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I
nterview with Dr. Luc Montagnier on Antioxidant Nutrients and AIDS: Exploring the Possibilities
 

Antioxidant Nutrients and AIDS: Exploring the Possibilities
Interview with © Dr. Luc Montagnier
as Interviewed By© Richard A. Passwater PhD

It doesn't seem like too many years ago that we learned of a dreadful new and mysterious disease that threatened to wipe out mankind. Little was known about this new disease, but it was rapidly spreading and some projected that it would be killing us by the millions within a few years and bankrupting our health care system along the way. Fortunately, this hasn't happened, and a large part of the reason why it has not is that scientists led by Dr. Luc Montagnier of the Pasteur Institute in Paris, determined the cause of the disease we now call Acquired Immune Deficiency Syndrome (AIDS) and how it's transmitted.

AIDS was formally recognized as a new disease in 1981. It is characterized as the breakdown of the body's immune system due to selected cells in the immune system being changed or their availability changed. These changes result in defects in immune function which then allows "opportunistic" infections that healthy people normally fight off to readily infect and soon kill AIDS patients. During 1980, there were a few reports of certain diseases such as rare cancers and serious infections that normally don't kill healthy people leading to quick "wasting" of the patient and rapid death. [1,2] The Centers for Disease Control established a task force led by Dr. James Curran to look for other cases, present and past, and to learn what they could about these alarming new reports. The earliest confirmed case they could find at that time was in 1978. These increasing reports were not recognized as a common disorder of the immune system until 1981. It was found that these patients had a depletion of certain white blood cells called T4- lymphocytes, which are cells that play an critical role in defending against invading organisms. Later investigation has identified several other immune changes, but the depletion of CD4+ T-helper lymphocytes has been related to AIDS ever since its first description.

Thanks to the research of Dr. Montagnier and his colleagues, the cause of this mysterious disease which behaved differently from normal viral or bacterial infections, was uncovered by 1983. [3] As a result, most of us don't have to worry about this disease and we don't give much thought to Dr. Montagnier's discovery. As an example, you can receive a blood transfusion today and not have to worry about Human Immune Deficiency Virus (HIV), the AIDS virus, being transmitted to you in the blood you receive. The fact that a test had been developed to detect HIV in blood was a comforting thought to me when I needed blood a few years ago. Even those who are at risk owe a huge "thank you" to Dr. Montagnier because the discovery of both HIV-1 and HIV-2 strains of virus that is the cause of AIDS has led to preventive measures that can protect those at high risk.

Dr. Montagnier's discovery goes beyond the development of measures to prevent the transmission of AIDS; it provides a means to identify those who are infected and allow treatment at an early stage, it also provides a means to develop a protective vaccine and drugs to cure AIDS. Otherwise, we would still be in the dark while AIDS would be mysteriously spreading throughout the general population, not just the high-risk groups. The fact that AIDS is being contained in developed countries by education and testing, while it is pandemic in developing counties, is testament to the effect of Dr. Montagnier's discovery.

AIDS is still a serious epidemic, but in the countries that take advantage of the knowledge provided by Dr. Montagnier's discovery, AIDS is under considerable control, rather than being pandemic as it is in other developing countries without extensive public health measures. Poverty, lack of education and exploitation of women can be considered risk factors for AIDS, and these are common factors in many of the developing countries. However, AIDS itself is only the tip of the iceberg of the HIV-infection. Although there was an estimated 13 million HIV-positive people worldwide in 1993, about eight million of those were in Sub-Saharan Africa. (In Africa, the transmission route of AIDS is different and the presenting symptoms are different than in the U. S. as will be discussed later.) The estimate for North America was about one million, Western Europe about one-half million, Latin America and the Caribbean was about one-and-a-half million, and South/Southeast Asia about one-and-a-half million. Of those who have contracted HIV worldwide, over two million had developed AIDS and died by mid-1993. Since the first reported cases in the U. S. in 1981, over 402, 000 AIDS cases and more than 241,000 AIDS deaths had been reported through mid-1994

