Who would you choose?
If you had to give a Nobel Prize to either Konnie Knox or Anthony, Fauci, which one would you choose?
The Historic Konnie Knox Interview in the New York Native, issue #678, April 15, 1996
Konstance Knox, Ph.D., is an HHV-6 researcher who has just published a study with extraordinary implications for AIDS research and treatment strategies. Along with colleague Donald R. Carrigan, Ph.D., Knox demonstrated that 100 percent of HIV-infected patients studied (ten out of ten) had active Human Herpes Virus 6 Variant A infections in their lymph nodes early in the course of their disease. Seventy-five percent of these patients, in fact, had CD4 cell counts higher than 200 (the cut-off for receiving a diagnosis of AIDS), up to as high a CD4 count as 700. This finding led Knox and Carrigan to conclude that "active HHV-6 infections appear relatively early in the course of HIV disease and in vitro studies suggest that the A variant of HHV-6 is capable of breaking HIV latency, with the potential for helping to catalyze the progression of HIV infection to AIDS."
This new study, in other words, presents data further implicating HHV-6, particularly Variant A (HHV-6A), as a cofactor (at the very least) in the development of AIDS. (The report is "Active HHV-6 Infection in the Lymph Nodes of HIV Infected Patients: In Vitro Evidence That HHV-6 Can Break HIV Latency," published in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology," April 1, 1996.)
Knox, who has a Ph.D. in Experimental Pathology from the Medical College of Wisconsin, is currently conducting cancer research in the Immunotherapy Program at St. Luke's Medical Center in Milwaukee, Wisconsin. She spoke to the Native on the day following publication of the new study.
Neenyah Ostrom: What is the bottom line, with respect to your new findings? Is it that Human Herpes Virus 6 (HHV-6) is present from the beginning of what we define as AIDS?
Dr. Konstance Knox: HHV-6 is present from very early in HIV infection. So we're not talking about waiting until people have opportunistic infections, and CD4 counts between 100 and 200. We're finding HHV-6 in the lymph nodes early-active infection; this virus is replicating. This is unheard of for any other opportunistic infection, even TB. The only opportunistic infections that you see in AIDS patients with CD4 counts above even 100 are TB and Herpes simplex and Herpes zoster. And all three of those, of course, also infect healthy people and cause disease.
So, what we found, when we examined the lymph node biopsies of HIV-infected patients, was HHV-6. We found both variants of HHV-6-HHV-6A and HHV-6B-but the predominant virus was HHV-6A.
And we're talking about finding the virus in lymph nodes of patients with CD4 counts of over 700. The mean CD4 count of 75 percent of the patients we examined was approximately 300. (There was a total of ten patients in this study just published, and we had CD4 counts on eight of them.) That's a unique finding. And one of the patients had a CD4 count of 711. So why is that virus, HHV-6A, there?
My personal impression, because of where we find HHV-6A-we find a predominance of infection in the germinal center of the lymph node, which is where we know HIV hangs out-is that the tat protein of HIV stimulates HHV-6A replication. And in the study that we have just published, the one that came out yesterday [April 1], we showed that HHV-6A causes an increase in HIV production. These findings are not based solely on this one study. We have done subsequent studies, and there is another already-published study by Charles Wood from Miami also demonstrating that tat protein from HIV induced more HHV-6A production.
So the theory-what seems reasonable to us-is, because these viruses hang out in the same place, and they infect the same cells, that it's not an accident that they co-localize-where you find HIV, you find HHV-6A.
I think that there is a mutual enhancement and potentially almost a mutual dependency for efficient replication. My impression is that HIV kind of acts as a wet nurse to HHV-6A, because in all the other immunocompromised patients that we have looked at-and primarily, these are bone marrow transplant patients-we don't find the A variant of the virus. We don't find it, and the best guestimates of how many people are infected with type A-well, the numbers are sketchy. Because of the blood tests previously available, we only know about type B.
You know, the classic numbers are that 90 percent of people by the age of two are infected with HHV-6. But that's the B variant, not the A variant. And the best estimate, up to about the age of 12, is that about five to 15 percent of people are infected with variant A.
The epidemiology of HHV-6A infection has not been done. Now, it's kind of curious to me why the studies have not been done. You know, there's been a lot of sort of pooh-poohing about the role of HHV-6 in AIDS. I think that's because people look at it, and they say, well, everybody's infected with HHV-6 by the age of two. Yes, everybody's infected with the B variant. But we don't know how many people are infected with the A variant.
We've just completed a study that we have submitted in which we examined 22 HIV-positive and AIDS patients. Every one of them has active replication of HHV-6A and it doesn't matter what stage of disease they're in, from frank AIDS, to autopsies, all the way up to people with CD4 cell counts of over 700.
We believe there is a special interaction between HIV and HHV-6A.
N. Ostrom: How different are variants B and A from each other?
K. Knox: Do you mean biologically?
N. Ostrom: Yes. I've heard speculation that they should have been classified as two different viruses, or that, conversely, HHV-7 is no more different from the two HHV-6 variants than they are from each other.
K. Knox: HHV-7 is probably more akin to HHV-6B. There was an interesting study-and it was a PCR [polymerase chain reaction, i.e. "DNA amplification"] study-which basically showed that, if you were to analyze peripheral lymphocytes, you can find HHV-7 and HHV-6B in about 83 percent and 25 percent of healthy people, respectively. HHV-6A is found much, much less frequently. We're talking about a very small percent-five percent of people.
HHV-6A is different. Probably a general rule of thumb is that HHV-6A can do everything that B can do, and more.
And it's also much more destructive. It is a very destructive virus. It's more similar to what people think of when they think of a herpes virus. It is very lytic-it kills very well, and it destroys tissue very well. It can infect the brain, the lungs, the lymphoid organs, and the bone marrow.
In all the dozens to hundreds of transplant patients we've looked at, if we find HHV-6 disease, it's variant B. We have only seen HHV-6A in, I think, five different individuals, from whom we've isolated it or stained it in tissues. These are not HIV-positive individuals.
So, we found HHV-6A in five out of 100 or so patients. Four of those patients were dead.
It is very destructive.
N. Ostrom: The question then becomes, in my mind, can HHV-6A do everything that HIV can do?
K. Knox: As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV.
And these are data from many people's laboratory studies, and that includes Paolo Lusso and Robert Gallo, as well as our own.
Where we have seen HHV-6A in tissue, we see dead tissue. And where you see HIV-you know, you can have HIV alone, and you may see some reactive changes, like the immune system reacting to a viral infection as if you have flu or something like that.
But you don't see dead tissue. You don't see destroyed organs and scar formation, and that's what you see when you see HHV-6A. We find replacement of the normal architecture of the lymph nodes with scar tissue. HHV-6A kills it. It kills the lymph node tissue.
If I were to place my bets-I do think the viruses HIV and HHV-6A are interactive. I think one of the reasons why you almost always find both of them is that there are viral products, some of the gene products that they make, that enhance each other's replication.
I think they're a team. And, when the two of them are present, they induce the production of more of each other. It's a mutually enhancing relationship.
It's our feeling that if you could interrupt or limit or suppress the HHV-6A infection, the levels of HIV would go down tremendously and HIV would become just a chronic viral infection. And, potentially, the antiviral agents that are out there would be able to manage that.
We don't have any evidence, looking in the tissue, that HIV is responsible for any of the destruction. And, if you think about it, HIV infects patients for years-a decade or more-without progressing to AIDS. When you look in their tissues, you have to ask how you can have such a long-term viral infection and have no damage?
Then something seems to happen somewhere in their course of disease. In some people, it happens earlier; in some people, it happens later; and there's that small percentage of people in whom it never seems to happen at all. Our hypothesis would be that, if we were to look in the lymph nodes of the long-term non-progressors, we would not find HHV-6A.
N. Ostrom: Do you have plans to do that study?
K. Knox: Well, last December I contacted Giuseppe Pantaleo-he's with Tony Fauci's group [at the National Institutes of Health], who had published the New England Journal of Medicine paper just about a year ago on the progressors and long-term non-progressors and the difference in the lymphoid organs between the two.
The basic difference is, in the non-progressors, even though they have replication-competent HIV, they don't have any evidence of degeneration or destruction of their tissue, even though HIV is there. So the hypothesis would be that those few percentage of HIV-infected patients that are long-term non-progressors don't have HHV-6A replicating in their lymph node tissues.
Pantaleo has agreed to send us what the NIH has in the way of tissues from that study. Now, I've been waiting-you know, they had the furlough, and all this other kind of stuff. And then I met with Dr. Pantaleo, actually, about the middle of February, and he again reiterated that he would be sending those tissues to me. Thus, he has personally assured me, but, until I have the tissues, we can't do the direct test of the hypothesis.
N. Ostrom: Why can't we get more funding for this research?
K. Knox: Well, I don't know if you've been tracking the kinds of exposes that Science magazine and others have published, that 80 percent of AIDS research monies are retained within the federal government programs on AIDS research. I think the science is very inbred. And I think there's been a real resistance to entertaining hypotheses or directions of AIDS research that aren't looking specifically at HIV, and that is the basic problem.
