Friday, December 31, 2010


You know the body-sniffing dogs that search for survivors in the rubble after buildings collapse? You know how the dogs’ handlers hide healthy people in the rubble to prevent the dogs from becoming too discouraged when the dead-body count starts piling up like so many sacks of potatoes?  That’s along the lines of how things have been going ME/CFS, with a bit of bright news followed by crashing blows for patients, who carry on much like their canine counterparts. The fallout can be worse than the original event.

In the U.K., for example, the NICE [National Institute of Health and Clinical Excellence] Guidelines issued in 2007 signaled to patients that they’d have a tough time finding physicians to treat them with more than antidepressants and cognitive therapy.  But the NICE guidelines also put the kibosh on pharmaceutical research into a promising ME/CFS antiviral drug, Isoprinosine.

A 2010 Newport Pharmaceuticals Limited email obtained by CFS Central stated that the company ceased drug trials of Isoprinosine not because the drug was not effective—a preliminary study on ME/CFS patients indicated that it was efficacious—but solely because of the NICE Guidelines, which, stated the memo, “advocated non pharmaceutical intervention for the treatment of the condition.”

Isoprinosine has proved helpful for some patients with ME/CFS. Several physicians have treated ME/CFS patients with  Isoprinosine, including Dr. Nancy Klimas in the U.S.  It’s believed the drug works as an immunomodulator, by shifting humoral (antibody) Th2 dominance into cell-mediated Th1 dominance, which rallies macrophages, natural-killer cells and cytotoxic T-cells.  Natural killer cell function is usually depressed in ME/CFS patients. In studies, the drug has been show to prevent HIV patients from developing AIDS, and has also been used to treat cancer.  It’s approved in Europe and Canada to treat viral infections. Once a drug is approved for a specific disease, it lends legitimacy to that disease.    

CFS Central queried Newport Pharmaceuticals with a list of questions:
  • Why did Newport Pharmaceuticals decide to investigate Isoprinosine to treat ME/CFS?
  • The company conducted a Phase II trial in Canada in 2003: “Clinical improvement in chronic fatigue syndrome is associated with enhanced natural killer cell-mediated cytotoxicity: The results of a pilot study with Isoprinosine.” Did Newport Pharmaceuticals conduct any other Isoprinosine drug trials with ME/CFS patients? If so, I’d be interested in reading those studies and knowing the results.
  • The ME/CFS Isoprinosine research stopped due to the NICE guidelines, which advocates using only antidepressants, GET [Graduated Exercise Therapy] and CBT [Cognitive Behavioral Therapy] to treat ME/CFS patients. What year did Newport terminate the ME/CFS research into Isoprinosine?
  • Would you explain why your company decided to stop the research because of these guidelines?  After all, treatment guidelines change over time, and research into new drugs is one of the ways that they do.
  • If the drug wouldn’t work for the U.K. market due to the NICE guidelines, why not for the American market, the Canadian market, or those of other countries?
  • Are there any plans to investigate whether Isoprinosine inhibits the retrovirus XMRV in patients with ME/CFS or prostate cancer?  As you may know, the newly discovered retrovirus has been found in patients with both diseases.  
The company declined comment.

Research guidelines and treatment guidelines are two different things—or should be:  Today’s experimental treatments often morph into tomorrow’s standard of care. ME/CFS patients can't get effective drug treatments until the research is done.  But the research isn't being done because the government in Great Britain appears all too willing to sweep ME/CFS under the proverbial rug, and at least one pharmaceutical company seems willing to follow.  

Thursday, December 23, 2010

Dr. Coffin Responds

While waiting for sources to get back to me, I thought I’d post preliminary comments from Tufts University’s Dr. John Coffin.  Coffin co-authored two of the four studies in Retrovirology on Monday that postulated that XMRV may be merely contamination from mouse DNA, as opposed to a new human retrovirus that has jumped species from mouse to man and has been found in patients with ME/CFS and prostate cancer.

CFS Central:  In your papers, you write that you obtained samples of WPI's [Whittemore Peterson Institute] XMRV positive lymphoblastoid cells.  Your papers, however, don't discuss testing these cells for evidence of mouse DNA….  Did you test these cells for evidence of mouse DNA?  If so, did you find contamination? If you did not test the 1282 cells for contamination, why did you decide not to test them?

JOHN COFFIN:  Not to my knowledge, since there was no particular reason to do so.  We have tested [prostate cancer] 22Rv1 cells, and some other human cell lines, with negative results.

CFS Central:  Were the cell lines you tested that had no mouse contamination (the 22Rv1 cells, for instance) XMRV positive or XMRV negative?

JOHN COFFIN:  22Rv1 is XMRV positive. It's the standard positive control.

CFS Central:  Have you tested or do you have plans to test XMRV positive patient samples from WPI or MLV [-related virus] positive patient samples from Drs. Alter and Lo?  

JOHN COFFIN:  We have no plans to do so at Tufts. However, the group I work with in the NCI [National Cancer Institute] is collaborating with the Blood Working Group, and we will look at samples from both the WPI patients as well as the same patients that Lo and Alter studied. [Lo and Alter are the principal investigators of the NIH/FDA/Harvard study published in August, which found XMRV-related retroviruses in the majority of ME/CFS patients and 7 percent of controls.]

CFS CENTRAL:  If you’ve already tested these retroviral positive samples from WPI and Alter/Lo, did you find mouse DNA contamination?  

JOHN COFFIN:  We haven't done that yet.

CFS CENTRAL:  If Tufts hasn’t tested these samples and has no plans to, wouldn’t that be the definitive way to determine whether there is mouse DNA contamination?

JOHN COFFIN:  We will test at NCI using the same assay.

Wednesday, December 22, 2010


I’m working on a piece about Monday’s Retrovirology papers that postulated that XMRV was merely lab contamination from mouse DNA rather than an authentic, new human retrovirus.  Please bear with me.

Wednesday, December 1, 2010

Disability Claims

 Linda Nee heads up Disability Claims Solutions, which helps ME/CFS patients in the U.S. and the U.K. apply—and if need be fight—for long-term disability.  

“Many insurance companies have the philosophy that they predetermine the outcome of ME/CFS claims—and that outcome is to deny the claims,” Nee says matter-of-factly.  Should the insurance company pay the claim, she says, there’s an enormous financial advantage to categorize ME/CFS as a psychological problem.  Group policies in Europe and the U.S. often cover psychiatric disorders for only two years, whereas coverage for a physiological disease usually continues until age 65. 

“You do the math,” Nee says. 

