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Re: Christine Maggiore, vocal skeptic of AIDS research, dies at 52
happyhealthygal Views: 7,088
Published: 12 years ago
Status:       RN [Message recommended for CureZone Newsletter!]
This is a reply to # 1,339,639

Re: Christine Maggiore, vocal skeptic of AIDS research, dies at 52

“Well the argument is far from settled with the so called dissidents. Their questions still remain unanswered.”

Would you post the specific questions that you believe to be unanswered? (Actually, it would probably be good to start this as a new thread, since it only peripherally relates to Christine Maggiore). In many cases, it seems to me that their questions are “unanswered” because they refuse to look at the research that would answer them! In some cases, they don’t even seem to be asking the right questions (if their real concern is getting to the truth of whether or not HIV is the sufficient and necessary cause of AIDS).

“My problem of accepting the HIV = AIDS hypothesis is there is AIDS without HIV*
*The CDC even came up with a classification for non HIV AIDS it is called 'CD4 lymphocytopenia'”.

A common problem when non-scientists (and even some scientists) make scientific arguments is that they do not provide precise definitions of their terminology. This is particularly important when someone is defining a term differently than its common usage. Nobody would suggest that HIV is the only cause of immunosuppression, or even more specifically, CD4 depletion. There are many other known causes of dramatic CD4 depletion. Examples include lymphoma, immunosuppressive drugs, sarcoidosis, Sjogren’s Syndrome, chemotherapy and radiation, etc…. Some people are born with genetic defects that result in a partial or total lack of CD4+ T-cells in the periphery (such as SCID, DiGeorge Syndrome, and MHC-II deficiency). There have also been reports of people with low CD4 counts where the cause can’t be determined – this has been termed “idiopathic CD4 lymphocytopenia” (ICL), which is exactly what it sounds like: a garbage-can category for people with low CD4 counts of undetermined origin! Some of the patients who have been thrown into the ICL bucket probably belong in other disease categories (for example, common variable immunodeficiency may be misdiagnosed as ICL:
It is clear that ICL is a heterogeneous construct – it’s a name for a group of people with a common symptom (and lack of explanation), but it’s almost certainly not caused by just one disease, defect, or disorder.

However, calling idiopathic CD4 lymphocytopenia “AIDS,” “HIV-negative AIDS”, or “non-HIV AIDS” is a misrepresentation (although perhaps a non-intentional one by most people, since they’re just repeating a catchy moniker they heard somewhere). The denialists make the fair point that the CDC definition of AIDS is dependent on the belief that HIV is the cause of AIDS. It is possible to come up with a definition of AIDS that is not dependent on HIV. So, let’s assume that you don’t know the cause of a disease: how do you define it so that it is neither too broad nor too narrow? Well, you would look at the pathology and the natural course of the illness.

It is clear that “CD4 depletion” is a very poor definition of AIDS, as is “CD4 depletion with opportunistic infections”, since these things occur for other known reasons (it would be like defining a common cold as “a runny nose”. It’s not very helpful because you already know that other things, such as allergies, cause runny noses). So, you look at AIDS patients and see what is unique about them. As it turns out, there are a whole lot of things that distinguish AIDS from other causes of severe CD4 depletion. Perhaps the most striking thing that distinguishes AIDS patients (so much so that it was noted in the case reports on the very first AIDS patients and has spawned tons of supporting research) besides the progressive nature of the CD4 decline is the incredibly high levels of immune activation (a good, non-technical description of the natural history of AIDS would be “a progressive loss of CD4+ T-cells in the face of profound immune activation”). So, you might also notice that the loss of CD4+ T-cells in AIDS patients is progressive, rather than stable. If you ran lab tests on this population, you would notice increased numbers of CD8+ and CD38+ cells, as well as increased B-cell activation and higher Ig levels. You might notice that this undefined syndrome was frequently accompanied by wasting, and that the general prognosis was very poor. It would also be hard not to notice that the disease appears in clusters. Does this look like the same disease as ICL? No.