Our studies themselves have been enthusiastically received, but the funding hasn't followed. And that is funding through the federal agencies-like the NIH-and I think one of the things that has stopped that has been the confusion with HHV-6B. People think, well, if everybody's infected with HHV-6, why doesn't everybody have AIDS?
Well, we're all infected with HHV-6B, but there's probably only a very small percentage of people infected with HHV-6A. And there's a very unique relationship between A and HIV-when we examine HHV-6B and HIV together, we don't see the same effects. They don't have the same interaction.
So, we're talking about two different viruses, essentially, A and B. And people have merged the two into just HHV-6 and have not appreciated the biologic differences between the two viruses. And actually, in our own research, this has only been clarified in the last year.
In our earlier studies, we only had reagents to look at HHV-6. We did not have the specific reagents to separate the two when we looked in the tissue; we could not tell if it was A or B. It's only been in the past year that we have developed the technologies to be able to distinguish between the two.
N. Ostrom: So you now have very reliable testing that will distinguish between Variant A and Variant B?
K. Knox: Yes.
N. Ostrom: Is it antibody testing, or DNA testing?
K. Knox: It is antibody testing. You could do both, but we use antibody testing.
N. Ostrom: And you test blood? Or do you look only at tissues?
K. Knox: We do tissue biopsies. We look in the tissue itself. And it is very difficult for people to dismiss the idea of HHV6-A because, frankly, nobody knows what the epidemiology is, how many healthy people are infected, how it's transmitted, those kinds of things. We don't know.
And there is a unique kind of collaboration between HHV-6A and HIV that HHV-6B does not have.
HHV-6B does cause disease. It kills immunocompromised patients. It kills transplant patients. But, with respect to AIDS and HIV infection, we believe that the A variant is what is important, because it has this special interaction with HIV.
And variant A is in all the AIDS patients. You don't find it, even in other immunocompromised patients, like bone marrow transplant patients.
There is something special about the interaction of the two viruses, HIV and HHV-6A.
N. Ostrom: Do you think they might have evolved together?
K. Knox: Actually, that is a very interesting thing to think about. Yes, I think that they have evolved together, and I think they really like hanging out together.
There seems to be a selective advantage to the two viruses being in close proximity-and the tat protein of HIV is something HHV-6A seems to like. There's something that HHV-6A makes as well that, in our laboratories, gets HIV really revved up.
If there's an advantage, viruses evolve together. If selective pressures are put on them, they will respond to make their environment more compatible. Viruses want to make more of themselves. They don't destroy things on purpose, because it's actually not to their advantage. It wouldn't surprise me, in their natural histories, if HHV-6A and HIV evolved together, because there's such an enhancement of the two viruses when they're together.
Although in vitro (laboratory) studies published over the last eight or ten years have suggested a synergy between HIV and HHV-6A, in vivo (in the body) evidence has been lacking. Finally, we have examined the tissue of HIV-infected patients and asked, why do all these people have HHV-6A replicating in their tissues when they're still healthy, and we can't even find it in other immunocompromised patients?
It's a very provocative finding.
There's also a study you'll find interesting, that was performed by Italian researcher Dario Diluca, published in the Journal of Clinical Microbiology, I think. Dario has also been doing HHV-6A and HIV research. What he just published last summer is a PCR study of HHV-6 in Chronic Fatigue Syndrome patients. The unique finding concerned HHV-6A. Whereas you can find it in the peripheral lymphocytes of about four percent of healthy people, you see it in 22 percent of Chronic Fatigue Syndrome patients.
There's no difference in the levels of HHV-7 and HHV-6B in healthy people and CFS patients, but the A variant was seen at four percent in healthy people and 22 percent in CFS patients, which is very significant.
N. Ostrom: In their natural killer cell paper, Lusso and Gallo showed that HHV-6 was infecting and killing NK cells in both AIDS and CFS patients. They identified the problem in both sets of patients, so it makes sense that HHV-6A would also be a problem in Chronic Fatigue Syndrome.
K. Knox: Yes, it's a very disregulating virus. Variant B is not benign, but variant A is especially destructive. This is not only when we look at tissues, but also in the test tube-variant A is especially destructive.
Which antiviral drugs do you know have effectiveness against HHV6-A?
We know that foscarnet does; we know that ganciclovir does; and we have treated patients with those agents. Actually, with foscarnet, we have treated specifically HHV-6A infections and seen very nice reversals of clinical syndromes. We don't always know which variant we're treating when we're treating HHV-6.
Also, if you look in the literature, there are three major studies looking at acyclovir in AIDS patients. These were patients with CD4s of less than 150. There was one study in particular that I'm recollecting in which there were about 300 patients. They treated half with AZT alone, and half with AZT plus acyclovir. What they wanted to do was to look to see if acyclovir could suppress CMV reactivation.
Well, what they found was that it had no effect on CMV infection, but there was a curious, significant prolongation of life in the patients who had AZT and acyclovir, as opposed to AZT alone.
There are three major studies in the literature like that, and the speculation as to why that is? They don't know. And they don't address it, because they haven't got a clue as to why it might be.
Now, we have never treated HHV-6 infections with acyclovir, because the B variant of the virus is resistant, and that's usually the virus that we see in transplant patients.
But in laboratory testing, HHV-6A is sensitive to acyclovir. So we have a curiosity as well. I mean, that would be pretty dandy, because certainly acyclovir has less toxicity than ganciclovir, and if you're talking about treating healthy people in a clinical trial, you're looking for something that people can take orally. You don't want them to have to come in for IV infusions, and foscarnet would require that.
So I would say that acyclovir and its analogs and ganciclovir would be very interesting.
N. Ostrom: So, what you have discovered should be viewed as good news?
K. Knox: Oh, I think it's tremendously good news.
I think it offers the best hope that we've seen in 15 years of this epidemic.
That's because it's the first new approach. And the difference is that we believe that actually what destroys the immune organs, the lymph nodes, is HHV-6A. It is not HIV. HIV keeps it going, and HHV-6A keeps goosing HIV, and together they keep secreting products that each other love. They stroke each other. And that's a hard team to break up. You can't do it just by targeting HIV.
N. Ostrom: Is there anything else you'd like people to know about your research?
K Knox: Now that we've made the distinction between the two HHV-6 viruses, A and B, we're really hoping that funding is loosened up and the abuses of how AIDS research has been managed by the government agencies, by NIH-certainly, we've been caught in that trap. I just hope that they loosen up soon enough that we don't have to abort our program. And it's getting pretty close. It's pretty close.
The Anthony Fauci Story
The Historic Konnie Knox Interview in the New York Native, issue #678, April 15, 1996
Konstance Knox, Ph.D., is an HHV-6 researcher who has just published a study with extraordinary implications for AIDS research and treatment strategies. Along with colleague Donald R. Carrigan, Ph.D., Knox demonstrated that 100 percent of HIV-infected patients studied (ten out of ten) had active Human Herpes Virus 6 Variant A infections in their lymph nodes early in the course of their disease. Seventy-five percent of these patients, in fact, had CD4 cell counts higher than 200 (the cut-off for receiving a diagnosis of AIDS), up to as high a CD4 count as 700. This finding led Knox and Carrigan to conclude that "active HHV-6 infections appear relatively early in the course of HIV disease and in vitro studies suggest that the A variant of HHV-6 is capable of breaking HIV latency, with the potential for helping to catalyze the progression of HIV infection to AIDS."
This new study, in other words, presents data further implicating HHV-6, particularly Variant A (HHV-6A), as a cofactor (at the very least) in the development of AIDS. (The report is "Active HHV-6 Infection in the Lymph Nodes of HIV Infected Patients: In Vitro Evidence That HHV-6 Can Break HIV Latency," published in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology," April 1, 1996.)
Knox, who has a Ph.D. in Experimental Pathology from the Medical College of Wisconsin, is currently conducting cancer research in the Immunotherapy Program at St. Luke's Medical Center in Milwaukee, Wisconsin. She spoke to the Native on the day following publication of the new study.
Neenyah Ostrom: What is the bottom line, with respect to your new findings? Is it that Human Herpes Virus 6 (HHV-6) is present from the beginning of what we define as AIDS?
Dr. Konstance Knox: HHV-6 is present from very early in HIV infection. So we're not talking about waiting until people have opportunistic infections, and CD4 counts between 100 and 200. We're finding HHV-6 in the lymph nodes early-active infection; this virus is replicating. This is unheard of for any other opportunistic infection, even TB. The only opportunistic infections that you see in AIDS patients with CD4 counts above even 100 are TB and Herpes simplex and Herpes zoster. And all three of those, of course, also infect healthy people and cause disease.
So, what we found, when we examined the lymph node biopsies of HIV-infected patients, was HHV-6. We found both variants of HHV-6-HHV-6A and HHV-6B-but the predominant virus was HHV-6A.
And we're talking about finding the virus in lymph nodes of patients with CD4 counts of over 700. The mean CD4 count of 75 percent of the patients we examined was approximately 300. (There was a total of ten patients in this study just published, and we had CD4 counts on eight of them.) That's a unique finding. And one of the patients had a CD4 count of 711. So why is that virus, HHV-6A, there?
