Lombardi, V. C. et al. Science 326, 585-589 (2009). | Article | PubMed | ISI | ChemPort |
    2. Urisman, A. et al. PLoS Pathog. 2, e25 (2006). | Article | PubMed | ChemPort |
    3. Coffin, J. M. & Stoye, J. P. Science 326, 530-531 (2009). | Article | PubMed | ChemPort |
    4. Erlwein, O. et al. PLoS ONE 5, e8519 (2010). | Article | PubMed | ChemPort |
    5. Groom, H. C. et al. Retrovirology 7, 10 (2010). | Article | PubMed | ChemPort |
    6. Van Kuppeveld, F. J. et al. Br. Med. J. 340, c1018 (2010).
    7. Lo, S. C. et al. Proc. Natl Acad. Sci. USA 107, 15874-15879 (2010).
    8. Switzer, W. M. et al. Retrovirology 7, 57 (2010).
    9. Robinson, M. J. et al. Retrovirology 7, 108 (2010).
    10. Oakes, B. et al. Retrovirology 7, 109 (2010).
    11. Sato, E. , Furuta, R. A. & Miyazawa, T. Retrovirology 7, 110 (2010).
    12. Hué, S. et al. Retrovirology 7, 111 (2010).

Source: Nature.com