How HIV Causes AIDS

 In the early 1980s Aids erupted onto the world stage as a completely unknown disease shrouded in absolute mystery. When Dr. Michael Gottlieb first noticed the syndrome at Harbor-UCLA Hospital in Los Angeles, California, and reported it to the US Center for Disease Control in June 1981, numerous questions begged to be answered. What kind of infectious agent caused this emerging disease? Where did it come from? How widespread was it? Would everyone who was infected die, or only a small percentage? How was it spread? How could this multifaceted, most complex of diseases be treated? And how did whatever caused this mysterious syndrome actually force the decline in CD4 white blood-cell count that results in chronic immune system depression?

Over the past three decades, thousands of scientists labored diligently to gradually untangle the enigma of HIV/Aids. They answered all these questions. All except one.

Researchers soon determined that Aids is caused by a virus that after some debate they named HIV. After twenty years of searching virologists tracked the origin of the disease back to chimpanzees living in the vast tropical forest that spans the border of Gabon-Cameroon. Those chimps harbor a simian/monkey immunodeficiency virus - SIVc - in their blood, that is virtually identical to the one now found in humans. A decade later geneticists determined that the HIV virus originated when two different simian viruses infected the same cell, exchanged genetic material, and formed a brand new hybrid virus. When this virus was eventually discovered in humans it was renamed human immunodeficiency virus – HIV. The SIVc virus began jumping the species barrier into humans approximately one hundred years ago via blood spilt during the butchering of bush meat. After physicians in Southern California finally noticed the illness in patients it did not take too many years for the medical profession to determine that almost everyone who was infected but not treated would eventually fall ill and die. People usually begin to get sick between six and twelve years after initial infection. The delay depends on several things including the strain of the virus, the genetics of the person, plus immune and nutrition related factors. HIV disease is spread via sexual intercourse and contact with contaminated blood, including intravenous drug use.

Subsidized by governments, over the past three decades pharmaceutical companies developed extremely effective anti-retroviral drugs – ARVs - to improve the health and extend the lives of those infected. They developed reverse transcriptase inhibitors during the 1980s and protease inhibitors in the 1990s. After the turn of the century fusion and integrase inhibitors were introduced. Overlooked, almost forgotten in this rush of scientific progress towards effective treatments lingered one curiously unanswered question. How does infection with the HIV virus actually cause the CD4 blood cell count to decline from a normal healthy level of 800-1200, to under 200, defining Aids; and then to less than 100 CD4 when most of the opportunistic infections and deaths occur?

Today most professionals working in the field of HIV/Aids still do not realize that there has never been a commonly accepted scientific explanation of precisely how the HIV virus causes CD4 cells to decline. People in healthcare assume that since the HIV virus infects CD4 cells and kills some of them, this is what causes CD4 counts to fall. However this unquestioned common knowledge is not the correct explanation of how HIV infection causes Aids.

Dr. David Ho is one of the most famous and respected Aids researchers in the world. He was named Time magazine’s Man of the Year in 1997 for his major contribution in developing protease inhibitors, the improved class of anti-retroviral drugs that quickly brought down the devastating death toll of the early 1990s Aids epidemic. Dr. Ho is a likely candidate for a Nobel Prize in Medicine.

In 2001, on the twentieth anniversary of the discovery of the Aids syndrome, the International Aids Society held its first “scientific” Aids conference in Buenos Aires, Argentina. The opening session keynote speaker Dr. David Ho addressed over 3,000 virologists and immunologists assembled from all over the world in the vast exhibition hall. Dr. Ho explained to that eminent audience that although over the past twenty years they as scientists had made great strides in understanding this new disease, there was still much work left to do. Ho highlighted the fact that scientists still could not explain precisely how HIV causes Aids. He threw this out as a challenge that needed to be solved. He explained that since HIV only infects about 1% of CD4 cells, killing just those 1% of cells could not possibly be the correct explanation of how HIV causes its devastation. Something else must be happening. He pointed out that the CD4 white blood cells that control the immune system live only four days on average. The body has to produce millions of new CD4 cells every day to replace those that are continuously lost.