When you look at these 2 diseases (AIDS and ICL), they actually appear quite different in a number of ways. For example:
- people with ICL have depressed antibody responses, and decreased activation of memory B-cells; people with AIDS have increased antibody levels and increased B-cell activation
- people with AIDS have increased CD8+ numbers, and marked increases in CD38+ CD8+ cells. People with ICL have normal or decreased CD8 and CD38 numbers.
- Without medication, AIDS patients do not spontaneously go back to having normal CD4 counts; In patients with ICL, the CD4 depletion is most often transitory
- people with AIDS have suffered progressive loss of CD4 cells; in those patients in whom ICL is not transitory, it is most frequently stable (rather than progressive).
- patients with ICL generally have a good prognosis; patients with untreated AIDS usually die
- AIDS occurs in clusters; ICL does not
- wasting syndrome is not seen in ICL patients
- Treatments that lead to a full recovery from ICL do not help patients with AIDS (e.g. IFN-g, IL-2, BMT)

If one wants to come up with a definition of AIDS that does not involve HIV and is diagnostically meaningful in any way, patients with ICL would probably not be included: without some proof that ICL and AIDS are connected (i.e. evidence that they are caused by the same thing), they just appear too different from each other to be manifestations of the same disease (it’s worth mentioning that ICL is heterogenous – it’s a garbage can category for people with a particular symptom (low CD4 counts) who do not fit into other categories. There are most likely multiple reasons that people have ICL. In some cases, investigators have found specific defects – problems with bone marrow production, decreased levels of certain proteins important in T-cell signaling, etc. – that are responsible for individual cases, but the condition is so rare that it’s hard to study).

However, suppose that ICL and AIDS were indistinguishable (which is not the case) – ask yourself, how would that function to suggest that HIV does not cause AIDS? That would be like saying “since people get runny noses when they don’t have colds (for example, from allergies), colds can not cause runny noses” or that

That is different from saying, “colds are not the only cause of runny noses”, which is obviously true. Similarly, HIV is not the only cause of immunosuppression; however, unless you define AIDS incredibly broadly, ignoring most of what is known about the clinical course of the illness and various aspects of its pathogenesis, HIV is the only known cause of AIDS. People who are immunosuppressed from HIV simply have a different illness than people who are immunosuppressed for other reasons. That doesn’t mean that the two groups may not sometimes have the same end-result (e.g. opportunistic infection, death), but that HIV-induced immunosuppression has unique features that are not shared by other causes of immunosuppression. Not all people with cirrhosis or liver cancer have Hepatitis C – does that mean that Hepatitis C does not cause cirrhosis or liver cancer? It is unclear to me why the AIDS denialists don’t apply the same arguments to just about every infectious disease (unless, of course, their motives are politics, not truth).

“and at THE VERY MOST HIV only infects 1 out of every 500 immune cells”.

Are you referring to immune cells in general? If so, that is obviously the case, since most of a person’s immune cells are neutrophils, a type of cell that HIV does not directly infect (although people with HIV have dysfunctional neutrophil activity, this is an indirect consequence of HIV’s effect on the immune system, not a result of direct viral infection of neutrophils. Not very many pathogens infect neutrophils – they’re a harsh place to live and they die too quickly!)

However, if you’re looking at CD4 T-cells (the cells that are primarily depleted by HIV), your 1 in 500 number won’t hold up. The T-cells most frequently infected are those in lymphoid tissue, not the peripheral blood, but peripheral blood is obviously easiest to study. Even in peripheral blood, in symptomatic patients, the numbers given are usually “at least 1 in 400” in peripheral blood mononuclear cells (only a minority of which are CD4+ T-cells, which would make the infection rate of these cells even higher); in lymphoid tissue (where the majority of T-cells reside), the number’s probably closer to 1 in 4 or 1 in 5 by late-stage AIDS. The percentage of infected T-cells differs in different stages of infection – it is very high in primary infection, goes down during the asymptomatic phase, and rises again during AIDS.