In November 1993, Drs. Linus Pauling and Raxit Jariwalla of the Linus Pauling Institute of Science and Medicine, and I had the privilege of lecturing to the Institute for Optimal Nutrition (ION) in London, along with several European scientists. After the ION lectures, Dr. Jariwalla and I were invited to speak at the Faculty of Medicine in Paris, standing on the same stones in the floor of the Grand Amphitheater that Louis Pasteur had given his lectures in the 1850s and 1860s as professor of chemistry and dean of the school of science.. Dr. Jariwalla spoke on his research in slowing HIV replication with vitamin C and I spoke on antioxidants in the prevention of cancer and slowing the aging process. After the lectures, I visited the Pasteur Hospital and the Pasteur Institute to survey their research on AIDS. I missed Dr. Montagnier, who is the Head of the Department of AIDS and Retroviruses, at that time, as he was out of the Country, but I was able to meet with him on my next visit on May 3, 1995.

Dr. Montagnier was kind enough to bring me up to date on his continuing research and particularly his research on the role of antioxidant nutrients as a key part in slowing the progression of HIV infection to the AIDS stage. You may also be interested in learning of the research into the possible roles of antioxidant nutrients and plant extracts in slowing the progression to AIDS. Dr. Montagnier has agreed to share part of our conversation with you.

Passwater: Dr. Montagnier, your experience at the Pasteur Institute was invaluable in leading you to isolate and identify the HIV virus. It was only fitting that the virus be first identified here at the institute that Louis Pasteur started over 100 years ago (1888) to treat rabies and to further his research on "germs." Pasteur's discovery that many diseases are caused by "germs" is a cornerstone of modern medicine and became the foundation for the science of microbiology.

You headed the Viral Oncology department since 1972, the Virology Department since 1982, and since about 1991, you have been Head of the Department of AIDS and Retroviruses.

You have been Professor and Director of the Virology course at the Pasteur Institute since 1980 and you are now the President of the World Foundation for AIDS Research and Prevention. The Pasteur Institute has been a world leader in virus research for decades, and has produced breakthroughs with vaccines for malaria, diphtheria, and tuberculosis. Several new viruses have been identified here and new cancer treatments have been developed at this prestigious Institute. With this experience and background, what made you suspect that AIDS resulted from a retrovirus infection, rather than a virus related to hepatitis B, or Epstein-Barr, or cytomegalovirus as others were suspecting? Was it the observed T-cell destruction leading to immune depression?

Montagnier: There were some models, such as with the mouse leukemia virus, suggesting that retroviruses of animals could induce immuno suppression. We had the techniques from our cancer research before the AIDS problem came along and we had the tools to detect retroviruses. It was not just my own ideas, it was ideas from my colleagues, plus some ideas coming from the U. S. as well.

Passwater: What led you to the isolation of what you first called Lymphadenopathy Associated Virus (LAV), which after acceptance as the cause of AIDS, had its name changed to HIV by the International Committee on Nomenclature of Viruses. Was it because AIDS patients had enlarged lymph nodes?

Montagnier: Yes, at that time we knew that most AIDS patients started with swollen lymph glands, and because many infectious agents are trapped in the lymph glands, it was logical to look there. We wanted to look at where the disease started so as to lessen our chances of following some agent that entered the scene later as an opportunistic invader. Opportunistic agents are normally found in the environment and they are harmful only to those having weakened immune systems. We had to find the causative agent, not an opportunistic agent.

Passwater: Was HIV easy to identify?

Montagnier: The first HIV (LAV at the time, now called HIV-1) was very difficult to grow in vitro (in laboratory glassware). Most viruses are far easier to grow in vitro than HIV is. This HIV was non-cytopathic and could have been overlooked. In many patients there are some changes in the virus with time, and the viruses isolated at the next stage of infection are more virulent and more cytopathic. Taking blood samples rather than lymph samples would not have isolated the original virus. The mutated viruses can be propagated in some cell lines, but the early form of the virus is not. Thus, we had a difficult time, at first, convincing others that the virus we isolated and identified was the causative agent for the infection that progresses to AIDS.