My personal impression, because of where we find HHV-6A-we find a predominance of infection in the germinal center of the lymph node, which is where we know HIV hangs out-is that the tat protein of HIV stimulates HHV-6A replication. And in the study that we have just published, the one that came out yesterday [April 1], we showed that HHV-6A causes an increase in HIV production. These findings are not based solely on this one study. We have done subsequent studies, and there is another already-published study by Charles Wood from Miami also demonstrating that tat protein from HIV induced more HHV-6A production.
So the theory-what seems reasonable to us-is, because these viruses hang out in the same place, and they infect the same cells, that it's not an accident that they co-localize-where you find HIV, you find HHV-6A.
I think that there is a mutual enhancement and potentially almost a mutual dependency for efficient replication. My impression is that HIV kind of acts as a wet nurse to HHV-6A, because in all the other immunocompromised patients that we have looked at-and primarily, these are bone marrow transplant patients-we don't find the A variant of the virus. We don't find it, and the best guestimates of how many people are infected with type A-well, the numbers are sketchy. Because of the blood tests previously available, we only know about type B.
You know, the classic numbers are that 90 percent of people by the age of two are infected with HHV-6. But that's the B variant, not the A variant. And the best estimate, up to about the age of 12, is that about five to 15 percent of people are infected with variant A.
The epidemiology of HHV-6A infection has not been done. Now, it's kind of curious to me why the studies have not been done. You know, there's been a lot of sort of pooh-poohing about the role of HHV-6 in AIDS. I think that's because people look at it, and they say, well, everybody's infected with HHV-6 by the age of two. Yes, everybody's infected with the B variant. But we don't know how many people are infected with the A variant.
We've just completed a study that we have submitted in which we examined 22 HIV-positive and AIDS patients. Every one of them has active replication of HHV-6A and it doesn't matter what stage of disease they're in, from frank AIDS, to autopsies, all the way up to people with CD4 cell counts of over 700.
We believe there is a special interaction between HIV and HHV-6A.
N. Ostrom: How different are variants B and A from each other?
K. Knox: Do you mean biologically?
N. Ostrom: Yes. I've heard speculation that they should have been classified as two different viruses, or that, conversely, HHV-7 is no more different from the two HHV-6 variants than they are from each other.
K. Knox: HHV-7 is probably more akin to HHV-6B. There was an interesting study-and it was a PCR [polymerase chain reaction, i.e. "DNA amplification"] study-which basically showed that, if you were to analyze peripheral lymphocytes, you can find HHV-7 and HHV-6B in about 83 percent and 25 percent of healthy people, respectively. HHV-6A is found much, much less frequently. We're talking about a very small percent-five percent of people.
HHV-6A is different. Probably a general rule of thumb is that HHV-6A can do everything that B can do, and more.
And it's also much more destructive. It is a very destructive virus. It's more similar to what people think of when they think of a herpes virus. It is very lytic-it kills very well, and it destroys tissue very well. It can infect the brain, the lungs, the lymphoid organs, and the bone marrow.
In all the dozens to hundreds of transplant patients we've looked at, if we find HHV-6 disease, it's variant B. We have only seen HHV-6A in, I think, five different individuals, from whom we've isolated it or stained it in tissues. These are not HIV-positive individuals.
So, we found HHV-6A in five out of 100 or so patients. Four of those patients were dead.
It is very destructive.
N. Ostrom: The question then becomes, in my mind, can HHV-6A do everything that HIV can do?
K. Knox: As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV.
And these are data from many people's laboratory studies, and that includes Paolo Lusso and Robert Gallo, as well as our own.
Where we have seen HHV-6A in tissue, we see dead tissue. And where you see HIV-you know, you can have HIV alone, and you may see some reactive changes, like the immune system reacting to a viral infection as if you have flu or something like that.
But you don't see dead tissue. You don't see destroyed organs and scar formation, and that's what you see when you see HHV-6A. We find replacement of the normal architecture of the lymph nodes with scar tissue. HHV-6A kills it. It kills the lymph node tissue.
If I were to place my bets-I do think the viruses HIV and HHV-6A are interactive. I think one of the reasons why you almost always find both of them is that there are viral products, some of the gene products that they make, that enhance each other's replication.
I think they're a team. And, when the two of them are present, they induce the production of more of each other. It's a mutually enhancing relationship.
It's our feeling that if you could interrupt or limit or suppress the HHV-6A infection, the levels of HIV would go down tremendously and HIV would become just a chronic viral infection. And, potentially, the antiviral agents that are out there would be able to manage that.
We don't have any evidence, looking in the tissue, that HIV is responsible for any of the destruction. And, if you think about it, HIV infects patients for years-a decade or more-without progressing to AIDS. When you look in their tissues, you have to ask how you can have such a long-term viral infection and have no damage?
Then something seems to happen somewhere in their course of disease. In some people, it happens earlier; in some people, it happens later; and there's that small percentage of people in whom it never seems to happen at all. Our hypothesis would be that, if we were to look in the lymph nodes of the long-term non-progressors, we would not find HHV-6A.
N. Ostrom: Do you have plans to do that study?
K. Knox: Well, last December I contacted Giuseppe Pantaleo-he's with Tony Fauci's group [at the National Institutes of Health], who had published the New England Journal of Medicine paper just about a year ago on the progressors and long-term non-progressors and the difference in the lymphoid organs between the two.
The basic difference is, in the non-progressors, even though they have replication-competent HIV, they don't have any evidence of degeneration or destruction of their tissue, even though HIV is there. So the hypothesis would be that those few percentage of HIV-infected patients that are long-term non-progressors don't have HHV-6A replicating in their lymph node tissues.
Pantaleo has agreed to send us what the NIH has in the way of tissues from that study. Now, I've been waiting-you know, they had the furlough, and all this other kind of stuff. And then I met with Dr. Pantaleo, actually, about the middle of February, and he again reiterated that he would be sending those tissues to me. Thus, he has personally assured me, but, until I have the tissues, we can't do the direct test of the hypothesis.
N. Ostrom: Why can't we get more funding for this research?
K. Knox: Well, I don't know if you've been tracking the kinds of exposes that Science magazine and others have published, that 80 percent of AIDS research monies are retained within the federal government programs on AIDS research. I think the science is very inbred. And I think there's been a real resistance to entertaining hypotheses or directions of AIDS research that aren't looking specifically at HIV, and that is the basic problem.
Our studies themselves have been enthusiastically received, but the funding hasn't followed. And that is funding through the federal agencies-like the NIH-and I think one of the things that has stopped that has been the confusion with HHV-6B. People think, well, if everybody's infected with HHV-6, why doesn't everybody have AIDS?
Well, we're all infected with HHV-6B, but there's probably only a very small percentage of people infected with HHV-6A. And there's a very unique relationship between A and HIV-when we examine HHV-6B and HIV together, we don't see the same effects. They don't have the same interaction.
So, we're talking about two different viruses, essentially, A and B. And people have merged the two into just HHV-6 and have not appreciated the biologic differences between the two viruses. And actually, in our own research, this has only been clarified in the last year.
In our earlier studies, we only had reagents to look at HHV-6. We did not have the specific reagents to separate the two when we looked in the tissue; we could not tell if it was A or B. It's only been in the past year that we have developed the technologies to be able to distinguish between the two.
N. Ostrom: So you now have very reliable testing that will distinguish between Variant A and Variant B?
K. Knox: Yes.
N. Ostrom: Is it antibody testing, or DNA testing?
K. Knox: It is antibody testing. You could do both, but we use antibody testing.
N. Ostrom: And you test blood? Or do you look only at tissues?
K. Knox: We do tissue biopsies. We look in the tissue itself. And it is very difficult for people to dismiss the idea of HHV6-A because, frankly, nobody knows what the epidemiology is, how many healthy people are infected, how it's transmitted, those kinds of things. We don't know.
And there is a unique kind of collaboration between HHV-6A and HIV that HHV-6B does not have.
HHV-6B does cause disease. It kills immunocompromised patients. It kills transplant patients. But, with respect to AIDS and HIV infection, we believe that the A variant is what is important, because it has this special interaction with HIV.
And variant A is in all the AIDS patients. You don't find it, even in other immunocompromised patients, like bone marrow transplant patients.
There is something special about the interaction of the two viruses, HIV and HHV-6A.
N. Ostrom: Do you think they might have evolved together?
K. Knox: Actually, that is a very interesting thing to think about. Yes, I think that they have evolved together, and I think they really like hanging out together.
There seems to be a selective advantage to the two viruses being in close proximity-and the tat protein of HIV is something HHV-6A seems to like. There's something that HHV-6A makes as well that, in our laboratories, gets HIV really revved up.
If there's an advantage, viruses evolve together. If selective pressures are put on them, they will respond to make their environment more compatible. Viruses want to make more of themselves. They don't destroy things on purpose, because it's actually not to their advantage. It wouldn't surprise me, in their natural histories, if HHV-6A and HIV evolved together, because there's such an enhancement of the two viruses when they're together.