Friday, November 26, 2010


From noon to 3 p.m. on Monday, ME/CFS patients in the U.K. are staging a virtual and onsite protest to mark the 25th anniversary of London’s St. Bartholomew’s Hospital ME/CFS service.  The hospital itself, however, is 900 years old, having been founded in 1123 by a courtier in King Henry I’s court.  The hospital’s future seemed precarious 400 years later, when King Henry VIII—the king who beheaded or divorced four of his six wives—ordered the dissolution of the monasteries, thereby depriving the hospital of income, until King Henry VIII reendowed Barts shortly before his death, in 1546.

Many ME/CFS patients believe that the treatment they’ve received at Barts is more appropriate for medieval times than today.

Rosie O’Grady (not her real name) is one of them. The 43-year-old disabled lawyer hails from Ireland but lives in England with a severe case of ME/CFS. Before she became ill in 1996, she reminisces, “I rowed on the weekends on the Thames with a rowing club in Greenwich. I loved traveling and my friends. My life was very full.” 

All that changed 14 years ago when she became ill with a flu from which she has yet to recover.  She was an outpatient at Barts several times from 1997 to 2005. To get government benefits in the U.K., she explains, there’s “intense pressure to show you’re doing ‘treatment.’  If you had a private income, you would not go there.”

O’Grady says the doctors and rehab team at Barts wanted her to become as physically active as possible. “I was told by the physio there everyone could do 10 percent more activity every few weeks. They told me that any time I felt unwell [I should] go for a walk and the fresh air would wake me up.  I completely placed my trust in them,” she says, but like most patients with ME/CFS pushing herself only made her worse. “Some days my power to my fingers was so weak I could not pick up a coin,” she remembers. “I was desperate to get well and would have done anything they said.”
Her ME/CFS case was so severe that she moved into a YMCA where all food and services were provided.  “I could not even change the duvet on my bed,” she says.  “I was unable to make a cup of tea and stay awake to drink it.”  Today she is bedbound or in a wheelchair, unable to work or remain upright for more than few minutes at a time.  She believes that her time at Barts contributed to her ill health.  Her sojourns there left her physically weaker and “emotionally spun out from the lies and double speak.”

Frustrated by the care at Barts, O’Grady made an appointment with a rheumatologist at a different hospital, who prescribed anti-inflammatories to treat the pain in her back and neck, which proved helpful.  When she had given her Barts doctor the same list of rheumatologic symptoms, “he looked bored, said nothing and started cleaning his fingernails,” she recalls.  “Another doctor claimed they didn’t need to run many tests on ME/CFS patients because “they would know the results simply by looking at the patients.”
For more information on the protest:
For information on how to email or fax a virtual protest:

Friday, November 19, 2010

2011 Open-Label
Ampligen Trial

Patients interested in participating in an open-label trial for the experimental ME/CFS drug Ampligen should contact Ali Allen or Kristin Pierce at Dr. Lucinda Bateman's office in Salt Lake City, Utah, for more information.  Depending in part upon patient response, Bateman may elect to conduct a trial in 2011. With an open-label trial, all patients receive the investigative drug.

The drug cost will be approximately $6,700 for the first six months, which will include extensive testing to determine eligibility, and $7,200 for each additional six-month period.  In addition, there will be procedure expenses (infusion costs, bloodwork, X rays, EKGs and other testing) of approximately $6,900 every six months, plus administrative costs of approximately $1,500 every six months.  For six months, expect to shell out more than $15,000 to participate in the study, plus housing costs if you're not from the area.

To qualify for the study, patients must be able to visit the clinic up to six times during the first 10 weeks for baseline testing before receiving the intravenous drug Ampligen.  Once you begin the drug, you must reside in the Salt Lake City area and visit the clinic at least twice each week, for one- to two-hour visits, for at least six months.  

Ali Allen:
Kristin Pierce:

Monday, November 15, 2010

Suzanne Vernon's Take on
Two XMRV Studies

Dr. Suzanne Vernon, scientific director of the CFIDS Association, recently penned a commentary on three recent XMRV studies.  Two of them—the Barnes study in England and the Henrich study in the U.S.failed to find XMRV.  Only the Donaldson study at Baylor College of Medicine in Houston found XMRV, in prostate cancer patients. 

Henrich looked at several groups of immunocompromised patients, including those with CFS, HIV, transplants and rheumatoid arthritis.  Barnes examined the blood of patients with HIV or hepatitis C.  

By email, I asked Vernon to expound on these two XMRV negative studies.  Her comments are in green.

CFS Central:  In the Henrich and Barnes studies—unlike the Lombardi 2009 Science study—the researchers calibrated the PCR assay with a synthetic clone instead of a clinically positive sample.  Synthetic clones have been used to calibrate PCR assays in other studies, including Dr. Myra McClure’s XMRV study done in England last winter. As you know, McClure is also one of the authors on the new Barnes study.  Do you believe using a synthetic clone may have contributed to Barnes and Henrich not finding XMRV? Why or why not?

Suzanne Vernon:  Negative results could indicate that assays are not sensitive enough. Positive controls and gold standards for XMRV detection in peripheral blood are needed.
CFS Central:  In addition, Henrich and Barnes examined HIV patients for XMRV—and didn’t find it. There is significant evidence to suggest that infection with two retroviruses is unlikely, that infection with one retrovirus helps prevent infection by another, a phenomenon known as retroviral superinfection resistance (  Would you comment on the possible role of retroviral superinfection resistance and negative XMRV findings in these patients?  

Suzanne Vernon:  The immune response to viruses that express similar antigens may help prevent dual infection. However, the role of superinfection resistance as it relates to XMRV has not been extensively explored.
CFS Central:  Moreover, some of the HIV patients studied had been on ARV [antiretroviral] therapy.  Do you believe being on ARVs could have made it more difficult to find XMRV in these patients?
Suzanne Vernon:  It is possible although the chronic HIV cohort had not received highly active antiretroviral therapy for an average of 14 months.
CFS Central:  Concerning the Henrich study, your article states that 32 patients met the Fukuda definition of CFS. However, in actuality these patients didn’t meet the Fukuda definition; they met the Empirical definition. The work of Dr. Leonard Jason has shown that 38 percent of patients who meet the Empirical definition actually have major depression. I think it’s an important point that Henrich is studying patients who don’t meet the Canadian or Fukuda definition, and who may be suffering from depression, not CFS.  Would you explain your point of view concerning the CFS definition in this study?

Suzanne Vernon:  Henrich et al used the 1994 CFS case definition criteria which is considered the revision of the 1988 CFS case definition published by Holmes.  We have confirmed use of the 1994 criteria with the investigators.  No one other than CDC has used the empiric approach in research.
CFS Central:  You mentioned in your review that investigators should seek to replicate “as much as possible the features of the CFS patients found to be positive for XMRV and related MLVS in the studies published in Science and Proceedings of the National Academy of Sciences.”  Shouldn’t a replication study replicate the patient group selected for the Science or PNAS studies precisely, by using the same definition—particularly in light of the divergent findings published and the resulting confusion that patients and researchers have been grappling with for a year?  Thus, in these XMRV studies, shouldn’t patients meet the 1994 Fukuda definition and/or the Canadian definition of CFS, while weeding out the Empirical patients used in the Henrich study? Why or why not?