Passwater: How long has the HIV virus been around?

Montagnier: In my opinion, a very long time before the AIDS epidemic. HIV may have been in Africa for centuries.

Passwater: Why did HIV infection and AIDS suddenly become epidemic about 1980?

Montagnier: HIV has been around for awhile -- it is only our behavioral changes that have caused the pandemic. AIDS is a complex disease. There are four factors that have come together to account for the sudden epidemic; HIV presence, immune hyper-activation, increased sexually transmitted disease incidence, sexual behavioral changes and other behavioral changes. All of these factors had to occur essentially simultaneously for HIV transmission. The first factor is the HIV virus, which is the causative factor without which there would be no AIDS. However, the other three factors are secondary factors or co-factors that make the HIV virus more easily transmitted from one person to another, and thus make the infection epidemic.

The second factor that is involved is that there must be hyper-activation of the immune system. What is striking in HIV infection is that abnormal activation (T cell receptor stimulation) of infected cells is continuous and lasts throughout the entire course of the disease, including pre-clinical and clinical stages. Apoptosis (programmed cell death) occurs rapidly after lymphocyte cell activation. The continuous CD4 cell depletion is the result of multiple mechanisms and the impairment of T4- cell renewal may contribute to CD4 cell depletion.

The HIV was already in Africa and Africans often have hyper-activated immune stimulation because in the tropics there are many infections caused by microbial parasites, fungi, viruses, etc., that stimulate the immune system. The stimulated immune system provides more targets for the HIV virus to invade. The CD4 differentiation antigen of the T- lymphocyte is the major cell surface receptor for HIV, thus the more CD4 activated T- lymphocytes, the more targets for HIV to infect.

The third factor involves changes in sexual behavior that resulted in more Sexually Transmitted Disease (STD) activity. The presence of conventional STD such as syphilis or chancroid increases the risk of HIV transmission by ten-to-a-hundred times. The birth control pill -- introduced about 1960 -- has led to more "sexual freedom" and with this new freedom has come change.

The fourth factor involved other behavioral factors. Behavioral factors include drug use, poor nutrition, stress, wider travel and migration, social changes, and the like.

Passwater: Thanks to your research and others, we have learned much about the transmission of HIV and how to prevent it. We know that HIV is transmitted mostly through blood and semen, but HIV is also present in -- although difficult to transmit via -- saliva, urine, tears, breast milk, vaginal and cervical secretions. Your research has led to the recognition of the three primary routes of transmission -- sexual intercourse (vaginal or anal) with an HIV-infected person, contact with HIV-infected blood or blood-products, and by infection passed from mother to child during pregnancy or birth. U. S. statistics for the late 1980s indicated that the high risk groups were homosexual and bisexual men (73 percent of cases) and intravenous drug-abusers (17 percent of cases). The public has been educated about the dangers of unprotected sex and dirty needles and these risks have been reduced. However, are there other factors that might further help prevent the transmission of HIV even in the educated, developed countries?

Montagnier: Well, two other cofactors for infection that come right to mind are poor nutrition and stress. Studies show that nutrition is a factor in immune system function. Likewise, psychological stress activates T- cell growth factors which could hyper-activate the immune system.

Passwater: Let's turn from HIV transmission to HIV progression to the AIDS stage. Some people develop AIDS more quickly than others after HIV infection. HIV appears to "lie dormant" for several months for a few people, while in most may not develop immune problems for several years, and in rare cases, some may go as long as ten years before detectable immune dysfunction. (Although the infection appears to be dormant, the virus is replicating actively in lymph nodes and lymphatic tissue and apoptosis is occurring.) Let me draw a graph to represent this progression through two major stages. Let point "A" represent the time that a person becomes infected with the HIV virus and is called "HIV-positive." Up until now, we have been discussing those factors that either facilitate or protect against "A." Now let point "B" represent the time that progressive T- and B-cell dysfunction begins. (T- and B- cells are immune system components and their decline in function reduces the body's resistance to disease and infection.)