Although in vitro (laboratory) studies published over the last eight or ten years have suggested a synergy between HIV and HHV-6A, in vivo (in the body) evidence has been lacking. Finally, we have examined the tissue of HIV-infected patients and asked, why do all these people have HHV-6A replicating in their tissues when they're still healthy, and we can't even find it in other immunocompromised patients?
It's a very provocative finding.
There's also a study you'll find interesting, that was performed by Italian researcher Dario Diluca, published in the Journal of Clinical Microbiology, I think. Dario has also been doing HHV-6A and HIV research. What he just published last summer is a PCR study of HHV-6 in Chronic Fatigue Syndrome patients. The unique finding concerned HHV-6A. Whereas you can find it in the peripheral lymphocytes of about four percent of healthy people, you see it in 22 percent of Chronic Fatigue Syndrome patients.
There's no difference in the levels of HHV-7 and HHV-6B in healthy people and CFS patients, but the A variant was seen at four percent in healthy people and 22 percent in CFS patients, which is very significant.
N. Ostrom: In their natural killer cell paper, Lusso and Gallo showed that HHV-6 was infecting and killing NK cells in both AIDS and CFS patients. They identified the problem in both sets of patients, so it makes sense that HHV-6A would also be a problem in Chronic Fatigue Syndrome.
K. Knox: Yes, it's a very disregulating virus. Variant B is not benign, but variant A is especially destructive. This is not only when we look at tissues, but also in the test tube-variant A is especially destructive.
Which antiviral drugs do you know have effectiveness against HHV6-A?
We know that foscarnet does; we know that ganciclovir does; and we have treated patients with those agents. Actually, with foscarnet, we have treated specifically HHV-6A infections and seen very nice reversals of clinical syndromes. We don't always know which variant we're treating when we're treating HHV-6.
Also, if you look in the literature, there are three major studies looking at acyclovir in AIDS patients. These were patients with CD4s of less than 150. There was one study in particular that I'm recollecting in which there were about 300 patients. They treated half with AZT alone, and half with AZT plus acyclovir. What they wanted to do was to look to see if acyclovir could suppress CMV reactivation.
Well, what they found was that it had no effect on CMV infection, but there was a curious, significant prolongation of life in the patients who had AZT and acyclovir, as opposed to AZT alone.
There are three major studies in the literature like that, and the speculation as to why that is? They don't know. And they don't address it, because they haven't got a clue as to why it might be.
Now, we have never treated HHV-6 infections with acyclovir, because the B variant of the virus is resistant, and that's usually the virus that we see in transplant patients.
But in laboratory testing, HHV-6A is sensitive to acyclovir. So we have a curiosity as well. I mean, that would be pretty dandy, because certainly acyclovir has less toxicity than ganciclovir, and if you're talking about treating healthy people in a clinical trial, you're looking for something that people can take orally. You don't want them to have to come in for IV infusions, and foscarnet would require that.
So I would say that acyclovir and its analogs and ganciclovir would be very interesting.
N. Ostrom: So, what you have discovered should be viewed as good news?
K. Knox: Oh, I think it's tremendously good news.
I think it offers the best hope that we've seen in 15 years of this epidemic.
That's because it's the first new approach. And the difference is that we believe that actually what destroys the immune organs, the lymph nodes, is HHV-6A. It is not HIV. HIV keeps it going, and HHV-6A keeps goosing HIV, and together they keep secreting products that each other love. They stroke each other. And that's a hard team to break up. You can't do it just by targeting HIV.
N. Ostrom: Is there anything else you'd like people to know about your research?
K Knox: Now that we've made the distinction between the two HHV-6 viruses, A and B, we're really hoping that funding is loosened up and the abuses of how AIDS research has been managed by the government agencies, by NIH-certainly, we've been caught in that trap. I just hope that they loosen up soon enough that we don't have to abort our program. And it's getting pretty close. It's pretty close.
The Anthony Fauci Story
November
2, 1984 was an especially tragic day in the Chronic Fatigue Syndrome/AIDS epidemic. That was the day Anthony
Fauci became the Director of the National Institutes of Allergy and Infectious
Diseases. (NIAID). (Good Intentions p.128) It was the day a
thin-skinned, physically ultra-diminutive man with a legendary Napoleonic
attitude was positioned by destiny to become the de facto AIDS Czar. In the fog
of culpability that constitutes what could be called "Holocaust II" one thing is clear: the HIV/AIDS
buck, on its way to the very top of the government, at least pauses at the
megalomaniac desk of Anthony Fauci.
In his book, Good Intentions, Bruce
Nussbaum writes, “Fauci looked as if he had just stepped out of a limousine.
Trim and athletic, Fauci’s tailored suits, cuff-linked shirts, and aviator
glasses set him far apart from the rest of the scientists and administrators at
the NIH.” (GI p.128) Fauci had risen quickly at NIH. According to
Nussbaum, he began work at NIH in 1968 after his residency and “by 1977 he was
deputy clinical director of NIAID.” (GI p.128) Nussbaum describes Fauci
as “an aggressive administrator,” not a “details man,” “a big picture kind of
guy.” (GI p.128) Nussbaum reports that “Fauci saw AIDS as a dreadful disease—and
an opportunity for NIAID to grow into a much bigger, more powerful institute.
AIDS was his big chance. He wasn’t known as a brilliant scientist, and he had
little background in managing a big bureaucracy; but Fauci did have ambition
and drive to spare. This lackluster scientist was about to find his true
vocation—empire building.” (GI p.128) Unfortunately, the empire his
extreme ambition would build was "Holocaust II." If the mantra during Watergate
was “follow the money,” the mantra for uncovering the crimes of "Holocaust II"
(other than “follow the heterosexism”) could be “follow the empire building.”
And one of the morals of the story is that “lackluster” can have extreme
consequences.
According to Nussbaum, in order to make
his dreams come true, Fauci had to fight “for a bigger piece of the AIDS
research pie” which he succeeded at by getting a sizable amount of the funds
that Congress appropriated for AIDS research. (GI p.129) Fauci also had
to fight to get AIDS out of the claws of the National Cancer Institute where
the virus that was believed to be the cause of AIDS had been discovered (or,
more accurately, stolen). Fauci argued that it was his institute’s right to
take on the lion’s share of the research because, although AIDS did involve cancer
(Kaposi’s sarcoma), it was, after all, an infectious disease. Fauci got his way
and his success is reflected in the evolving financial numbers Nussbaum
provides: “A growing budget for AIDS research, like a rising tide, lifted Tony
Fauci’s profile considerably on the NIH campus. In 1982, NIAID received
$297,000 in AIDS funding. In 1986 it received $63 million. In 1987, the sum
reached $146 million. By 1990, NIAID’s annual AIDS funding was pushing half a
billion dollars. Tony Fauci’s ship had come in.” (GI p.132)
Fauci’s ship coming in meant the gay
community’s would be sinking fast. It would fall to Anthony Fauci to be the
Enforcer-in-Chief of the "homodemiological" (and "Afrodemiological") HIV/AIDS and
“chronic fatigue syndrome is not AIDS” paradigms of Holocaust II. No one can
argue that he didn’t do a spectacular job of paradigm enforcement for three
dreadful decades.
Starting in the mid 1980s an organization
called the American Foundation for AIDS Research (amfAR) played a multifaceted
role of raising money for HIV research and enlisting celebrities in a glamorous
and ultimately shameful HIV propaganda campaign that made the putatively private
organization essentially a de facto arm of the government’s HIV/AIDS
establishment. If one considers the HIV theory of AIDS a Potemkin biomedical
village that gays were forced to live in, then amfAR as one of its leading real
estate agents. John Lauritsen, in his book, The AIDS War, writes
that “[amfAR] was founded as an alternative to the AIDS establishment, to
provide funding for research that was not predicated on the ‘AIDS virus’
hypothesis. It didn’t last long. . . . I am not aware that even a penny has
ever been given to a researcher who publicly expressed doubts as to the
etiological role of HIV or the benefits of the nucleoside analogues.” (AW
p.437)
In addition to becoming one of the leading
private promoters of the government’s HIV/AIDS paradigm propaganda, amfAR
played a disturbing role in squelching serious scientific criticism of the HIV
hypothesis and in helping turn the entire field of AIDS into a world of
heterosexist, totalitarian, abnormal science. Lauritsen describes an
historically important amfAR moment in the AIDS disaster in his first book Poison
by Prescription: “A ‘Scientific Forum on the Etiology of AIDS,’ sponsored
by the American Foundation for AIDS Research (amfAR), was held on 9 April 1988
at the George Washington University in Washington, D.C. In the words of the amfAR
‘fact sheet’, the forum was convened to critically examine the evidence that
human immunodeficiency virus (HIV) or other agents give rise to the disease
complex known as AIDS.” (PBP p.143)
According to Lauritsen, it was supposedly
an opportunity for Peter Duesberg, the University of California at Berkeley
retrovirologist who first challenged the HIV theory of AIDS “to confront
members of the ‘AIDS Establishment’ over their hypothesis.” (PBP p.143)
He reports, however, that “Despite these praiseworthy intentions, the forum
appears to have had a hidden agenda; to discredit Duesberg.” (PBP p.143)
Lauritsen characterized the forum as a “Kangaroo Court.” The forum would make
great scene in a play about the nasty, zany world of AIDS and HIV
pseudoscience. It was anything but an honest, open collegial discussion about
the nature of AIDS. Scientific philosopher Thomas Kuhn Kuhn would roll over in his grave if anyone called it
genuinely scientific. By Kuhn’s standards, some of the leading voices at the
forum may have even demonstrated that they should not even have been considered
real scientists. Politicians, yes, scientists not so much. Even the HIV
theory’s ardent acolyte, Michael Specter, the reporter from The Washington
Post (and future New Yorker writer) who was among the 17
journalists at the Forum, saw through the charade, noting that the meeting “was
billed as a scientific forum on the cause of AIDS but was really an attempt to
put Duesberg’s theories to rest.” (PBP p.144) It was more like they
wanted to put Duesberg himself permanently to rest.