Suzanne Vernon:  Study subjects in replication studies should be as similar as possible to those studied by Lombardi et al and Lo et al and should meet 1994 and/or Canadian.

Wednesday, November 3, 2010

Month Five of
Dr. Michael Snyderman's
Antiretroviral Boilermaker

Dr. Michael Snyderman, an oncologist with Chronic Lymphocytic Leukemia and ME/CFS, started the HIV drug AZT five months ago to treat both diseases.  Five days after beginning AZT, he added another HIV drug, raltegravir (Isentress).  The third FDA-approved HIV drug shown in test-tube studies to be effective against XMRV is tenofovir (Viread), which he plans on adding to the mix next month.  "I haven't started tenofovir yet because I want to collect enough data to sort out what is happening," Snyderman explains.  He calls his cocktail a boilermaker.

For the year before he began the HIV meds, Snyderman experienced lower extremity neuropathic pain but couldn't figure out why.  And for a few weeks before beginning treatment he became more fatigued than usual and couldn't concentrate by the end of the workday, "which isn't good if you are taking care of sick people, so I started thinking I would have to retire." In addition, his pain had become "agonizing."

During the first two weeks of treatment, there was no improvement, and the only drug side effect was mild nausea. At the third week, however, the pain resolved completely and his concentration and energy began to improve.  "I am still tired though maybe 25 percent better," Snyderman says.  "I believe it must take a long time to heal the damage done directly by the virus and done by the elevated cytokines. Stopping the virus and lowering the cytokines must be important and should be our initial goal, but there are other issues like dealing with the deconditioning. I am not an expert on CFS so I can't go beyond that."

On the HIV drugs, Snyderman's elevated cytokines have normalized, and his cancer markers have improved as well.

Link to Snyderman's most recent posters here:  or here:

Monday, November 1, 2010

New British ME/CFS Print Ad

The British advocacy organization Action Now begins its new “Policy Change: NOW” campaign today.  The campaign, which will run for two weeks, was inspired by the “Time for Action” campaign started by three ME/CFS patients in the U.S.

The U.K. campaign dovetails with today’s demonstration at the Department of Health in London. Today marks the first day that British ME/CFS patients are banned from donating blood.

A spokesperson says that today’s protest was organized in response to the government position that there is no infectious pathogen associated with ME/CFS and that the British ban is in place for only one reason: to prevent patients’ health from getting worse. For more information on the campaign, click here.

Action Now has developed a foreboding two-color print ad campaign:

Wednesday, October 27, 2010


Senator Harry Reid of Nevada is in the fight of his senatorial life.  But ME/CFS patients and the families of children with autism can reelect him on November 2

by W. L. Karns

The tight and nasty race between U.S. Senate Majority Leader Harry Reid and Tea-Party Republican challenger Sharron Angle is down to the wire in Nevada. The race may come down to a few hundred votes. Harry Reid is one of the few politicians willing to stand up for ME/CFS patients, and we help ourselves by voting for him and supporting his campaign.

Voting in Nevada began last Saturday, and loyal Republicans are already turning out in disproportionate numbers. Voter turnout is critical for Reid—and his campaign wants Nevadans to cast their votes by Friday. After Friday, early voting stops, and voters have to wait until Election Day.

Reid has long been a staunch supporter of ME/CFS research and healthcare reform. Angle hasn’t weighed in on ME/CFS research, but here are her views on key health issues: She doesn’t believe that insurance companies should be mandated to cover mammograms and colonoscopy screenings. She also believes that insurance companies shouldn’t have to cover autism treatments. Indeed, she questions whether autism really exists.

In other areas, she wants Social Security to be phased out, and she doesn’t believe in global warming or that the U.S. Constitution mandates a separation of church and state.  She believes same-sex marriage should be banned on the federal level. She doesn’t believe in abortion—even in cases of rape and incest. 

Donations of time or money and calling voters to increase turnout may reelect Harry Reid, the senior and rational senator from the silver state—and keep Sharron Angle out.

In Nevada, ME/CFS patients and parents of autistic children need to call upon friends, relatives and neighbors to vote as well. If ME/CFS patients and families of autistic children can make a difference in this election, other politicians will, no doubt, sit up and take notice.

W. L. Karns has lived with ME/CFS for 23 years and is XMRV positive.

Tuesday, October 26, 2010

More Monkeys

Here are patient advocate Joe Landson's messages delivered by nine anthropomorphic macaques.  Landson sends these emails to government officials every day as part of the “Time for Action” campaign.  On October 4, patients Rivka Solomon, Charlotte von Salis and Robert Miller launched the campaign to get the government's attention concerning ME/CFS.

Landson chose the macaque because researchers at Emory University’s primate lab who injected XMRV into macaques reported that even when the retrovirus was undetectable in the blood, it thrived in the reproductive organs as well as the spleen, gut, bladder, lung, liver and lymph nodes.

Monday, October 18, 2010


An Editorial on
Homographs and Outside Voices

It’s an odd thing looking back at this disease, realizing that 17 million patients all over the world have waited for help for decades, their pain and disability steadily worsening until for many that's all they have left.  Along the way, thousands have died of lymphomas, heart failure, heart attacks, suicide, pneumonia.  Many spouses have deserted them, many friends have written them off as malingerers or head cases.

Georgia resident Leanne Hyneman, whom I interviewed in 1994 for an investigative article I wrote for Philadelphia magazine on the experimental ME/CFS and HIV drug Ampligen, was the sickest ME/CFS patient I’ve ever spoken with.  She was 30 years old in 1994, slept 22 hours a day, rising around midnight, and was cared for by her mother.  (Though Ampligen helped many patients, it only made her worse.)  She lived with seizures, nystagmus, profound weakness, her teeth broke off at the gum line, but she remained soft-spoken and hopeful despite the living death her life had become. After 20 years of living with ME/CFS, she died of cardiac arrest in 2007 at the age of 43.

What terrible isolation Leanne Hyneman and many others like her have endured every day! At least the Internet has helped mitigate that. Finding XMRV and related retroviruses in patients have helped too.  Buoyed for the first time in a long time, patients have been taking matters into their own hands, comparing notes on ME/CFS forums and in private messages and, more recently, shopping for a compassionate doctor who might write them antiretroviral scripts.