However, this is all sort of irrelevant! You are assuming that HIV can only kill a T-cell by directly infecting it. At one point, the general belief among HIV scientists was that most CD4 depletion was the result of direct infection (the denialists like to argue that HIV scientists are so entrenched in “orthodoxy and dogma” that they cannot reevaluate their hypotheses when the data requires it. They haven’t paid much attention over the last 25 years! As new experiments have been performed and new data collected, consensus beliefs about AIDS pathogenesis have changed too) – this is clearly not the whole story. There is so much research on how HIV could lead to CD4 depletion, and so many results, that it’s almost difficult to summarize the mechanisms by which HIV leads to depletion of CD4 numbers and function, but here are some examples:

- HIV proteins (especially envelope glycoproteins) induce apoptosis of uninfected bystander cells (e.g.,,,

- HIV is capable of infecting and killing thymocytes (the cells of the thymus, which is where T-cells develop), resulting in decreased supply of naïve T-cells to replace those die (e.g.,,

- HIV destroys follicular dendritic cell networks, leading to loss of antigen-presenting capacity (

- HIV infected cells form syncytia with uninfected cells (

- HIV infection leads to massive immune activation, followed by activation-induced cell death: (,

- HIV induces lymph node homing in resting lymphocytes, leading to their premature death (

”It is strange that numerous virus vaccines have been developed since Ed Jenner’s pox vaccine in 1793 yet HIV is somehow different.”

Different from what? There are a LOT of diseases that there are no vaccines for. There aren’t vaccines for Hepatitis C, malaria, Chlamydia, HSV, schistosomiasis, or dozens of other infectious diseases, despite a lot of effort to create them. There aren’t even vaccines for the viruses that cause the common cold. Some of our current vaccines aren’t all that great (e.g. cholera vaccine, flu vaccine, BCG could all stand to be a lot better).

It’s not really all that strange at all that there are vaccines for polio, measles, HBV, etc., but not for HIV. The difference between HIV and the diseases we have vaccines for? HIV is a lot harder to vaccinate against! The immunization strategies that can induce protective immunity against pertussis (injection of the killed pathogen) or Hepatitis B (injection of recombinant surface antigen), for example, have not worked with HIV. A lot of the most successful vaccines involve live, attenuated pathogens – the measles vaccine is a live measles virus that has been so weakened that it’s very easy for most people to fight it off and develop protective immunity. It’s possible that a live, attenuated vaccine could provide some protection against HIV, but this is research that can’t really be performed: the risks of giving even a weakened version of HIV to people is just too high. Some people are naturally infected by weakened versions of HIV. A small number of people were infected with a less competent virus (the HIV was missing the nef gene), and over a decade ago, people were talking about using nef-deleted HIV as a vaccine because the people with the less competent virus seemed to be OK after a long period of time. However, the idea was canned after one of them developed AIDS in the late 90s. Same with some of the primate studies: even though the virus used in the vaccine had been seriously weakened, the monkeys developed AIDS. One doesn’t have to think too hard to realize the problems of creating a live, attenuated vaccine with a retrovirus that mutates rapidly.

One also has to consider the practical and ethical difficulties of trials for HIV vaccines (plenty to read on that if you’re interested).


You’re conflating two different issues:
Issue 1: Does HIV cause AIDS?
Issue 2: Do scientists know how to induce protective immunity against HIV?

You seem to be assuming that (1) scientists can make a vaccine that prevents a person from being infected with HIV; but (2) such a vaccine does not prevent people from getting AIDS. This is incorrect – the problem is that scientists have not yet been able to create a vaccine that can prevent a person from being infected with HIV.

Why are some infectious diseases easier to create a vaccine for than others? It all has to do with the correlates of protective immunity. With some diseases, people get sick once, some (or all) people mount an immune response to the pathogen, and they are protected for life (or a long time) – when this occurs, you can look at those people, see what the immune response was, and try to induce the same response with a vaccine. For example, people who recover from Hepatitis B create antibodies to the Hepatitis B surface antigen – the HepB vaccine gives people a dose of the surface antigen (without the viral DNA – it’s basically just a shell) so that they can create those same antibodies. At sufficient levels, those antibodies are able to prevent a person from being infected. The problem with HIV is that despite a lot of research, scientists have not yet identified a particular immune response that provides protective immunity (i.e. prevents people from being infected). The majority of people with HIV mount strong immune responses to the virus, but these immune responses are not protective: people with HIV can be re-infected with new HIV strains or with drug-resistant versions of the same strain. The antibodies do not lead to the virus being cleared in infected people.