0 HIV-infection (point A) progresses through several stages. This is illustrated here by point A, the time of HIV-infection, by point B, the final HIV-infection stage called AIDS which is the time of noticeable progressive T- and B-cell dysfunction, that leads to death (point C). The time scale has no dimensions due to the fact that this period varies from individual to individual.

What can be done to extend the time between HIV infection (point A) and the beginning of serious immune problems (point B)?

Montagnier: Our goal in following those people who are HIV-positive, but asymptomatic is to learn how to delay this progression or to completely halt it. I think that this is possible. There are examples in animals where they are infected with Simian Immune deficiency Virus (SIV, a monkey retrovirus similar to HIV) and yet they are not sick. So we have to understand the complex action between the virus and the immune system. We have to try to make the immune system take over the virus, and not the other way around.

The complex pathophysiological basis of the profound and seemingly irreversible immune depression that follows this retroviral infection is still obscure. At present our best hope is to prevent further immune depression. Based on animal studies, the indicator as to how fast the immune system fails is in the lymph nodes. We have shown that when there is rapid HIV replication in the lymph nodes at an early time, then there is rapid acceleration towards AIDS. The rate of virus replication in the first few weeks after HIV exposure is directly related to the progression. If the replication is high in the first few weeks, then the progression is more rapid.

Oxidative stress is a key factor. There is a higher free radical production in stage II of HIV infection that could be caused by several factors including the overproduction of oxygen radicals by polymorphonuclears. The key may be to reduce oxidative stress at the earliest stage of HIV infection. Antioxidants and AZT or other drugs could be used at this stage to prevent progression to AIDS. If the oxidative damage is slowed, then the progression may be slowed or halted.

I strongly believe that one important factor is the activation of the T-helper cells. Consecutive T-cell receptor stimulation induces T-cell deletion by apoptosis. [4] Recognizing the importance of apoptosis in AIDS progression may have dramatic implications for developing new treatments for AIDS. Apoptosis may induce oxidative stress. We know also that oxidative stress can mediate apoptosis. This is a circular cascade.

Being able to reduce apoptosis to a normal rate in lymphocytes of HIV-infected individuals would put HIV infection in a class with mononucleosis and other chronic infections where cell death does occur, but the immune system goes back to normal after a period of time. In the middle and later stages of HIV infection, apoptosis is a chronic and permanent problem. Antioxidants including NAC might slow the rate of apoptosis. Apoptosis is not limited to HIV infection, but proceeds at a higher rate in HIV-infected cells.

Other cofactors may be some ordinary proteins or some external factors which are present before infection or even carried along with the HIV, and oxidative stress. If we act on the causative agents that lead to increased apoptosis -- free radicals, microbial factors, viruses -- or interact with the many steps of the apoptosis process, we can reduce cell death to a normal rate.

We should treat oxidative stress at the earliest possibility. This requires measuring the oxidative stress markers in the blood and tailoring the treatment to the individual based on the results of these tests.

Passwater: What might be done to "flatten" or extend the time between point "B," the beginning of progressive T- and B-cell dysfunction and point "C," death?

Montagnier: That's more difficult than treating it earlier. I won't say it is impossible, perhaps gene therapy might be useful. Still antioxidants and drugs might delay the more rapid decline.

Passwater: Have you investigated N-acetyl cysteine or other antioxidants as possible mediators of the progression to AIDS?

Montagnier: Yes. We have started some open trials with NAC following the work of the Herzenbergs at Stanford and that of Droge in Germany. In HIV infected patients, the glutathione system is depressed even at early stages. The rationale is to restore the oxidative protection system back to normal. When we treat patients for less than six months with NAC, we don't see much change. However, when the NAC treatment is longer than six months, NAC will restore apoptosis back to normal levels. This is a preliminary result and we will repeat the study in our new applied research laboratory.. We plan to open a new research center at the end of this year for HIV asymptomatic patients, in which we will follow a battery of laboratory markers and treat patients accordingly.