Desperate ME/CFS patients plead sotto voce for a triple cocktail of HIV medications and other antivirals like the desperate women of an earlier time who sought clean, illegal abortions from a sympathetic M.D. What person who learns that they’re HIV positive is relieved?  But most patients who learn that they’re XMRV positive are relieved, for it’s validation that their illness is in their bodies and not their minds. That ME/CFS still is not acknowledged as a serious and sometimes fatal physical illness remains for many the worst aspect of having it.

Measuring the effects
Given how sick many patients are and how long they have suffered, why the reluctance of some researchers to begin clinical trials? Several test-tube studies have shown that three approved HIV meds—AZT, tenofovir and raltegravir—have efficacy against XMRV.

There’s also clinical data to suggest FDA-approved antivirals like Vistide and B-cell depleters like the cancer and rheumatoid-arthritis drug rituximab may also be effective for ME/CFS. There are markers to chart patient’s progress, including an XMRV viral load test, cytokine panels, V02 max (maximum capacity of the body to transport and use oxygen during exercise), IQ testing and actometers, which measure activity level.  Desperate patients are experimenting with medications now, but few are monitoring markers, so they’re flying blind. 

Of course, these medications may not work and, worse, can cause kidney and liver toxicity and anemia, among other problems. But the scientific community needs to stop wagging a collective finger at ME/CFS patients trying experimental treatments and, instead, begin clinical trials.  Paternalistic physicians and researchers have come close to equating antiretroviral therapy with lunacy, calculating the damage it’ll wreak on patients’ already compromised immune systems, cautioning about the early days of HIV drugs, which hurt as many sufferers as they helped.  They may be right.  These medications may turn out to be the devil for ME/CFS, but no one is going to know without clinical trials. 

When the healthy reprove the sick that they’re impatient and reckless and foolish and need to wait for treatment, I say isn’t it funny how healthy naysayers get to enjoy their lives while admonishing the sick to be grateful that life is not any worse.  It is sickening.  It’s also a way for the fit to distance themselves from those who are suffering.  The only people who can put a stop to this paternalism and delay are the patients themselves, by acting up, by challenging every inaccurate and inappropriate comment and action.

Gottesman, Plotz and Straus
Case in point: The National Cancer Institute’s Michael Gottesman told patients before the start of the National Institutes of Health (NIH) XMRV conference that they lost a devoted advocate when the NIH’s Dr. Stephen Straus died.  The NIH’s Dr. Paul Plotz made a similar surreal comment last week about the “excellent” work of Stephen Straus on journalist Llewellyn King’s PBS show White House Chronicle.  To Michael Gottesman and Paul Plotz I say:  “What have you been smoking?”  Gottesman and Plotz may be well meaning, but they’re certainly misinformed.

For those who don’t know much about the late researcher who headed up “CFS” research for years at the NIH, Straus holds the distinction as the only physician who seriously injured the health of several patients, during his acyclovir trial in the 1980s.  Acyclovir is an antiviral used to treat herpes viruses, including Epstein Barr virus (EBV), which causes mono.  ME/CFS patients often have elevated antibodies to EBV, and early on scientists hypothesized that the virus caused the disease.  How did Straus injure patients? He didn’t give them enough fluids.  It’s acyclovir 101, not exactly brain surgery, to hydrate patients to prevent renal toxicity problems with antivirals.

The Vapors
After the EBV theory fell apart, Straus started blaming patients for the illness. As outlined in Hillary Johnson’s seminal book Osler’s Web, Stephen Straus launched a 1994 ME/CFS workshop with a slide of a Victorian woodcut of a woman recumbent on a couch with her hand clasping her forehead.  For Straus and some other government scientists in the U.S., as well as a group of psychiatrists in the U.K., ME/CFS became nothing more than an updated name for the Victorian Vapors. 

In 1986, according to Johnson, Straus theorized to fellow physicians:  “Maybe these are the individuals who… don’t want to drive their BMW unless they feel up to it, and they need our help to get behind the wheel.”  When it came to ME/CFS patients, Straus was misogynistic, cruel and, as he proved in the acyclovir trial, incompetent.  That’s who Stephen Straus really was, Dr. Plotz and Dr. Gottesman.

Dr. Elizabeth Unger
Likewise, at last week’s CFS Advisory Committee meeting, the tremulous acting head of CFS research at CDC, Dr. Elizabeth Unger, trotted out the CDC’s usual party tricks: the agency’s fantasy that childhood abuse causes the disease, plus the tried-and-true Cartesian mind-body dualism (though CDC investigates only the mind part).  “Enough, Dr. Unger," I wanted to say to her.  "This is a physiological illness that’s killed thousands of people in the past twenty-six years.  Four of the ME/CFS patients whom I interviewed in 1994 have since died, including my friend Nancy Kaiser.  She died in 2008 of pneumonia after struggling with ME/CFS for 33 years.  No doubt childhood trauma makes individuals susceptible to any chronic illness, but you don’t see any studies on childhood trauma and contracting HIV, do you?  Of course not; it would be absurd.”

Outing gay politicians
Recently I watched a documentary called Outrage.  It chronicles the work of gay journalists, bloggers and activists who’ve outed closeted gay politicians—not because they’re gay but because they’re hypocrites, voting against any issue that would afford  homosexuals the same rights and protections as heterosexuals.  Before AIDS, the late activist Rodger McFarlane says, being closeted was more an issue of privacy.  “After AIDS,” he intones, “that was collusion with genocide.” 

ME/CFS for many is slowly progressive.  After 10 or 20 or 30 years, patients develop cancers, heart disease, heart failure and some die.  By denying the reality of what this disease is, by morphing fact into fiction, by playing Animal Farm head games with the CFS case definition (using the “Empirical” definition which isn’t CFS at all but depression), by reciting the spurious childhood-trauma mantra, many government officials in this country and many “CFS” psychiatrists in Great Britain are in my view intentionally or unwittingly committing slow genocide of the 17 million people worldwide with this disease. Many patients have allowed this crime—it is a crime—to continue for years because they’re so sick and because they bought the company line that they’d recover.

The gay reporters and activists in Outrage implemented a strategic shift in their way of thinking once gay men started dying from AIDS.  Instead of the hounds chasing the foxes, the foxes turned the tables and started hunting the hounds. This switcheroo has, finally, begun in the ME/CFS community. After
decades of quiescence, of hoping that help was just around the bend, the new mood feels different because many patients have reached critical mass. There is a focused determination to effect change.

Inside voices
The use of “inside voices” that CFIDS Association’s Kim Kenney McCleary advocates in an aggravating post on the organization’s website may be well intentioned but it’s out of touch with what’s necessary for change.  Change won’t come easily.  As I’ve said in a previous post, change is always bitter and bloody, with the old guard on tenterhooks, desperate to stave off its own obsolescence—and to keep its secrets secret.  And it will not be easy because adult women comprise the largest segment of this disease, and most girls are taught in childhood to cooperate and not to make waves, and to use their inside voices—even if it kills them.