The early HIV vaccines mostly tried to stimulate antibody responses. Some of them worked at this. People given the vaccine had antibodies to certain components of the virus. However, these antibodies weren’t protective – they couldn’t stop HIV from infecting cells (if anti-HIV antibodies could do this, HIV wouldn’t be the problem that it currently is). Denialists like Duesberg are straight-out lying when they say that the presence of antibodies means that a person is “immune” to the pathogen that the antibodies are specific for. People make antibodies to herpes simplex, Hepatitis C, and a whole host of other chronic diseases that they are not “immune” to.

The fact that HIV vaccines don’t work has nothing to do with whether HIV causes AIDS (the outcome being measured in most vaccine trials is whether the person is capable of being infected; HIV vaccines have not protected from HIV infection, and that would be the case whatever the ultimate outcome of HIV infection is).

The fact is, it is frequently the case that scientists can identify a pathogen, know what disease that pathogen causes, and still not know how to protect against it. The early vaccines were the “easy targets”. As the history of immunization proceeds, new vaccines seem to require exponentially more effort (and basic Science understanding) than was required to create the vaccines that came before it. Vaccine research (on all infectious diseases, not just HIV) is undergoing something of a revolution, moving from inactivated and live attenuated vaccines (and some subunit vaccines) to DNA vaccines and recombinant vector vaccines. However, if it’s possible to vaccinate against HIV, we still don’t know how.

A lot of study has gone into people who seemed to have some protection against HIV – people who were exposed to HIV in high-risk situations multiple times, but never were infected. Some of these people turned out to have genetic mutations (e.g. CCR5d32) that protected them, but in most of them, no obvious genetic protection was found. The reason these people were studied is because scientists wanted to know if they were having some sort of special immune response that offered true protection. You can read the results of some of these studies if you wish (,,
are just a few studies of many). The results have been interesting, but unfortunately they have not given us a clear direction (likely to be successful) for new vaccine research.

A lot of money has been tossed down the drain on certain HIV vaccine trials. There were some trials that just about every immunologist really doubted would work, but our government, having backed the wrong horse, apparently couldn’t stand to switch mid-stream.


I doubt it. Lysenkoism in the former USSR was the disregarding of data, the triumph of ideology over evidence, the inability to throw away hypotheses that turned out to be garbage (although after a few decades of the shit hitting the fan, the Soviets rejected Lysenko’s agricultural theories. One can only choose dogma over pragmatism for so long!) Personally, I think comparing present-day movements to movements like Lysenkoism, Fascism or Nazism is usually just name-calling – ad hominem attack by (usually false) analogy (“we’re like Galileo and you’re like Goebbels!” “No! We’re like Einstein and you’re like Lysenko!” – none of these comparisons make substantive points).
However, it can be instructive to play out the analogy a bit. I would argue that it if anyone in this “debate” is analogous to Lysenko and his supporters, it is the HIV denialists:

AIDS denialists resemble Lysenkoists in the following ways:
- A refusal to re-evaluate hypotheses based on data.
- reliance on political arguments when the Science does not support their case (e.g. wild accusations about the allegedly evil motives of others)
- refusal to engage in honest data collection or experimentation
- resurrection of old, dead, thoroughly disproven hypotheses (e.g. the hypotheses that AIDS is caused by hemophilia, drug use, poppers, anal sex, etc. [rather than a retrovirus] have been disproven just as most hypotheses on the inheritance of acquired characteristics had been disproven when Lysenko refused to let it go)
- effective use of propaganda (full of inaccuracies and misrepresentations that are nevertheless convincing to laymen without the time or scientific literacy to look up the primary literature)
- the appeal of being the “outsider” (Lysenko claimed that the academic biologists studying Mendelian genetics were bourgeois, enemies of the Soviet people, etc. By contrast, he painted himself as a peasant and a revolutionary who was outside of that nasty old establishment. HIV Denialists do something quite similar in their caricatures of the “scientific establishment”)

“The AIDS orthodoxy states that HIV is/can be the SOLE cause of AIDS without CONCLUSIVE peer reviewed experiments, articles or papers”

What would you consider conclusive proof? There has been a tendency in the dissident movement to say “you haven’t conclusively proved that HIV causes AIDS until you’ve shown X and Y” – then, as the Science progresses, and X and Y are shown, they change to “but you haven’t shown Z yet!” This “moving of the goalpost” indicates that they’re not actually looking for the truth.