I am convinced that oxidative stress is indeed involved in the progression of going from HIV infection to the AIDS stage. I believe, therefore, that antioxidants are necessary in the treatment , but antioxidants are not sufficient by themselves.

I advocate adapting the treatment to the patient. Antioxidants are important, but in order to be effective, they must be rationally used. We must take into account the parameters of each individual. Some may lack selenium, or zinc, or vitamin E, or other nutrients, or any combination. So our treatment must be planned according to these parameters, and thus, our treatment may change from one individual to another. The treatment must be adapted to the individual to restore these parameters that we are measuring back to normal.

We should monitor the markers of oxidative stress such as lipid peroxides which increase when opportunistic infection occurs, as well as the carbonyl content of lymphocyte proteins, cytokines and Tumor Necrosis Factor (TNF). We have laboratory studies showing that the proteins of lymphocytes are very rapidly degraded due to oxidative stress.

These parameters will be evaluated and then patient treatment may include several antioxidants such as NAC, beta carotene, vitamins A, C and E, the enzymes superoxide dismutase (SOD) and catalase, proteins such as metallothionine, plant extracts and other nutrients as indicated.

Passwater: Will you give the SOD orally or by injection?

Montagnier: Both.

Passwater: I am pleased that you are using oral SOD, because so many researchers have been dissuaded from using it because of a very questionable report incorrectly claiming that SOD can't be absorbed orally due to its molecular size.

Montagnier: There are ways to make SOD assimilable orally. Some preliminary data support that oral SOD is sufficiently absorbed.

Passwater: Could you comment more on the use of plant extracts?

Montagnier: Plants have invented many more compounds than we have and before we will. Plants are much richer sources of antioxidants and other useful nutrients or pharmacologically-active compounds than man. Let nature help us. They give us a wide spectrum of compounds to work with.

We should not try to purify plant extracts too much. They might contain several compounds that are effective only when in combination with each other.

Passwater: You have suggested that mycoplasmas could increase oxidative stress and thus be a co-factor in how quickly HIV infection progresses to AIDS.

Montagnier: In 1989 and 1990, I suggested that mycoplasmas may be cofactors in some individuals. We are still investigating the role of mycoplasmas trying to verify this hypothesis. We have several types of evidence. One is the fact that from 20 percent of individuals to almost 40 percent at the AIDS stage of HIV infection, have antibodies against mycoplasmas such as Mycoplasma fermentans, Mycoplasma penetrans or Mycoplasma pirum.

Mycoplasma may play a role in signaling lymph nodes to start the integration of HIV into cells where they can replicate. There is some evidence that HIV replication does not take place in non-activated cells. The _____ mycoplasmas is a silent infection, but they may influence HIV pathogenesis by contributing to oxidative stress, or activating the immune system or producing superantigen. Mycoplasmas could induce inflammatory cytokines and TNF. They could be sexually transmitted along with HIV. [5]

Passwater: Is there a switch from "T-helper 1" response to "T-helper-2" response which seems to promote the progression to AIDS, and if so, is this "switch" affected by antioxidants?

Montagnier: This concept was put forth by Gene Shearer and Mago Clerici at NIH. There is still some debate about it. It seems that it is not a clear cut switch, but that there are some changes. What is observed in patients progressing to AIDS, is an increase of cytokines which are involved in T-helper 2 immunity which promotes B-lymphocytes, but inhibit the cellular immunity important in controlling HIV infection.

Passwater: Is the decline of T-cell proliferation and Interleukin-2 production decline, and the increase of interleukins -4, -5, -6 and -10, plus immunoglobulin production affected by antioxidants or other nutrients?

Montagnier: I haven't seen evidence of this, but it is possible. You have to tell me if you know. .

Passwater: Yes, I have seen some very preliminary results by Dr. Ron Watson of the University of Arizona where the antioxidant Pycnogenol(R) restored these immune components towards normal levels in a Murine AIDS model in the mouse.