Few boys are sold that phony bill of goods in childhood.  In Outrage, AIDS activist Larry Kramer recalls an incident during the Reagan administration when at a party he ran into Terry Dolan, at the time the head of the National Conservative Political Action Committee. President Reagan still had not uttered the word “AIDS” in public and had done nothing to contain the disease or help thousands of people dying an agonizing death from it. “How dare you come to a party of gay people after what you’re doing to us?” Kramer asked Dolan and threw a drink in his face. “You’re raising money to kill us.”

I’m not advocating throwing drinks in anyone’s face.  But I am advocating that patients discard their inside voices every time those in power turn ME/CFS into a benign psychiatric problem when it is, in fact, a severe neuroimmune disease, until scientists get the message that patients aren’t going to put up with the lies and doublespeak anymore, until duplicitous scientists become so embarrassed and beleaguered from being besieged by emails, faxes and phone calls, that they give up the charade or, better yet, retire. 

Clinical trials now
At the recent Chronic Fatigue Syndrome Advisory Committee meeting, the National Cancer Institute’s Dr. Stuart LeGrice informed patient advocate Cort Johnson, without any irony: “I don't think this ‘What Have You Done For Me Lately’ campaign is helping. I don’t need to have [NIH Director] Dr. Collins call me and ask me, ‘What are you doing for CFS?’ ” Wow.  What a light-bulb moment that was! Clearly, as Cort Johnson pointed out, the campaign is working. 

The next step is standing up to those who deny patients with ME/CFS the clinical trials that they deserve now, not a year from now or five years from now or 25 years from now, or, if the CDC has its way, a week from never. With our government, patients won’t get what they want unless they articulate exactly what drugs they want and how the trials should be conducted.  For instance, it would be unethical to conduct placebo-controlled drug trials. Early on, HIV patients established that precedent.  The reasoning is this:  Since there are no approved ME/CFS drugs for control patients to take during such a study, it would be unethical to give them a placebo.

Latin declensions and phony definitions
One thing I found stupefying as I watched the Chronic Fatigue Syndrome Advisory Committee (CFSAC) meeting of last week was that the CDC’s Dr. Elizabeth Unger justified using different definitions of the disease, as if they were, say, Latin declensions.  One of those definitions, the Canadian Consensus definition, is the real ME/CFS.  That’s the CFS that causes immune abnormalities, seizures, autonomic dysfunction, excruciating pain, short-term memory loss, dramatic drops in I.Q., swollen lymph nodes, lesions on the brain, cancers and death. 

And there’s the phony CFS that the CDC studies, which meets the Empirical definition (which the CDC sometimes calls the revised Fukuda definition). That’s the CFS that causes depression, minor aches and pains, and weight gain.  In fact, many patients whom the CDC recruits for its studies don’t even know they’re ill, so mild are their symptoms. Why is the CDC studying patients who aren’t very sick when many ME/CFS patients are dying?  It’s as if CDC scientists aren’t familiar with the concept of triage.  At this point, who else but ME/CFS patients can teach them?

Perhaps they could explain how the Canadian Consensus CFS and the Empirical CFS are homographs:  Words that sound the same but have different meanings like bow (shoots arrows) and bow (tied with a ribbon).  That’s all they have in common.  No researcher on the CFSAC committee voices umbrage at the muddling of these disparate groupsthis lunacy that passes for sciencefor fear of alienating the government agencies that feed them.  It’s not their fault.  They’ve got to earn a living.  Which is why CFSAC needs scientists with very sick spouses or very sick children because they’ll have different priorities.  Which is also why CFSAC needs patient advocates: They’ve got nothing left to lose and they have the sense of urgency that’s sorely lacking now.

Congressman Barney Frank, who is gay, believes that the reason many people hate homosexuals is because their leaders tell them to.  I believe the reason most people think that ME/CFS is a benign mental disorder is because scientists and the government have been telling them that for a quarter century.  There’s a great moment in Outrage when activist Michael Rogers pronounces that all activism is driven by rage. “People are suffering and dying because some self-promoting asshole is telling a lie,” he says.  Doesn't that sum up what’s been happening with ME/CFS in the United States since the Incline Village, Nevada, outbreak of 1984?  It’s time that patients once and for all get angry enough—and stay angry enough—to put an end to it.

This article is copyright CFS Central 2010. All Rights Reserved. You may quote up to 150 words from this article as long as you indicate in the body of your post (as opposed to a footnote or an endnote) that the excerpt is from CFS Central. You may not reprint more than 150 words from this article on blogs, forums, websites or any other online or print venue. Instead, refer readers to this blog to read the article.

Wednesday, October 13, 2010

Dr. Michael Snyderman's
MD Anderson Poster

Dr. Michael Snyderman, an ME/CFS patient with chronic lymphocytic leukemia (CLL), began a trial of two HIV drugs shown to have efficacy in treating XMRV in test tube studies.   Here's the poster presentation that Snyderman, who's an oncologist, is presenting at MD Anderson Cancer Center in Houston, Texas, at 7 p.m. this evening.  Snyderman concludes on the poster:

"A patient with CFS and CLL with adverse prognostic factors was shown to have XMRV in plasma and CLL cells. Within the first 100 days of treatment with AZT and raltegravir, he showed multiple benefits simultaneous with disappearance of infectious XMRV.  These findings suggest that XMRV is etiological for both the CLL and CFS and that virus-direct treatment was beneficial in this patient.  Further CLL patients should be studied especially as CLL has been statistically associated with an increased risk for other neoplasia. Questions to be answered are what neoplasms are associated with XMRV, will existing antiretrovirals have antineoplasticactivity in these neoplasms and what is the optimal combination of antiretroviral drugs."

Snyderman continues to have more energy on the drug cocktail. However, the doctor's trisomy 12 marker--which is elevated in 25 percent of patients with CLL--initially dipped significantly on the drugs, but has begun to rise again. 

Tuesday, October 12, 2010


Joe Landson emailed CFS Central three macaque cartoons that he's sent to government officials, as part of the “Time for Action” campaign.  On October 4, patients Rivka Solomon, Charlotte von Salis and Robert Miller launched the campaign to get the government's attention concerning ME/CFS.

"Should the CDC ever be inundated by banana peels, I categorically disavow all knowledge," Landson wrote to CFS Central.  Last week, Landson posted this comment on this blog:
"Right, so I've started faxing cartoons, annotated with the suggested messages, to Dirs. Collins and Fauci. Every day, it's another observation about ME/CFS, told by a rhesus macaque I draw myself. (All else is computerized.) Why the macaque? Because macaques have arguably done more to advance CFS research than senior NIH officials have."  Landson is referring to the study done by researchers at Emory University’s primate lab who injected XMRV into macaques and reported that even when the retrovirus was undetectable in the blood, it thrived in the reproductive organs as well as the spleen, gut, bladder, lung, liver and lymph nodes. 
Macaque 1, Macaque 2, Macaque 3.