The meeting had the tone and style that was
endemic to HIV/AIDS research and characteristic of abnormal science. Lauritsen
reported that “While no blows were struck, some of the HIV protagonists fell
below the standards of civility that are expected in scholarly debate . . . .
At all times Duesberg retained good manners and a sense of humor, in the face
of invective, insults, and clowning from his opponents.” (PBP p.144)
One of the signs that AIDS in general was
being conducted in the opposite world of what could be called abnormal, totalitarian science was the
uncanny willingness of the scientists to abandon the traditional rules of
evidence known as Koch’s postulates. Instead, AIDS researchers, including the
ones at the amfAR forum, were willing to “revise Koch’s in a more permissive
direction: it would no longer be necessary to find the microbe in all cases of
the disease. Mere correlations between microbial antibodies and the
progression of the disease would be sufficient. HIV could be proved
‘epidemiologically’ to be the cause of AIDS.” (PBP p.145) Given the unrecognized
sexual politics of the science that was operative among this crowd, they were
basically saying, without realizing it, that causation could be established "homodemiologically."
The presumptions of heterosexist and political epidemiology would trump the
traditional rules of evidence. And those rules could basically be summed up as
“Heads I win and tails you lose.” “You” basically being gays and eventually
blacks.
Lauritsen caught the powerful HIV
advocates in the act of doublespeak that is common to abnormal, totalitarian science:
“Actually, the HIV advocates talked out of both sides of their mouths with
regard to Koch’s postulates. On the one hand, they disparaged them as in need
of ‘modification’ (read abandonment); on the other hand, they were doing their best
to come up with data that would satisfy at least the first postulate.” (PBP
p.145)
Duesberg’s opponents at the forum included
a living, breathing example of scientific conflict of interest, William
Haseltine, a scientist who was in the process of making a lot of money from HIV
testing, and Anthony Fauci, the empire-building Director of NIAID.
At the amfAR Forum, Fauci and others
played a curious unfair game with Duesberg. Hypocritically they accused
Duesberg of citing research that was out of date even though it was basically the
same research quoted at that time by the AIDS establishment. On the other
hand, when Duesberg would ask Fauci and others for actual references to support
their statements at the amfAR forum, he was “rudely rebuffed,” and
according to Lauritsen, they tried to shore up their viewpoint about HIV with
unpublished data, or “their own private facts.” (PBP p.147) “Private
facts” not on the public record are another sure sign that AIDS was a
manifestation of the opposite world of abnormal science. Unfortunately their
private facts about AIDS were also connected to each other by a private
scientific logic.
The 800-pound gorilla at the amfAR forum
was the fact that evidence of HIV could not be found in all AIDS patients,
which should have been strong—damning even—evidence that HIV couldn’t possibly
be the cause of AIDS, that is, if Kuhnian normal science was being practiced.
As scientist Marcel Beluda pointed out at the meeting, “sometimes even a single
exception is sufficient to disprove a theory.” . . . This is the crux of the
matter. The virus cannot be found in all cases of AIDS.” (PBP p.151) One
could say that still believing that HIV is the cause of AIDS in the face of
evidence that it could not be found in all patients is Exhibit A that delusion
and denial were running the show.
Fauci’s answer belongs in a beginner’s
textbook on the card tricks of abnormal science: “Fauci responded to Beluda by
saying that a good lab was able to isolate the virus in 90-100% of the cases,
that there was ‘no question about it.’ Fauci did not provide a reference to
published data, nor did he indicate what the ‘good labs’ were, or how exactly
they differed from the not-so-good labs.” (PBP p.151) References belong
to the abandoned Kuhnian world of normal science.
Duesberg made a number of arguments, based
on his years as one of the celebrated deans of retroviral research, about why
HIV could not possibly be the cause of AIDS.
Lauritsen wrote that Fauci’s presentation
“while aspiring to be a point-by-point rebuttal to Duesberg, consisted mainly
of disconnected assertions, delivered in a tone of petulant indignation.
Epidemiological studies conducted in San Francisco and unpublished laboratory
reports seemed to be the basis of most of his statements. So far as I could
tell, he understood none of Duesberg’s arguments . . . .” (PBP p.155)
The role of the AIDS politics of
epidemiology in AIDS research showed itself dramatically at the forum.
According to Lauritsen, “In the question period, Beluda asked if the evidence
were sufficient that HIV is necessary for the development of AIDS, Fauci
replied that he hoped the epidemiologists would answer that question.” (PBP
p.157) (Given the political and heterosexist nature of AIDS epidemiology, one
could guess how that was going to turn out.)
The most shocking and downright hilarious
episode at the forum occurred when Harvard Medical School’s William Haseltine
spoke. Lauritsen reported that “His presentation was devoted largely to
personal attacks on Duesberg.” (PBP p.157) Ironically, he
accused Duesberg of resorting to
personal attacks. In another telltale moment of abnormal science, Lauritsen
caught Haseltine trying to explain away the anomalies about the evidence of
AIDS in men and women in America: “He attacked Duesberg’s ‘paradox,’ that the
AIDS virus seemed to be able to discriminate between boys and girls, by saying
that this was not true outside the U.S.—in Africa, about equal numbers of men
and women develop AIDS. (He seemed oblivious to the paradox that a microbe
should be able to discriminate in one country, but not in another.)” (PBP
p.158) In a memorable moment that perfectly captured the essence of the past
and future of AIDS research, Haseltine showed the audience a slide of a graph
that was meant to absolutely demolish Duesberg’s argument. The slide was
supposed to show a correlation between the rise in HIV titers with the decline
of T cells in the progression of AIDS. There was just one small problem:
Duesberg quickly noticed that there were no units on the vertical axis of
the slide. Haseltine was angry and flustered by the charge and had to ask
Dr. Robert Redfield, an AIDS researcher from the military, how the slide was
prepared. At the forum Redfield said “different measurements were used,” but
later that night at a post-forum party, according to Lauritsen’s report,
Redfield told Duesberg and other people at the gathering that “the graph had
been prepared to illustrate a theoretical possibility. It had no units on it
for the simple reason that it was not based on any data at all. In other
words the slide was a fake.” (PBP p.161) That’s the kind of
ideology-based data that was used to back up the HIV theory of AIDS which
changed the course of millions of lives and fostered the autism catastrophe.
In terms of the habitual use of political
epidemiology (or "homodemiology") rather than real science to deal with AIDS
during Holocaust II, the most disturbing talk was given by Warren Winkelstein,
Professor of Biomedical Environmental Health Sciences at U.C. Berkeley.
Essentially, he too suggested that AIDS would require a new kind of science.
According to Lauritsen, “the point of Winkelstein’s presentation is that Koch’s
postulates should be superseded by new standards for establishing the causal
relationship between microbes and disease, and that these standards should be
based upon ‘epidemiology’ or, as it were, correlations of various kinds.” (PBP
p.162) If this crowd had superseded traditional science anymore than they did,
we all would probably be dead. (But wait. There is still time.)
Most of the scientific world was not aware
of the degree to which this zany cast of characters was improvising a questionable
newfangled science as they went along. And it was being done in a Fauci-style
of “petulant indignation,” to reprise Lauritsen’s very apt phrase. That it was
all dependent on a loosey-goosey, all too subjective political “discipline”
like epidemiology should have disturbed Lauritsen’s sixteen journalistic
colleagues who were at the amfAR affair. But there was already a tragically
cozy relationship between the media and the abnormal scientists of Holocaust
II. For three decades as the HIV/AIDS paradigm held sway, most of the reporters
who covered AIDS were a self-satisfied, inattentive, group-thinking,
intellectually slothful bunch who wouldn’t know independent, journalistic due
diligence if it bit them.
Lauritsen’s eyewitness record of the forum
(originally published in New York Native) was an important contribution to the history of the flakey beginnings of the
science and politics of AIDS. His diligent and critical reporting is proof that
not every journalist was hoodwinked by these charlatans. He didn’t buy into
this new improvised epidemiological science that the AIDS establishment was
dumping on the public: “I do not accept the proposition that Koch’s postulates
should be abandoned in favor of epidemiological correlations. This would be a
step backward, a step away from scientific rigor, a step towards impressionism
and confusion.” (PBP p.162) Lauritsen didn’t acknowledge it, but it was
also a big heterosexist (and ultimately racist) step backwards.