So if what most people think how HIV causes Aids is not correct, what can HIV’s true mechanism of action be? Have we learned anything more since 2001? Certainly there has been no major announcement by medical authorities or the international press that scientists have finally solved this largely unmentioned question. There must be a reason a question so full of implications is never asked or examined publicly.

So if what most people think how HIV causes Aids is not correct, what can HIV’s true mechanism of action be? Have we learned anything more since 2001? Certainly there has been no major announcement by medical authorities or the international press that scientists have finally solved this largely unmentioned question. There must be a reason a question so full of implications is never asked or examined publicly.

Selenium is essential to life. It is a constituent of every cell in the human body. Virtually every living cell in both plants and animals contain this chemical element. Most viruses need it too. Selenium atoms form the active component of the universal anti-oxidant enzyme glutathione-peroxidase – GPx - that helps clean and detoxify every cell in the body. GPx keeps them, and us, healthy. The mineral selenium is concentrated in the cells and organs of the immune system and all aspects of complex immune responses require this trace element. Over twenty-five human proteins and many enzymes that play critical roles in various bodily functions require selenium for their formation.

Structurally the HIV virus is nothing more than a string of RNA genetic programming wrapped in a protein membrane “envelope”. This outer envelope coat partly consists of selenium molecules. Every time an HIV virus is formed, it uses up a minute amount of the body’s store of selenium. As HIV disease progresses to Aids, viral load increases dramatically and billions of viruses are produced daily. This progressively depletes the level of selenium in the body. As selenium levels decline, CD4 levels decline in tandem. Why?

There are three likely places where selenium could potentially exert action in increasing CD4 or where the decline in selenium would cause the production of CD4 white blood cells to fall. These are the thyroid gland, the bone marrow, and the thymus.

The thyroid gland is one of the master glands of the body. It controls the metabolic rate and influences the functioning of most of the other glands and organs. The thyroid contains the highest concentration of selenium of any gland or organ in the body. Eleven of the body’s twenty-five selenium proteins are found in the thyroid. One of these enzymes, Iodothyromine deiodinase – ID - converts inactive thyroid hormone to active thyroid hormone. Active thyroid hormone directly stimulates production of immature CD4 precursor cells that originate from the bone marrow.

My original hypothesis was that the selenium containing ID enzyme that converts inactive into active thyroid hormone is highly sensitive to the level of selenium in the body. When selenium levels fall, the level of this critical thyroid enzyme might also fall, thus causing active thyroid hormone levels to decline. Since active thyroid hormone is the primary stimulant to the production of immature CD4 cells from the bone marrow; when it falls, so would CD4 count. Since the body needs to replace millions of CD4 cells every day, if the signal to produce those cells is weak or lacking, the body will not create enough new cells to replace the millions that die every day. This would easily explain why CD4 counts gradually decline when selenium declines. However some researchers suggest the ID enzyme is not very sensitive to the level of selenium so this may not be the correct explanation. Nevertheless, the thyroid gland remains one likely suspect as to where the deficiency of CD4 cells may originate. It has the highest concentration of selenium in the body, has the highest number of different seleno-proteins in the body, and it has an influence on blood cell formation in the bone marrow.

The abbreviation “CD” as in CD4, stands for “cellular designation”. “T” as in T-4 stands for “thymus”. CD4 and T-4 are two names for the same cell. This class of cell controls the overall immune response. They are the generals of the immune system army and direct other immune cells when to turn on and off, where to go, and what to do. That is why CD4 cells are so vital to health and their quantity reflects the overall competence of the immune system.