Sunday, October 10, 2010

Dr. Michael Snyderman at
MD Anderson

Oncologist Michael Snyderman will present his latest poster on his one-man trial to treat ME/CFS and chronic lymphocytic leukemia with HIV meds at 7 p.m., October 13 at MD Anderson Cancer Center in Houston, Texas.  Snyderman, who is XMRV positive, has both ME/CFS and chronic lymphocytic leukemia (CLL), which is relatively common in ME/CFS patients.  About 5 percent of ME/CFS patients get it, compared with .02 percent in the general population.  Snyderman's taking AZT and raltegravir, two HIV drugs with efficacy against XMRV in test tube studies.

Snyderman continues to feel significantly more energetic than he was prior to initiating antiretroviral therapy.  His elevated cytokine signature, particularly interleukin 8, improved on the cocktail and his XMRV viral load dropped. His CLL cells expressed XMRV. Snyderman, however, is concerned that attending the poster presentation may be discouraging for some patients because of the recent upturn in a CLL marker called trisomy 12, which is elevated in 25 percent of patients with CLL.  Initially on the drugs, this marker plummeted.

Monday, October 4, 2010


Three ME/CFS patients launch a campaign to get the government’s attention

Beginning today, ME/CFS patients Rivka Solomon, Charlotte von Salis and Robert Miller are launching the “Time for Action” campaign. Using email, fax and phone, the trio are asking ME/CFS patients to contact Director of the National Institute of Allergy and Infectious Disease Dr. Anthony Fauci and Director of the National Institutes of Health Dr. Francis Collins every day and pose the same question: “What have you done for ME/CFS today?  Patients and their families are waiting.” 

Robert Miller organized the September 7 meeting of nine patients and their families with NIH scientists Michael Gottesman, Paul Plotz and Roland Owens, in Bethesda, Maryland, right before the NIH's first international XMRV conference began. Along with Miller, Solomon and von Salis were among the patients who attended.

Solomon’s mother was also there—and came up with the idea for the new campaign. “Bug them every day!” she advised her daughter.  It was a light-bulb moment for Solomon.  “It lets the government know we’re watching them, waiting for them to help us," she explains. "And it’s what we’re calling ‘advocacy made easy.’ This way we can include everyone in the action campaign—even the severely ill. The way I see it, and I'm speaking for myself personally here, this illness and we patients who suffer from it have been ignored, delegitimized, psychologized and marginalized since the early 1980s, when many of us first got sick.

Solomon, a playwright from Boston, and Miller, a former fire boss in Utah (who moved to Reno, Nevada, last year for the experimental HIV and ME/CFS intravenous drug Ampligen from CFS-literate physician Dr. Daniel Peterson) have been ill for a quarter century.

Von Salis, a lawyer, lives outside Washington, D.C., and has spent the last two decades bed-bound or house-bound. “NIH Deputy Director Gottesman pointed out during our meeting that AIDS activists definitely had an impact on the NIH's response to their disease,” von Salis recalls. “ME/CFS requires as strong a response from the NIH as AIDS did, especially in light of recent research indicating a retroviral association. Increasingly greater numbers of patients, their families and friends are completely fed up with the lack of governmental response to ME/CFS and are prepared to act, just as PWAs [persons with AIDS] did. This simple campaign puts the NIH on notice that we’re not about to remain silent and accept the status quo. If we don’t get a response or the response is inadequate, we will follow up with another action."

Solomon agrees.  Although she was pleased with the September 7 meeting between ME/CFS patients and NIH officials, as well as the NIH two-day international XMRV conference, she’s looking for a little less conversation and a little more action on the part of both patients and government.  "We won't get fast-track clinical trials by waiting for them," she says. "We need to demand them. We won't get funding for ME/CFS centers of excellence by waiting for them. We need to demand them. The NIH will see a repeat of the ACT UP days of AIDS activism if they don’t move to actually help us ME/CFS patients, and fast."
Contact info:
National Institutes of Allergy and Infectious Disease
Director Anthony Fauci
Phone: 301-496-2263
Fax: 301-402-3573

National Institutes of Health
Director Francis Collins
Phone: 301-496-2433
Fax: 301-402-2700

Robert Miller is tracking patient response to the Time for Action campaign and would appreciate patients sending him a copy of any emails sent to Fauci and Collins:

Wednesday, September 29, 2010


Dr. Michael Snyderman, an oncologist at the State University of New York at Buffalo, also has Chronic Fatigue Syndrome and chronic lymphocytic leukemia (CLL), one of the cancers that's relatively common in CFS patients.  His poster presentation at the NIH conference showed that on a trial of AZT and Isentress (raltegravir)—two HIV drugs with efficacy against XMRV in test tube studies—several inflammatory cytokines decreased.  Cytokines are proteins secreted by immune and glial cells.  For Snyderman, the drop in interleukin 8 was particularly striking.  His CLL numbers decreased as welland his CLL cells expressed XMRV. 

In an email, Snyderman wrote to CFS Central, “I believe there is excellent supporting data for treatment trials to start right now (as long as a good lab like Judy's [Mikovits] is involved). I am upset by delays when people with neurological, autoimmune and neoplastic disease are suffering. I don't know if treatment will work but my personal data validates trials. This is why I have put myself through this. I knew I was working with a center of excellence (WPI), and if there was anything important to learn, we would.  Waiting more to do these studies will not make the data stronger or more convincing. The studies can be modest at first to learn the parameters before doing a multi-million dollar study.”

Snyderman promises a longer interview with CFS Central in two weeks.  Right now, he’s snowed under finishing another poster presentation, this one for MD Anderson Cancer Hospital at the University of Texas.

Friday, September 24, 2010


I emailed a few questions to Richard Easingwood, one of the New Zealand coauthors of a 1994 study that identified retroviral particles from the peripheral blood lymphocytes of ten of 34 CFS patients and none of the controls. Back then, the scientists reported that the majority of viral particles were similar to lentivirus and and murine leukemia virus. Now a senior electron microscopy technician at the University of Otago, Easingwood wrote back:

"That [study] was a long time ago! I have not revisited this research since then. My role in that study was fairly limited—I performed the electron microscopy and that was about it. To comment intelligently on it I would need to review the images (which I still have in storage) and possibly prepare more sections from the specimen blocks (which I still have) in the light of my electron microscopy experience now. I have 15 years+ extra experience since that paper was published and may look at the data differently.  If I did this and reviewed the current literature I would be better able to form an opinion about this research.  However, I will attempt to answer your questions as best I can.