Like many others, Lauritsen came face to
face with totalitarian, abnormal science. Unfortunately, even though he was
openly gay himself, he didn’t grasp the manner in which the infernal game was
being played—or what the game was actually concealing. He didn’t fully perceive
the homodemiological underpinnings of what was happening before his very eyes.
But he definitely grasped the fact that the science of the budding AIDS
Establishment was utterly bogus. He concluded his report by writing “I am more
convinced than ever that HIV is not the cause of AIDS. If the HIV advocates
were sure of their hypothesis, they would want to enlighten Duesberg and the
rest of us; they would want to publish their arguments in a proper scientific
journal complete with references. They would not need to resort to
stonewalling, deception, and personal abuse.” (PBP p.168)
The 1988 amfAR Forum was another one of
the tragic “What if?” moments in the dark history of AIDS. What if the reporters
had looked closer at Haseltine’s fake slide and realized that it was the tip of
the iceberg, a little like the scientific version of the Watergate break-in
that would have led them to a much bigger crime if they only followed the lies?
What if they had reported that AIDS science, as practiced by Anthony Fauci, was
simply out-to-lunch? What if they had been independent enough to notice that
epidemiology was overplaying its arrogant, biased hand and that, in reality, it
is actually a soft, subjective enterprise vulnerable to political manipulation?
Why was it beyond the pale to wonder if this petulant, hostile gathering was
actually the expression of some rather unsavory feelings and hostilities
directed at the so-called beneficiaries of this new kind of “science,” namely
the gay community? Maybe someone should have asked if there was something funky
about a group of hostile, petulant, white heterosexual mostly-male scientists performing
their jerry-built kind of seat-of-the-pants epidemiological science on gays. Wasn’t
that a formula for all kinds of prurient, heterosexist pseudoscientific mischief if ever there
was one? In terms of majorities doing their science on minorities, hadn’t
anyone ever heard of Nazi science or the Tuskegee Syphilis Experiment? God only
knows what personal sexual issues were being acted out by this elite motley
crew under the cover of what has turned out to be high-falluting retroviral
claptrap. Why didn’t anyone other than Lauritsen notice the peculiar,
unscientific defensiveness of the whole affair, i.e. that the ladies had protested
too much? And most importantly for the main event, why was HHV-6, which had
been discovered in AIDS patients two years before that curious amfAR forum, not
put on the table for discussion?
Fauci believed in the kind of transparency
and communications with the public that are typical of abnormal science. He
laid out the draconian media policy that he would maintain for the nearly
thirty years he ran the totalitarian HIV/AIDS empire in a brief piece he wrote
for the AAAS Observer on September 1, 1989.
Fauci wrote, "When I first got
involved in AIDS research, I was reluctant to deal with the press. I thought it
was not dignified. But there was a lot of distortion by those who were speaking
to the press so I changed my mind." The "distortion" was, of
course, coming from those who didn't agree with the very dignified Fauci about
the etiology of AIDS. Fauci had his own idea of what the media's responsibility
is. He notes that his interpretation of what the media is supposed to do
"doesn't even jibe with what competent journalists think." He asserts
that the big dilemma for journalists is between what is "important"
and what is "newsworthy" and he notes that they sometimes "are
not the same." He whines about the fact that journalists are more
interested in the latest story of a cure than the "magnificent
science" involving the regulatory genes of HIV.
Fauci describes what he thinks is the
hierarchy of media. It ranges from The New York Times and The
Washington Post all the way down to publications that "care only
about sales or have axes to grind." (He had yet to face the unwashed
barbarians of the blogs and the commenters of the online forums.) One can
safely assume that the publications with axes to grind were the ones who didn't
agree with the axe that Fauci himself was grinding.
It is amusing that Fauci pontificated in 1989 that "the media are no place for amateurs, particularly when talking about a public health problem of the magnitude of AIDS." Especially when one considers the magnitude of the public health problem that this very self-reverential scientist (that Bruce Nussbaum described as "lackluster") himself helped create for the whole human race. While Fauci would make one think that the real problem in AIDS journalism was the clownish journalist who can’t spell "retrovirus" or one who didn’t listen carefully after asking questions, his real quarry in this peevish little piece is something far more serious. Fauci's real problem was journalists who not only could spell “retrovirus" but could also actually hear what he was saying all too well. The kind of journalists who also knew things about retroviruses and listened to what he was saying so closely and critically that they could make life unpleasant for Fauci and his powerful AIDS cronies by asking inconvenient questions.
It is amusing that Fauci pontificated in 1989 that "the media are no place for amateurs, particularly when talking about a public health problem of the magnitude of AIDS." Especially when one considers the magnitude of the public health problem that this very self-reverential scientist (that Bruce Nussbaum described as "lackluster") himself helped create for the whole human race. While Fauci would make one think that the real problem in AIDS journalism was the clownish journalist who can’t spell "retrovirus" or one who didn’t listen carefully after asking questions, his real quarry in this peevish little piece is something far more serious. Fauci's real problem was journalists who not only could spell “retrovirus" but could also actually hear what he was saying all too well. The kind of journalists who also knew things about retroviruses and listened to what he was saying so closely and critically that they could make life unpleasant for Fauci and his powerful AIDS cronies by asking inconvenient questions.
Fauci's nose should have grown several feet
when he wrote, "We know that reporters must consult more than a single
source and make room for dissenting opinions." What was yet to come in the
AAAS piece made that one of the biggest fibs in the history of American
science. Under the pretense of giving us a little lesson in the relationship
between science and the media and warning that people too often believe what
they read in the papers, Fauci reveals his real agenda: "One striking
example is Peter Duesberg's theory that HIV is not the cause of AIDS. I laughed
at that for a while, but it led to a lot of public concern that HIV was a hoax.
The theory had a great deal of credibility just on the basis of news
coverage." This was Fauci being intellectually dishonest on a couple of
counts. Duesberg never said it was a hoax. He said it was a mistake. A
hoax is a whole other ball of wax, and it is an example of using language politically
to deliberately misrepresent the opposition. Duesberg wasn't saying something
similar to those who say that the landing on the moon was just staged with
props and a camera. He was a Nobel caliber expert on retroviruses pointing out
the deficiencies of the HIV theory in AIDS using basic logic and analyzing the
available evidence. And blaming the media for the credibility given to
Duesberg's ideas ignored all the scientists, (eventually including two Nobel
Prize winners), who publicly supported Duesberg's skepticism
Fauci then introduces us to the smarter
member of his family, his sister: "My barometer of what the general public
is thinking is my sister Denise. My sister Denise is an intelligent woman who
reads avidly, listens to the radio, and watches television, but she is not a
scientist. When she calls me and questions my integrity as a scientist, there
really is a problem. Denise has called me at least ten times about Peter
Duesberg. She says, 'Anthony’—she is the only one who calls me Anthony, 'are
you sure he's wrong?' That's the power of putting someone on television or in
the press, although there is virtually nothing in his argument that makes any
scientific sense." This captures how touchy Fauci was. No one was
questioning his "integrity as a scientist.” His sister was simply asking
him if it was possible that he was wrong, and the answer that would have
shown some scientific integrity would have been "Yes, my dear Denise, it
is always possible that I'm wrong, although I think the evidence suggests I'm right."
The fact that Fauci took this soooooo personally speaks volumes about
the petulant chip-on-the-shoulder attitude problems of those in charge of AIDS. Fauci
put it all on the line. Questioning his so-called science was a threat to his
very being. It shouldn't surprise anyone that he was willing to viciously fight
for so long during Holocaust II to keep everyone from seeing what a house of
cards he had helped build. The funny thing is that in a number of ways this
very piece of his writing suggests he did have serious problems in the
integrity department. (Between the lines of the piece Freudian historians may
one day even find the glimmer of a guilty conscience.)
Fauci, like most of the crowd that gave us
"Holocaust II," knew only too well what normal science is supposed to look like:
“People are especially confused when they see divergent viewpoints about the
same thing. They do not understand that the beauty of science is that it is
self-corroborating and self-correcting, that it is important for scientists to
be wrong.” (If that’s really the case Fauci was indeed doing something
incredibly important with HIV.) It was actually Fauci who didn’t understand
that the whole process of self-corroboration and self-correction was being
short-circuited by the totalitarian hijinks of the petulant HIV/AIDS establishment that
was growing more dominant by the day. The very tone of Fauci’s piece, its
extraordinary imperiousness and presumptuousness about the stupidity of the
public, points to the fundamental problem for a society in which petulant elite
scientific communities have more and more power. Fauci would not only be the
judge and jury of what was true in science, but he also wanted to decide who
deserved to write about it and what they should write. He clearly left no room
for the possibility that the really good journalists would be the kind that
questioned what he had to say.