Like immune system B-cells that produce antibodies, CD4 cells originate in the bone marrow from undifferentiated progenitor cells. Immature CD4 cells known as “precursor cells” then migrate to the thymus gland for processing and testing before they are released into the blood stream. Once they are processed and matured, CD4 cells have to be tested to determine if they are auto-reactive or not. If a CD4 cell is tested and reacts negatively against proteins that are a natural part of the human body, it is destroyed through a process known as programmed cell death or apoptosis. CD4 cells are supposed to react only against foreign antigen, “non-self” proteins that are not naturally part of the human body, like bacterial, viral or fungal proteins. They are not supposed to react to “self” proteins that are part of the body. Otherwise, once released into the bloodstream, they would attack human cells and cause damage, sometimes resulting in autoimmune disease. Unfortunately, as we age the thymus shrinks and develops lesions. It does not work as well. HIV disease accelerates this deterioration and contributes to the premature aging of the thymus. However, selenium supplements increase the size of the thymus and help protect it from lesions. This may prevent damage to the thymus. That would allow it to process CD4 cells properly with fewer cells undergoing programmed cell death, thus resulting in the release of more fully functional T-4 cells

The continuing loss of selenium due to increased viral replication might easily affect the production of CD4 cells at any one of the three major points in the cellular production line; the thyroid, the bone marrow, or the thymus. The loss of selenium may have an impact at one or more of these points. But it seems clear that the loss of CD4 cells that is the hallmark of Aids is due to the failure to produce enough fully fledged CD4 cells rather than the destruction of infected CD4 cells as most people have been led to believe.

A fundamental principal of science is cause and effect. This hypothesis presents a simple chain of cause and effect where HIV infection and rapid viral replication leads to a depletion of selenium levels. This leads to potential reduction in thyroid activity, damage to the thymus or perhaps a disruption of cellular processes in the bone marrow. Any one of these would contribute to a dramatic fall in CD4 count. Wherever the problem lies, this cascade of cause and effect can be significantly reversed through supplementation with selenium tablets. Using selenium supplements reverses this chain of causality, rapidly increasing CD4 count and improving health. Consistent with this explanation, selenium is the only nutritional agent that has been proven to slow down the progression of HIV infection becoming Aids. It is the only nutrient that individually can substantially increase CD4 count and improve the CD4/CD8 ratio. Researchers from Harvard University in conjunction with the Nigerian Institute for Medical Research showed that in advanced Aids patients, supplementing one standard selenium tablet daily more than doubled the benefits of triple-ARV therapy in increasing CD4 count. Adding only one standard 200mcg selenium tablet a day reduced hospitalizations by half compared to ARVs alone. Still, this combination is not a cure for Aids since it cannot totally eliminate the virus. Nothing yet can. However, used in conjunction with ARVs, selenium supplements constitute a “practical cure” for this disease, allowing people to be more healthily than using ARVs alone. Selenium has proven effective in helping treat all Aids related opportunistic infections including tuberculosis, Kaposi’s sarcoma, thrush, pneumonia and muscle wasting. Nothing can explain this except that selenium is absolutely central to this disease and to understanding HIV disease progression.

Some physicians have raised the question that if the HIV virus needs selenium in order to be formed, would adding selenium just increase HIV replication? In fact this does not occur. Just the opposite. Selenium works as an anti-viral agent to reduce HIV production in four different ways. First, just like many ARVs, it inhibits the reverse transcriptase enzyme. It is not as strong as newer reverse transcriptase inhibitor drugs (RTIs), but it does have that effect. Second, selenium supplements inhibit nuclear factor-kappa binding - NF-kB - a primary stimulant to HIV replication in the nucleus of the CD4 cell. Third, selenium inhibits HIV’s TAT trans-activating gene, that helps regulate viral transcription. Finally, sodium selenite, a common form of selenium found in nutritional tablets helps prevent the HIV virus from gaining entry into CD4 cells through the cellular membrane in the first place. Exhibiting four different anti-viral mechanisms makes selenium an effective anti-retroviral even if it does not quite compare to the best of today’s multiple-combination ARVs in anti-viral activity. Instead of through their direct antiviral activity, selenium supplements provide their strongest effect by potently increasing CD4 count through their action on the thyroid, thymus, or the bone marrow. They also improves the CD4/CD8 ratio, considered a better barometer of overall immune competence that CD4 count alone. Excluding the most effective ARVs, selenium supplements are by far the best HIV medication on the market today. Combining selenium tablets with ARVs certainly improves overall HIV therapy.