Do you believe that XMRV may be what you found back in 1994?  Why or why not?
They may have been virus particles. The structures we found were intriguing but it is possible that they were normal structures or artefactual.

Back in the 1990s, did you believe that a virus or retrovirus was likely the cause of ME/CFS?
I had no opinion on that back then.

Are the blood samples from those patients still frozen somewhere—or have they been discarded?
I don't know what happened to any of the samples other than those that I prepared for TEM [transmission electron microscopy]
, which I still have. If there were frozen samples I don't know their fate. However, the resin-embedded cells I have are stable indefinitely.

If the frozen specimens are still around, would you be interested in looking at them again?
I would be very happy to review the existing old negatives (most of which haven't been published) and the stored resin-embedded samples. I suspect some kind of ethical approval may be required, I would have to check this.

Monday, September 20, 2010


From a 1995 article by Dr. Dharam Ablashi:  "At the CFS Research and Clinical Conference 1994, Diack et. al. reported the identification of retrovirus particles from the peripheral blood lymphocytes of 10/34 CPS patients and none of the controls. The majority of viral particles were similar to the ultra structure of visna virus (lentivirus) and murine leukemia virus. According to the authors, virus-like structures were compatible with various maturation stages of lentivirus. No reverse transcription activity or possible target cell phenotype was found. Considerable work is needed to prove that these ultra-structures resembling a retrovirus are not artifacts."

Diack D, Easingwood R, Cross J, Carlisle B, et. al. Electron microscopic immunocytologic profiles in Chronic Fatigue Syndrome. Proc Res & Clin CFS Conf. p. 24, 1994 (Oct. 7-11, Ft. Lauderdale, FL). 

Monday, September 13, 2010

XMRV Conference Recap

One thing that resonates from the two-day XMRV conference at the National Institutes of Health is the, at times, testy battle between two camps of scientists. The cohort that believes that mouse retrovirus contamination accounts for the positive XMRV and related murine leukemia virus studies was pitted against the cohort that believes contamination has been ruled out and that the positive studies show a clear link between this family of retroviruses and Chronic Fatigue Syndrome and prostate cancer.  Not surprisingly, the discussions around CFS grew more heated than those around prostate cancer.  Dr. Mary Kearney of the National Cancer Institute may be the one to resolve this issue, as she reported on a test that discriminates between mouse retroviruses and XMRV with, she said,100 percent accuracy.

Despite several positive retroviral findings, by the time the Q and A began at the end of the second day, the upbeat mood many felt due to the recently published FDA/NIH/Harvard murine leukemia virus study—which found XMRV-related MLV viruses in 86.5 percent of CFS patients—had morphed into uncertainty.  Dr. John Coffin of Tufts University, however, reassured the audience that it takes time to grind the sausage—his oft-used phrase—and that the XMRV findings were, in fact, moving along at a brisk clip.

Lyme expert Dr. Joseph Burrascano asked one of the most salient questions of the conference that so far has no definitive answer:  Why are some scientists finding XMRV and related MLVs in most of their samples while others aren’t finding it at all?  What is responsible? Is it the reagents, the collection, the processing, the methods, the patient cohorts or a combination of the above?  The representative of the Blood Working Group suggested that blood collection and processing may hold the key. Dr. Judy Mikovits echoed that sentiment.

Here are some highlights of the conference:

--Dr. Sam Chow of UCLA discussed data from a Chinese study of men with prostate cancer and healthy controls. Of the 117 controls, 17 or 14.5 percent were positive for one of several types of MLVs, including XMRV, polytropic MLVs and modified polytropic MLVs.  (Polytropic viruses infect the original host—in this case mice—as well as other species, whereas xenotropic viruses like XMRV infect species other than the original host.)  Of the 34 men with prostate cancer, five or 14.5 percent were also positive.  One reason for the hefty numbers in controls may be that Chinese keep mice as pets. Chow said that older men were more likely to have an MLV than younger men.  In addition, Chow reported that XMRV has entered the blood supply in China: 3.4 percent of blood donors were positive for XMRV. There was no association of the RNASE-L genetic defect in the Chinese study.

In contrast, Dr. Robert Silverman of the Cleveland Clinic and co-author of the first study linking prostate cancer to XMRV,  talked about the RNASE-L mutation in his cohort.  In one family of five sons, for instance, four had prostate cancer, along with the RNASE-L mutation.  He also discussed the study he coauthored on macaques infected with XMRV.  In these animals, he explained, the prostate epithelium is infected early on, followed by the seminal vesicles and epididymis, and finally the stromal fibroblasts. Prostate cancer is often preceded by inflammation and XMRV stimulates proinflammatory genes, so it’s conceivable, he said, that XMRV infection could cause inflammation and eventually prostate cancer. The enzyme APOBEC3G, a potent inhibitor of XMRV, mutated XMRV DNA in blood cells of the macaques. Silverman also said that androgen stimulates XMRV, and anti-androgens inhibit the retrovirus.

--Dr. Eric Klein, chair of the Glickman Urological and Kidney Institute at the Cleveland Clinic and co-author of the first study linking prostate cancer to XMRV, discussed his findings on prostate cancer and XMRV. Klein said that XMRV is in urine.  He also gave possible explanations for why some groups haven’t found the retrovirus, including geographical differences, which is what is seen with another human retrovirus, HTLV. Klein stressed that PCR “details” are important in doing studies correctly.

He also discussed how most prostate cancer is relatively benign: though 17 percent of men get the disease, only 3 percent will die from it.  But scientists can’t always predict which prostate cancers need to be treated aggressively, and as it stands now, 90 percent of men with the disease opt for treatment.  Treatment, however, carries it own constellation of possible long-term complications, including incontinence and erectile dysfunction.  Perhaps, Klein said, the XMRV positive patients will prove to be among those who should be treated. Klein said given that many viruses have been shown to cause cancer, “It’s not unreasonable to assume that the retrovirus XMRV could cause cancer.”  Mutations, he said, in RNASE-L and MSR1 genes are associated with an increased risk of prostate cancer. In addition, eunuchs may have a decreased risk of prostate cancer not because of their diminished production of testosterone, but due to the fact that they’re not exposed to pathogens through sex. 

--Dr. Ila Singh of the University of Utah and co-author of a study linking XMRV to prostate cancer voiced that XMRV may become a marker for prostate cancer.  It’s conceivable, she said, that XMRV status may eventually prove to be a better indicator than the current PSA test, and perhaps antiretroviral therapy will be effective in treating the disease. She explained that the XMRV gag (the basic physical infrastructure of the retrovirus) cross-reacts with Moloney mouse MLV.  However, the envelop (the retroviral protein that makes up the outside of the retrovirus) reacts only to XMRV.  Of 233 men with prostate cancer in her study, 27 percent were XMRV positive.  Interestingly, the higher the Gleason score—which is used to determine the prostate-cancer prognosis and ranges from two to 10—the more likely the men were to be infected with XMRV. 