Fauci also made it pretty clear in the
piece that, try as they might, AIDS critics and dissidents would get absolutely
nowhere because he was permanently stacking the deck against them: “The lack of
clear-cut black-or-white answers plagues the biomedical sciences compared with
the physical sciences. Stanley Pons and Martin Fleishmann said they had
achieved nuclear fusion at room temperature. Other scientists tried, but they
could not reproduce it. Bingo it’s over. But because we cannot ethically do
clinical trials to establish that he is wrong, I am probably going to be
answering Peter Duesberg for the rest of my life.” Someone near him should have
tried to convince Fauci that it wasn’t all about him. One also loves the
presumption that he was going to control the official etiology of AIDS for
the rest of his life. Unfortunately he almost has. Beyond the breathtaking
megalomania of the statement is the stupidity that the only way to show HIV
wasn’t the cause of AIDS was to do clinical trials with patients. All it would
have taken would have been a few patients with AIDS who had no evidence of
HIV. The only people that would be hurt by the implications of that finding
would be the scientists, like Fauci, whose undeserved reputations and incomes
had depended upon the HIV theory. Those HIV-negative patients would be
forthcoming—in spades. In fact those patients were basically the very
immune-compromised chronic fatigue syndrome patients Richard DuBois had seen in
his Atlanta practice in 1980 before the
socio-epidemiological construction of the heterosexist and racist HIV/AIDS
paradigm.
Hillary Johnson reported on the DuBois
Atlanta cases in Osler’s Web Inside the Labyrinth of Chronic FatigueSyndrome Epidemic, her epic work of journalism detailing the CDC’s failure
to acknowledge the true nature of the chronic fatigue syndrome epidemic. It is
now all too painfully obvious that the DuBois cases—with the telltale signs of
hypergammaglobulinemia, t-cell perturbations and persistent reactivated EBV and
CMV infections—were the beginning of the real AIDS/CFS/autism/HHV-6 disaster.
According to Johnson, in 1980 Richard DuBois “saw a thirteen-year old girl who
suffered from a seemingly endless case of mono. As the months passed, he
identified several more cases of the curious syndrome in his practice.” (OW
p.7) He wasn’t alone. According to
Johnson he was in touch with other clinicians who had seen similar cases and he
and his colleagues eventually had a research article published about it in the Southern
Medical Journal in 1984, the same year the big consequential government
mistake of certifying HIV as the official AIDS virus occurred. According to
Johnson, “they [DuBois and his colleagues] had believed that they were
describing a new syndrome, one that would have increasing importance and was
worthy of national attention.” (OW p.7) The DuBois patients morphed into the millions of chronic fatigue
syndrome and HHV-6 patients that Fauci and his organization (which was supposed
to handle infectious diseases) were willfully ignoring while building their
Potemkin AIDS empire.
At the end of Fauci's little AAAS piece comes the
shot across the media’s bow from the uberpetulant AIDS czar: “Scientists need to
get more sophisticated about expressing themselves. But the media have to do
their homework. They have got to learn the issues and the background. And they
should realize that their accuracy is noted by the scientific community.
Journalists who make too many mistakes, who are sloppy, are going to find that
their access to scientists may diminish.” In other words, the scientists that
journalists reported on were going to be the petulant final arbiters of what the public
knows about science. They could decide to cut off journalists they defined
as making mistakes and being sloppy, and one would assume that one of those
sloppy mistakes would probably entail giving any coverage to scientists like
Peter Duesberg, who raised serious questions about what was being called good
science by Fauci and the rest of the HIV/AIDS establishment. Fauci was
basically saying that he and his cronies would only be accountable to
themselves which is the hermetically-sealed, closed-community essence of should be called totalitarian, abnormal science.
If anyone ever makes a serious film about
"Holocaust II" it will have to include the shocking revelation that came to light
during the Eighth International Conference on AIDS in Amsterdam during July of
1992. Its historic importance rivals that of the Wannsee conference during
World War II or the Gulf of Tonkin incident. It was the moment of no turning
back, the moment a line was crossed, a life of virtual pseudoscientific crime against humanity was
virtually signed onto and those responsible for "Holocaust II" lost all forms of
plausible deniability. AIDS almost overnight became AIDSgate and a very unique
biomedical assault against humanity. And, ultimately, the man who stood at the
center of the developments that came out of Amsterdam was Anthony Fauci. Before
Amsterdam one might be able to say that Fauci wasn’t exactly the Bernie Madoff
of the Ponzi Scheme that maintained AIDS, chronic fatigue syndrome and the HHV-6 spectrum catastrophe. But not
after Amsterdam
Hillary Johnson provided a detailed
account of what happened at that Amsterdam conference in her book, Osler’sWeb. She recounts how the conference was electrified by news from a small
press conference that was held in California at which a scientist named “Subhir
Gupta, a University of California immunologist, reported he had isolated
particles of a previously unknown retrovirus from an HIV-negative, ailing
sixty-six-year-old woman, her symptomless daughter and six other patients.” (OW
p.600) According to Johnson, “Investigators and the lay press gathered in
Holland were riveted by Gupta’s announcement that the older woman suffered from
an ‘AIDS-like’ condition wherein a component of her immune system, a subset of
T-cells called CD4 cells, were severely depleted. In addition, she had suffered
a bout of Pneumocystis carinii pneumonia, a so-called opportunistic
infection that afflicted many AIDS patients whose CD4 cells were depleted.” (OW
p.600)
That announcement was soon outdone by a
flurry of shocking revelations from additional scientists at the Amsterdam
conference who had “findings of retrovirus particles in HIV-negative patients
with AIDS-like symptoms.” (OW p.601) A near panic was almost set off
internationally by the possibility that there was a second previously unrecognized
AIDS epidemic on the horizon that was caused by a non-HIV agent. (OW
p.601)
According to Johnson, it turned out that
the Centers for Disease Control was already aware of such HIV-negative cases of
an AIDS-like illness. (OW p.601) Johnson reported that months before
Gupta’s press conference two CDC scientists had reported on “six cases of
non-HIV positive AIDS.” (OW p.601) Their conclusion was that “HIV may
not be the only infectious cause of immune deficiency.” (OW p.601)
The HIV-negative cases of AIDS-like
illness set off an explosion in the press, most notably from Lawrence Altman,
the reporter who guided The New York Times dreadful, sycophantic reporting on
AIDS throughout "Holocaust II." In the Times Altman wrote that the CDC’s
embarrassment was “huge because the agency had lost control over the
dissemination of new information in the field of AIDS.” (OW p.602) (That
anyone at the Times could stress the importance of a government agency controlling
information with a straight face is pretty amazing. And revealing)
According to Johnson, the CFS research
community was especially fascinated by the fact that the Gupta HIV-negative
AIDS-like cases were chronic fatigue syndrome sufferers. (OW p.604) And for anyone following
the bizarre scientific politics of AIDS, it was interesting that Gupta’s
colleague, the man who supposedly isolated the new retrovirus was none other
than Zaki Salahuddin, the scientist who had worked for Robert Gallo and had
faced criminal charges for creating a company that garnered illegal self-dealt
income from his position at the National Cancer Institute. Johnson reported
that when Salahuddin was asked whether HIV-negative AIDS might be chronic
fatigue syndrome, he said, “It’s a fair statement. But I’m not a prophet. Time
and money [are] required for this.” (OW p.604) Johnson also reported
that “Salahuddin confirmed that he and Gupta, who had a cohort of CFS patients
in his clinical practice and who had presented papers on the immunology of CFS
at medical conferences on the disease, had discussed the possibility that CFS
and non-HIV positive AIDS were the same disease.” (OW p.604) Also,
according to Johnson, the non-HIV positive AIDS cases caught the attention of
Paul Cheney, one of the two pioneering Lake Tahoe chronic fatigue syndrome
researchers. Johnson reported that “For years he had observed that some CFS
patients met the government’s defining criteria for AIDS on every count except
infection with human immunodeficiency virus.” (OW p.604) He also told
Johnson that “It was hardly unheard of . . . to diagnose the kinds of
opportunistic infections that torment AIDS victims—maladies like thrush,
candida and pneumonia—in CFS.” (OW p.604)
The AIDS conference in 1992 should have
been one of those great moments in normal science as described by Thomas Kuhn.
It could have been a moment when “anomalies” should have attracted the
“attention of a scientific community.” (The Structure of Scientific Revolutions p.ix) But this would not be
a moment for AIDS research that “the profession can no longer evade anomalies
that subvert the existing tradition of scientific practice” which would “begin
the extraordinary investigations that lead the profession at last to a new set
of commitments, a new basis for the practice of science.” (SSR p.6) This
would not be one of those eureka moments in science characterized by “the
community’s rejection of one time-honored scientific theory in favor of another
incompatible with it.” (SSR p.6) There would be no “transformation of
the world within which science was done.” (SSR p.6) There would be no
“change in the rules governing the prior practice.” (SSR p.7) As a
result of what happened in Amsterdam, scientists would not alter their
“conception of entities with which [they] had long been familiar.” (SSR
p.7) Amsterdam would not cause the AIDS researchers’ worlds to be “qualitatively
transformed as well as quantitatively enriched by fundamental novelties of
either fact or theory.” (SSR p.7) After the revelations of HIV-negative
AIDS cases, the researchers would still not give up their “shared paradigm.” (SSR
p.11) No new AIDS (or chronic fatigue syndrome = AIDS) paradigm was allowed to
reveal itself in Amsterdam and subsequently be fairly examined and debated. The
HIV-negative cases of AIDS would not be recognized as an important scientific
surprise that would lead scientists “to see nature in a different way.” (SSR
p.53) The scientific world of AIDS researchers did not change “in an instant” (SSR
p.56) the way it might have if AIDS research was taking place in the world of
normal science. (And consequently, immune-system-destroying HHV-6 would remain locked in the basement of "science.")