Using selenium nutritional supplements to treat HIV does not eliminate the need for extremely effective, standard ARV therapies. Instead, they provide a much needed additional dimension to HIV treatment. That is especially welcome for the majority of people with HIV who are recently infected but who do not yet need ARVs. This is also good news for those who are already on ARV treatment but are not responding quickly or strongly enough to their therapy. That is due to government funding limits where some people do not receive the latest drugs. Since selenium increases CD4 count so potently and rapidly, it is the most powerful immune booster found in nature. Using selenium in Africa to slow down disease progression from the start offers people an incentive to get tested, years prior to becoming sick. Making selenium supplements a standard part of the HIV treatment protocol could boost disease prevention efforts and help governments worldwide get a better grip on this epidemic. Doctors and scientists who know these facts often recommend that all HIV positive people use selenium tablets to help maintain and improve their health. That would greatly reduce hospitalization rates saving governments and medical aid schemes billions of dollars annually.

Once a person’s CD4 blood cell count falls below 350, ARVs are indispensable for treating people with HIV. However taking those drugs without adding selenium is like fighting Aids with one hand tied behind their back. Combining selenium with ARVs helps delay development of resistance to each revised combination of ARV therapy, preserving and extending antiviral treatment options. Used earlier in infection, selenium can keep CD4 counts higher for longer and help delay the need to commence anti-viral therapy.

How can international Aids organizations claim they are serious about fighting this pandemic when over thirty years after this terrible viral scourge came to light, scientists still cannot explain precisely how HIV causes Aids? Why do governments and NGOs worldwide apparently remain ignorant of and fail to utilize these simple facts of medical science? Why has this most basic of scientific questions been swept under the rug and ignored? Is it because pharmaceutical companies control the development of drugs, the discussion of research issues, and the education of doctors on this? Do those companies suppress or avoid the discussion of the unmentioned question of how HIV causes Aids because they do not like the answer? As a result, tens of millions of people with early HIV infection tragically receive no effective treatment to help slow down the progression of initial infection becoming Aids. In many cases, those laying dying in hospices could be quickly revived by using an appropriate, moderately high daily dose of selenium to rapidly increase CD4 count and significantly reverse immune system depression.

Many scientists certainly should agree with the above explanation of how HIV causes Aids. The above explanation is both highly logical and fits all the known science surrounding this disease. Until someone postulates a better hypothesis this one should stand despite the fact that some details remain unclear. It should not be that difficult to fill in the missing science. No other scientist has set forth an alternative theory that fits more precisely all the pieces of this complex, scientific puzzle.

Based on the above analysis, I suggest that the term Acquired Immune Deficiency Syndrome - Aids - should be changed to Acquired Immune Deficiency of Selenium. This redefined acronym much more accurately reflects the disease process and focuses attention on an effective way to treat HIV. It allows people to understand HIV/Aids more clearly as a slowly progressing disease of selenium nutritional deficiency caused by a virus in the lentivirus – slow virus - family of viruses.

Adding affordable selenium supplements to current ARV combination therapies creates a better, longer lasting treatment strategy that comes close to being a practical cure for this disease. They are complementary to ARVs, not an alternative. The sooner selenium is added to national standards of care for HIV, the sooner doctors, hospitals, governments and NGOs can gain better control over this tragic, ongoing pandemic. Not only individuals, communities and nations would benefit, but the whole family of man.