I ask this because it is not clear what question you are asking, or what your current beliefs are. If you believe that HIV alone is capable of causing AIDS, but that other things are capable of causing AIDS, then you need to define what you mean by AIDS (I assume you have a definition that does not involve HIV, which is fine, but you really do need to state what your definition is) – it may be that you are arguing a point that no one would disagree with, but that isn’t really relevant to the question at issue.

There will never be 100% conclusive proof that HIV is indeed “the SOLE cause of AIDS” because one can never prove a negative – you are essentially asking that one prove a negative (i.e. prove that there is NOTHING else that could cause AIDS). Nobody can prove a negative because even if you’ve looked at a million potential “co-factors” and determined that none of them were the cause of AIDS, you could never actually rule out the possibility that there is a million-and-1th that could cause AIDS.

The weight of the evidence that HIV is both sufficient and necessary to cause AIDS is overwhelming. At this point, the onus is on the AIDS denialists to find another sufficient and necessary cause, test it, and publish the data. As far as I can tell, no HIV denialist has ever actually done any scientific research on AIDS. Some are scientists in other realms, but when it comes to HIV and AIDS, they are “armchair scientists” (and I don’t mean that term as a compliment!). Nevertheless, when their testable hypotheses (e.g. poppers cause AIDS, heroin causes AIDS, promiscuous sex causes AIDS, hemophilia causes AIDS, mycoplasmas cause AIDS….) have been examined, they’ve been refuted!

“this is akin to the university of Liverpools research that found that 97% of women with Breast Cancer test positive for cytomegalovirus(CMT) and then stating CMT causes breast cancer.”

I have no idea what research you’re talking about (a link would be nice), but as cytomegalovirus (which is abbreviated CMV, not CMT BTW) is ubiquitous and just about everyone’s been exposed, I’m not sure what this is supposed to prove? Again, a link to the study would be nice if you want me to know what you’re talking about! A review of associations between HCMV and cancer (that came out just a week ago) doesn’t seem to mention this study. If you’re interested in HCMV + cancer, it’s a decent review, worth a read:
I could not find a single study on PubMed that stated that CMV caused breast cancer.

I think the point you’re trying to make is that “correlation alone is not sufficient to establish causality”. On this, you would be correct. However, there is much more than a correlation between HIV and AIDS. Even excluding HIV from the definition of AIDS (to remove what some would see as a tautology), the correlation between AIDS and HIV is nearly perfect (close to 1). So start by asking yourself, what are the other possibilities (besides HIV being the cause of AIDS), and what is the evidence to support them? I actually think this is an important enough question to warrant its own post (several alternative hypotheses are possible), so I’ll answer that one separately when I get a chance (I’ll title it something along the lines of “Alternatives to HIV being the cause of AIDS” so you’ll be able to find it).

“Here are some more interesting quotes regarding HHV-6A.

’HHV-6A was shown to dramatically accelerate progression from HIV to full blown AIDS in macaques, by causing an early depletion in both CD4+ and CD8+ cells.” (Lusso 2007)’”

It accelerated the progression to AIDS; it did not cause it. From the study:
“No long-term clinical and hematological alterations were seen in animals singly infected with HHV-6A, despite the occasional detection of low levels of plasma viremia (_100 genome equivalents/ml). In particular, their CD4_ and CD8_ T cell counts remained stably within the normal range. By contrast, a progressive loss of circulating CD4_ T cells was seen in all SIV-infected animals (Fig. 2B), associated with a marked reduction of lymphocyte
proliferation indices”.

The animals with SIV (the simian analogue of HIV) but not HHV-6 still developed AIDS!

It is certainly possible that HHV-6 influences the course of HIV infection, but it is not necessary for the development of AIDS.

“HHV-6A may cause more of the destruction of lymphoid tissue and apoptosis of immune cells than HIV”.