Does research at the Pasteur Institute suggest that there may be a second HIV receptor, a co-receptor, which is a cell surface protein called CD26, in addition to CD4?

Montagnier: I personally am not working on that, but some of my colleagues are. This question is more complex that what it first appeared. The evidence may not be convincing at this stage, but the research is not at a dead end, however. CD26 may be involved in the induction of apoptosis along with the CD4 receptor when the virus envelope glycoprotein gp120 binds to the cell.

Passwater: What can we do for the people of Africa where the AIDS epidemic is now exploding?

Montagnier: We have seen that international campaigns to educate the public about AIDS has almost brought AIDS under control in some developed countries. However, this education is not efficient in some populations with high drug use. Our educational efforts have almost completely failed in areas where cultural and epidemic factors collide. Poverty is at the root of many of Africa's problem, as are cultural factors. There is poor hygiene where there is poverty. Where, in addition, there are poor conditions for women then there is an AIDS pandemic. In Africa, AIDS is transmitted mostly heterosexually,.and both sexes are nearly equally infected with HIV. Most African males that are HIV-positive are promiscuous heterosexuals, and many of the females with HIV infection are prostitutes. There are areas where the culture dictates that women cannot resist sexual contact with men. In some areas, single men are sent to work and they are supplied with prostitutes, who are often HIV-infected. In these areas STD are high. HIV is the virus that causes AIDS, but as we discussed earlier, cofactors such as STD and parasite infection increase the efficiency of spreading the infection. Poor nutrition resulting from the poverty handicaps the immune system. The lack of availability of medical treatment allows these cofactors to be rampant. This is why studying the cofactors is so important in these countries.

We can reduce the pandemic even without a vaccine. If we can improve hygiene, or provide chlorine bleach to disinfect, or even electricity, we can reduce the spread of AIDS in Africa. If we could improve the economic conditions and educate the population, we could do much more.

Even though AIDS is not spreading out of control in our countries, we must be vigilant and try to do something for the rest of the world. It is the humane thing to do, and otherwise we can't eradicate AIDS in developed countries. There will still be a danger as long as HIV infection is epidemic anywhere on Earth.

This is why I created, along with Federica Magor, the World Foundation for AIDS Research and Prevention. Our immediate goal is to launch three or four centers in sites where HIV infection is high.

Passwater: Well, you have accomplished so much. I know your empathy for the people, but only political solutions may help there. Let's look ahead. What's next in your research.

Montagnier: There are many pressing problems. Before working on AIDS, I was doing cancer research. I want to get back to that, and to also study Alzheimer's disease, heart disease and arthritis. There is so much to do.

Passwater: Yes, there is. Even though you have done so much already. Thanks for taking the time to bring us up to date. Who knows, maybe one of our scientific readers will get an idea from your discussion and help solve some of these problems.

REFERENCES

    1. M. S. Gottlieb and I. Pozalski, Morb. Mortal. Wk. Rept. CDC, 30:250-2 (June 5, 1981)

    2. A. Friedman, Morb. Mortal. Wk. Rept., CDC, 30:305-8 (July 3, 1981)

    3. F. Barre-Sinoussi et al., Isolation of a T-lymphotropic retrovirus from a patient at risk foracquired immune deficiency syndrome (AIDS), Science 220:868 (May 20, 1983)

    4. M-L. Gougeon and L. Montagnier, Apoptosis in AIDS, Science 260:1269-70(May 28, 1993)

    5. A. Blanchard and L. Montagnier, AIDS-associated mycoplasmas, Ann. Rev. Microbiol.48:687-712 (1994)


All rights, including electronic and print media, to this article are copyrighted by © Richard A. Passwater, Ph.D. and Whole Foods magazine (WFC Inc.)

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Richard A. Passwater, Ph.D. has been a research biochemist since 1959. His first areas of research was in the development of pharmaceuticals and analytical chemistry. His laboratory......more
 
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