Singh’s CFS study involves 200 healthy controls and 105 patients, all from the Utah area. Singh said she won’t use nested PCR, because in her view contamination can result.  Other ways to reduce contamination:  Handle only one specimen at a time, and have a negative control.  Her tests, she said, are very sensitive at a 97.5 percent detection rate, with a specificity of 100 percent (i.e., no cross reaction with other retroviruses).

--Dr. Maureen Hanson of Cornell University is studying 30 subjects, with a mean age of 39.  Ten of those patients supplied by longtime CFS physician Dr. David Bell were severely ill with CFS, with less than three hours of daily upright activity.  Another ten had recovered from CFS, with 13.5 hours of upright activity daily. And, finally, 10 healthy controls weighed in with more than 15.5 hours of daily upright activity.  Hanson’s findings are consistent, she said, with the Lombardi Science study (which found XMRV in 67 percent of CFS patients) and the recent FDA/NIH/Harvard MLV study (which found XMRV-related MLVs in 86.5 percent of patients). She also said that she’s never worked with mice in her lab, making contamination with a mouse retrovirus less likely. 

--Dr. Judy Mikovits of the Whittemore Peterson Institute and principal investigator of the first study linking XMRV to CFS talked about a London CFS cohort (and then, I believe, it was British researcher Dr. Jonathan Stoye who corrected her and said that the cohort was nearer to Kent) who met the Canadian consensus and suffered from severe cognitive dysfunction, joint pain, vertigo and tender lymph nodes; more than 50 percent were homebound. The predominant MLV was XMRV, and the rate of infection among CFS patients was 70 percent.  Fifty blood donors served as controls. Dr. Jonathan Kerr (who, like Jonathan Stoye, was an author on the second negative British XMRV CFS study) drew their blood. Four percent of the controls were positive for XMRV.

--Dr. Mary Kearney of the National Cancer Institute discussed the assays she developed to detect XMRV, which she said can discriminate between XMRV and mouse retroviruses.  She explained that  mouse retroviruses emit a lower level of florescence than XMRV.  She claimed she can distinguish between the two with 100 percent accuracy. Perhaps her assay will be used to render a final verdict on the mouse-contamination theory.

--Dr. Ross Molinaro of Emory University, co-author on the first study linking XMRV to prostate cancer, said that XMRV encodes a previous unknown Orf3 protein with punctate patterns.  In macaques, he explained, the prostate epithelium is infected early on, followed by the seminal vesicles and epididymis, and finally the stromal fiberblasts. 

--Dr. Francois Villinger of Emory University chronicled the infection of macaques with XMRV.  He said their CD4, CD8 and natural killer cells were infected and was surprised that monocytes were not.  "The viral load in blood was contained very quickly," he said. Chronic infections, Villinger said, were seen in the spleen, epididymis, macrophages in the lung, the seminal vesicles, cervix and vagina. Villinger said he didn't look at the breast or spinal cord.  Someone in the audience brought up screening sperm banks for MLVs.

--Dr. Jonas Blomberg of Uppsala University in Sweden looked at CFS and fibromyalgia in Swedish patients. Judy Mikovits supplied five samples, and Blomberg found three to be positive, so he was able to detect the retrovirus, just not in the Swedish cohort. Of the 35 CFS patients and 15 fibromyalgia patients, all were negative. 

--Dr. Graham Simmons of the Blood Working Group discussed the different phases of study for the blood people.  Phase 1:  assay evaluation. Of all the assays, he said, the CDC’s and the FDA’s were the most sensitive. Phase 2: pilot clinical study.  Phase 3: clinical sensitivity specificity.  Phase 4: blood donor clinical panel. While phase 2 to phase 4 are not complete, “We do think we have begun to figure it out,” Simmons said and indicated that proper collection and processing of blood are vitally important.

--Dr. Nicole Fischer of University Medical Center Hamburg-Eppendorf found XMRV in one out of 300 men with prostate cancer and one out of 70 controls in Germany.

--Dr. Shyh-Ching Lo of the FDA talked about the findings in FDA/NIH/Harvard paper, which he co-authored, and said that different primers yield different results.

--Dr. Brigitte Huber of Tufts University focused on contamination as the cause of XMRV positive samples. Veteran CFS physician Dr. Susan Levine supplied the 111 patients, all of whom met the Fukuda CFS definition; 25 percent were severely disabled. Only one of the 111  patients—less than 1 percent—proved positive. 

Last fall, Huber collected new blood:  three CFS samples and 36 healthy controls.  Using  nested gag PCR, two out of the three CFS patients and 17 of the 36 controls were positive. Twelve samples were negative. Mouse DNA probes detected mouse DNA in those 17 positive samples from CFS patients, and Huber called the correlation “shocking.”  Her conclusion was that a common lab reagent is contaminated with mouse DNA.  Most of her samples contained several MLVs.  Her lecture drew criticism from several members of the audience.  One outspoken critic shouted to Huber that heparin tubes were a “nightmare.  Why are you still using it?” The heparin naysayers used EDTA tubes instead.

--Bill Switzer, lead investigator of the CDC’s negative XMRV CFS study, reported on the agency’s prostate cancer study of 162 patients.  Switzer said that the CDC found a gag sequence in one and pol sequences in three. (Pol proteins synthesize viral DNA.)  Other scientists are looking at RNA, Switzer said, and the CDC is looking at DNA.  Switzer made the point that the Robert Koch Institute in Germany didn’t find XMRV in prostate-cancer patients either. 

--Dr. Frank Ruscetti of the National Cancer Institute and co-author of the first study linking XMRV to CFS said that there are 17 million people in the world with Chronic Fatigue Syndrome, and all of them have contacted Judy Mikovits.  That line drew a huge laugh from the audience.  Single round PCR, he explained, locates only 15 percent of cases, whereas nested PCR finds 69 percent. XMRV reservoirs, he said, have not yet been identified. One patient who was studied had both XMRV and a polytropic MLV.  When I asked if that person was more ill, Judy Mikovits replied yes.

Coming up:  A look at the salient posters presented at the conference.

This article is copyright CFS Central 2010. All Rights Reserved. You may quote up to 150 words from this article as long as you indicate in the body of your post (as opposed to a footnote or an endnote) that the excerpt is by Mindy Kitei for CFS Central. You may not reprint more than 150 words from this article on blogs, forums, websites or any other online or print venue. Instead, refer readers to this blog to read the article.