That eentsy-teentsy word “may” is pretty damn important! While this MAY be the case, I haven’t seen any research showing that it IS the case! It also may be the case that AIDS is caused by invisible aliens sucking the T-cells out of HIV-positive people while they are sleeping (perhaps our T-cells are tastier than those of the HIV-negative?) – however, until someone shows that this IS the case, I’m not giving the theory too much credence.

The overall influence of HHV-6 on HIV progression in humans is currently unclear. There is also some evidence that HHV-6 can inhibit HIV replication in vitro (and vice versa, e.g.,
but overall, the data on HHV-6's influence on HIV progression is very equivocal.

It appears most likely that HHV-6 is re-activated as a result of HIV-induced immunosuppression, not the other way around. However, this doesn’t mean that HHV-6 doesn’t contribute to CD4 depletion, or that there isn’t synergy between HIV and HHV-6.

“Bob Gallo spoke on this subject at the last HHV-6 conference in Barcelona, telling the group that HHV-6A is an important progression factor in AIDS and has been wrongly ignored.”

It’s possible! It may even be probable! But none of this leads to the conclusion that HIV is not the cause of AIDS. As I’ve said before, people use the word “co-factor” in different ways, which often leads to confusion. There are a million things that influence the rate of progression to AIDS – Age is a VERY important determinant. All sorts of things influence rate of progression – host genetics, viral genetics, other infections, nutritional status….. I don’t think anyone would doubt that you could throw HHV-6 into that category. But no reasonable person would say that it is the cause of AIDS.

“Of note, HIV can not invade CD8 cells until HHV-6A has first infected the cell to induce the CD4+ receptor. (Lusso 1991)”

Nope! That’s just not true! See this article here: “HHV-6 independent HIV infection of CD8+ T cells in vivo”
(found gp120 [an HIV envelope protein] and CD8 co-expression on 4.5-10% of CD8+ T-cells in both early and late HIV infection; in early infection, this was independent of HHV-6 – i.e. the CD8+ T-cells were infected with HIV but not HHV-6).

Incidentally, the Lusso 1991 study didn’t even claim that the ONLY way HIV could invade a CD8 cell was if the cell was infected with HHV-6 – it merely showed that HHV-6 infection of CD8+ CD4- T-cells could lead to the re-expression of CD4, not that nothing else could (or did) do so. The misstatement of the evidence by the people running the HHV-6 site makes me a bit uneasy. Obviously they’re trying to drum up money to study their pet virus, which is fine, but they shouldn’t misstate the evidence in order to do so.


I have to say, I get pretty disgusted by these sorts of sites and their “quote-mining”. They use quotes instead of data (otherwise known as “appeal to authority”: “look! This guy said it! So it must be true!” rather than presenting data and making a logical argument). They often use quotes from questionable sources, pull quotes out of context (often misrepresenting the actual intent of the speaker), and ignore quotes (and data!) that don’t support their position (otherwise known as “cherry-picking”).

"Carrigan and Knox, meanwhile, were pursuing a theory that had been considered, and rejected, by researchers earlier - that HHV-6 might be a "co-factor" in AIDS, aiding and abetting HIV in the destruction of victims' immune functions.”

Where had it been rejected? I’ve found no articles that reject the possibility, although I’ve found articles that present data making it seem unlikely. The reason people haven't jumped on the possibility is because the data is very equivocal.

“ Soon, Regush relates, Knox was wondering, "was HIV doing any killing, or was HHV-6 the lone assassin?" But in 1997, after Carrigan and Knox found evidence suggesting HHV-6 might be killing alone, the British medical journal The Lancet rejected their paper for publication." --Mark Nichols

Actually, Carrigan and Knox WERE published in the Lancet, in 1994, and have been published in other journals, but there was no evidence presented in their papers that HHV-6 was solely responsible for CD4 depletion in AIDS patients.

One thing I DO know is that Regush is a propagandist rather than a reporter. His 14 articles at
are political rants devoid of supporting evidence. The main point of most of them seems to be to paint himself as the intrepid reporter who questions authority and stands up to the man, not to impart any actual information (I’m not sure if that’s a good or a bad thing, given his generally atrocious level of scientific literacy). It would almost be humorous, if it weren’t so pathetic.

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