Tragically, the HIV-negative AIDS cases
were not a wake-up call for the scientists that “something had gone wrong” and
hence the anomalous cases were not “a prelude to discovery.” (SSR p.57)
Even though the HIV-negative AIDS cases “violated deeply entrenched
expectations,” (SSR p.59) they were not allowed to change anything about
the AIDS paradigm. In Kuhn’s world of normal science the “traditional pursuit
prepares the way for it own change.’ (SSR p.65) Amsterdam showed
that
AIDS research was being conducted in normal science’s opposite world,one
that should be called "abnormal, totalitarian science." Even if
the HIV-negative AIDS cases could have ultimately led to a new paradigm
that
was “able to account for wider range of natural phenomena,” (SSR p.66)
they were dead on arrival. No “novel theory” about AIDS which was a “direct
response to crisis” (SSR p.75) was allowed to emerge because the
abnormal, totalitarian science of AIDS was politically invulnerable to crisis. At that conference there
was never any chance that the HIV/AIDS theory would be “declared invalid” even
though a new “CFS is a form of AIDS” paradigm was staring out at the conference
from the new anomalous data and was a perfectly credible “alternate candidate.”
(SSR p.77) Kuhn wrote that the decision to reject one paradigm is always
simultaneously the decision to accept another, and the judgment leading to that
decision involves the comparison of both paradigms with nature and with each
other.” (SSR p.77) The HIV-negative AIDS cases were not allowed to
catalyze that kind of intellectual process in Amsterdam. Kuhn would probably
argue that absent a new paradigm to examine and accept in Amsterdam, there was
no exit from the HIV/AIDS paradigm because “To reject one paradigm without
simultaneously substituting another is to reject science itself.” (SSR
p.79) In a way, much of what happened at the AIDS conference was based on
appeals to something quite characteristic of the AIDS establishment and
abnormal science: authority. The petulant HIV/AIDS authorities basically said “Nothing
here, folks. Please move along.” And unfortunately the scientific community and
the media (with a few notable exceptions) did exactly that. Kuhnian anomaly
didn’t turn into Kuhnian crisis and that in turn did not explode into
Kuhnian scientific revolution as it should have. The HIV-negative cases
in Amsterdam should have led to a period of what Kuhn called “extraordinary
science” (SSR p.82) in which “the rules of normal science become increasingly
blurred.” (SSR p.83) (Although one could argue that the rules of AIDS
research already actually were a shocking mess.) Amsterdam would not be the
moment when “formerly standard solutions of solved problems are called into
question.” (SSR p.83) The conference should have been a fruitful time
when scientists were “terribly confused.” (SSR p.84) If things had gone
the way they should have at that conference, the assembled AIDS researchers
would have ultimately changed their view of “the field, its methods, and its
goals.” (SSR p.85)HHV-6 might have been allowed to reveal itself in all its viral glory.
Had the science of Amsterdam been normal,
both AIDS research and chronic fatigue syndrome research might have morphed into
one unified discipline. The dismantling of the “chronic fatigue syndrome isn’t
AIDS” paradigm should have begun in earnest. HHV-6 (and its spectrum or family)
might have emerged quickly as the unifying viral agent(s) of those two
epidemics which should have always been considered one in the first place. What
happened in Amsterdam was a virtual scientific crime. It was the deliberate
attempt to use sheer political force to make a legitimate scientific crisis
disappear. As a result, scientists would not turn to what Kuhn describes as a
“philosophical analysis as a device for unlocking the riddles of their field.”
(SSR p.88) The crisis was not allowed to play itself out and would not
loosen what Kuhn calls the “stereotypes” and provide “the incremental data necessary
for a fundamental paradigm shift.” (SSR p.89) There would be no Kuhnian
“transition from normal to extraordinary research.” (SSR p.91) It should have
been painfully clear in Amsterdam “that an existing paradigm [had] ceased to
function adequately in the exploration of an aspect of nature to which that
paradigm itself had previously led the way.“ (SSR p.92)
A potentially life-saving scientific revolution in AIDS research
was politically nipped in the bud in Amsterdam and in the months that followed.
No “new theory” was allowed to surface that would “permit predictions that are
different from those derived from its predecessor” (SSR p.97) Kuhn
asserted that “the price of significant scientific advance is a commitment that
runs the risk of being wrong.”(SSR p.101) Those in control of the
abnormal science of AIDS had no interest in engaging in any kind of
science that would prove them wrong. “Wrong” was not in their petulant
vocabulary. They had bet their white heterosexual malereputations and the credibility of American
science on their ridiculous and dangerous HIV/AIDS and “chronic fatigue
syndrome is not AIDS” paradigms. Fake dividends of their scientific Ponzi Scheme would be paid out for decades.
What happened in Amsterdam was the opening
and almost simultaneously closing of a Pandora’s Box of incredibly important
scientific questions. The person most responsible for keeping that box closed
then and for the next two decades was the de facto AIDS Czar, Anthony Fauci.
This may have been the last chance for Fauci and the HIV/AIDS establishment to
turn back from the precipice of the HHV-6 spectrum catastrophe.
According to Hillary Johnson, “On August
15, federal scientists convened a meeting in Atlanta to discuss the emerging
health threat of non-HIV positive AIDS. In the three weeks since Sudhir Gupta’s
paper on his isolation of a new intracisternal retrovirus in a handful of
cases, the number of reported cases had risen from approximately thirty to
fifty. Nobel prize winners, members of the National Academy of Sciences, CDC’s
AIDS administrators, and Anthony Fauci, head of the National Institute of
Allergy and Infectious Diseases, formed a panel to query scientists Gupta,
David Ho of the Aaron Diamond AIDS Center in New York and Jeffrey Laurence, a
Cornell Medical College cancer and AIDS specialist and associate professor of
medicine, each of whom had been studying cases of the syndrome and discovered
evidence of retroviral infection in patients.” (OW p.606) It didn’t
matter how many brilliant scientists from different institutions were queried
at the meeting, because their mindsets about HIV were all the same. It was like
a mini-Woodstock of groupthink. There was no turning back from the HIV/AIDS and
“chronic fatigue syndrome isn‘t AIDS” paradigm. It was eight years old at that
point and the nation’s heterosexist and racist AIDS propaganda and public health policies had been
built around it. It was another moment in abnormal science in which the foxes
had formed a panel to investigate the henhouse. The homodemiological and
Afrodemiological HIV/AIDS and “CFS is not AIDS” paradigm was in very little
real danger.
The manner in which Fauci and his
colleagues basically covered up the shocking anomalies of HIV-negative AIDS was
relatively simple and Orwellian: they disingenuously gave the HIV-negative
cases an obfuscational new name (Idiopathic CD4 T lymphocytopenia or ICL) and
they insisted by fiat that they were not really AIDS cases. The HIV/AIDS elite
insisted that because there was no unifying geographic or chronological “risk
factor” (OW P.603) to be found in these ordinary Americans and they shared no
official AIDS risk factors, there was no HIV-negative AIDS or AIDS-like
epidemic covertly occurring in the general population.
Because the “chronic fatigue syndrome is
not AIDS” paradigm was not challenged by what happened at the Amsterdam
Conference in 1992, for at least another two more decades, the chronic fatigue
syndrome patients were locked into their pathetic heterosexist wild goose chase to find a
cause while constantly avoiding the obvious links between their medical issues
and AIDS. They had Tony Fauci’s blessing for that fool’s errand. His basic
attitude toward CFS was that people shouldn’t be ashamed of being told that
their problem was psychiatric, (OW p.334) which was how the disease was
deceptively framed by the government for nearly three decades. And of course
they were only the tip of the iceberg. Everyone suffering from multi-systemic
problems of the HHV-6 spectrum (like multiple sclerosis, autistic spectrum and even Morgellons
patients) would ultimately pay a heavy price for the intellectual dishonesty of
the 1992 AIDS conference.
Fauci and his colleagues told the public
that the HIV-negative cases of AIDS-like illness were rare, but of course it
all depended on deisease definitions and who was doing the defining and counting. Fauci
disingenuously sent out a call that summer asking that all HIV-negative cases
be reported immediately to him. An editorial in New York Native heeded his call: “Last week
Anthony Fauci of the National Institute of Allergy and Infectious Diseases
asked that all cases of HIV-negative AIDS be reported to him. We reported
thirteen million American cases. That’s the estimate of the number of cases of
chronic fatigue and immune dysfunction, a condition that research (if anyone
bothers to read it) suggests is essentially HIV-negative AIDS.” (OW
p.605)
The editorial had no impact on Anthony
Fauci and it would not be the only time he would ignore the New York Native during
Holocaust II.
One could ultimately say that Denise Fauci's petulant brother
himself represented one of the most significant paradigm shifts, one
that moved the whole world from normal to abnormal, totalitarian
science. During the Fauci years, The Age of Scientific Racketeering
began in earnest.