Email Our Editor

Join Our Mailing List

View Our Archives

Search our archive:

The Last 20 Days' Editorials

12/11/2017 "The Black Economy 50 Years After The March On Washington"

Email This Article  Printer Friendly Version

The Tour That Bono and Secretary O’Neill Should Have Taken

The recent tour of Africa by rock star Bono of U2, and Treasury Secretary O'Neill will one day be noted as one of the most patronizing, irrelevant, vanity-filled and ignorant activities ever taken by two such powerful White men, since Blacks were taken from Africa and brought to the Western Hemisphere some 400 years ago. We are confident that once fully conscious and arisen, the leading historians in the international Black community will arrive at such a conclusion, if they even care to. That does not mean that the much-celebrated tour was not informative, or even educational. We do remember the old maxim which states: "The more unlikely an event is, the more information it yields".

Rarely, if ever has such an event put on public display the two dominant streams that run through the mindset of White Supremacy - both its supposedly benevolent, socialist sympathetic disposition embodied by Bono, and its supposedly just, "rugged individualism" and capitalist disposition represented by Secretary O'Neill. In America, most Blacks are led to believe that the former stream, loosely referred to as "liberalism" is substantively in their better interests than the latter stream, referred to as "conservatism".

But for those who study history - particularly the Black experience in America, the bottom line result of the supposedly different solutions to endemic problems offered by the White cultural, political or economic establishment, whether under liberal or conservative regimes, is the same: a structural and accepted level of poverty, ignorance and disease for tens of millions of Blacks. Nowhere in recent memory has this dynamic been on such public display as was the case with this mockery of a "humanitarian" trip led by two members of the White cultural, political and economic elite.

For a media, political, economic and cultural establishment that styles itself as relative experts on the subjects of history and current events, when the subject is the root causes of poverty, ignorance and disease in Africa the answers are half-true, incomplete and skewed - with a mixture of African corruption in government, famine, and helplessness made to shoulder the vast majority of the responsibility for the problems on the continent. The White-supremist history and present context that serves as the real backdrop to the wickedness that Black Africans commit on each other today, is a mere after-thought for the White intellectuals and policy-makers (whether liberal or conservative) who have come to "save the day" or reform wayward African leaders.

The establishment answer, though lifting aspects of the problem to view, is not near correct. This trip exemplified this dishonest and inadequate spirit that dominates Western governments and intellectuals, in stark terms.

On one hand, we are presented with the "radical", "progressive", "liberal" Bono whose heart bleeds for the suffering Blacks and who has a bagful of solutions to save the natives, if only he could write legislation and executive orders for a day.

On the other hand, we see coming into view the arch-calculating, bottom-line businessman, in Secretary O'Neill, who has come to model, again, for the benefit of the natives, the "tough love" that they have been lacking and the standards of right and wrong, the accountability, yes, the holy and pristine "rule of law" that Africa longs for and has been deprived of, not by colonialism or apartheid for the last few centuries, but, of course, by corrupt African despots and dictators in power the last few decades.

The two streams, embodied by the rock star and the Treasury Secretary, go toe-to-toe, waging intellectual war, in front of our very eyes and we are made to choose a winner or, if President Bill Clinton were to prevail - we would find a "third way"; the quintessential synthesis of the thesis of Secretary O'Neill and the anti-thesis of Bono. O'Neill thinks harder but Bono feels harder, placing the entire Black world in the valley of decision, forced to helplessly hope that Bono and O'Neill can arrive at a solution, a happy "Clinon-esque" medium where there are no true winners or losers. The quest is for the "Win-Winners" with each side getting what they have longed for.

Anyone who truly believes that Bono or Secretary O'Neill has the right approach or that a third way that merges their respective approaches would mean nirvana for Africa is absolutely deceived. If that person is a Black person living in the Western Hemisphere or Africa, then they truly suffer from the Black inferiority complex, which today, does as much harm as its twin, White supremacy.

Let's take a look at the tour that both leaders should have taken if they were serious about "saving Africa". It does not even require that either gentleman leave the mid-atlantic region of the country where they both have made their millions, much less her borders.

Here is the itinerary

Day 1: Washington D.C.

Tour Guide(s): Oduor Ongwen, Chair of the National Council of NGOs in Kenya; and Bishop Akologo, Deputy Executive Director of the Integrated Social Development Centre in Accra; Lawrencia Adams, Coordinator, Organisation Pan Africaine Pour Le Developpment Durable ;and Bruce Bartlett, senior fellow at the National Center for Policy Analysis

Since Bono and Secretary O'Neill are open to listening to Africans, we figure we would start our guided tour with the help of three of the more informed African-based individuals on the subject of how U.S. trade policy has been more unfair to Africa than to any other part of the world, historically.

It just so happens that they were in Washington D.C. several days ago as part of a group of 21 African NGO leaders. We expect that, during our tour Oduor Ongwen would repeat, for the benefit of the esteeemed Treasury Secretary and rock star what he told, when he explained that for, " the last 400 years an international division of labor has been responsible for our underdevelopment. This international division of labor requires us to produce what we don't consume, and consume what we don't produce. And any African country that has tried to break out of this, has been isolated and has got a lot flogging...from institutions that are controlled by the U.S. and the countries of the G8." We would then count on Bishop Akolgo to add his previously-reported comment, " No country develops by lowering barriers, opening up and letting everybody in." Lawrencia Adams would be more specific stating, " There is no way, where agriculture is concerned, we will be able to compete effectively when America is protecting or nurturing its agricultural sector."

On this issue, we think Secretary O'Neill's ear is a bit more important than that of Bono, so we will leave the African experts and head over to the National Center On Policy Analysis and ask Mr. Bruce Bartlett, the senior fellow to break it down for Mr. O'Neill. We expect something along the lines of what Mr. Bartlett offered in his recent column at National Review where he wrote:

If Western governments really wanted to do something to help Africa, the easiest thing they could do is open their markets to African products. The fact is that domestic subsidies and import tariffs prevent Africans from selling much of their agricultural output in Europe, North America, and Japan. These nations, it seems, would rather tax their citizens and force them to pay higher prices for food than allow poor farmers in Africa to sell their produce in their countries.

This is an insane policy because it hurts domestic consumers as well as African farmers. By allowing African farmers simply to sell what they have produced in the West at market prices, consumers would have cheaper food and African farming would benefit, possibly obviating the need for aid.

A recent World Bank study found that full elimination of import tariffs in Europe, Canada, Japan, and the U.S. would raise African exports by $2.5 billion per year. This is a trivial sum in the context of their economies, but would lead to a major increase in growth for Africa.

Day 2: Washington D.C., The Federal Reserve Board Of Governors

Tour Guide: Alan "The Maestro" Greenspan

No true quest to find out why Africa is so poor, and remains so, would be complete without having the central banker of the world show Secretary O'Neill and Bono how his mis-management of Federal Reserve monetary policy has impoverished Africa. It is a subject that only a handful of Africans, to our knowledge have explored and one that the U.S. press corps are frightened to touch. Here is how I explained the problem to Mr. Greenspan in an open letter to him last year. Although the price of gold is currently hovering near $320 per ounce, it can't undo the devastation that was caused by Chairman Greenspan's mismanagement of dollar liquidity. I wrote to the Federal Reserve Chair:

"In 1966 for the Objectivist newsletter you wrote the following words, which later appeared in Capitalism the Unknown Idea by Ayn Rand "In the absence of the gold standard, there is no way to protect savings from confiscation through inflation. There is no safe store of value". Mr. Chairman, do you not see the same danger in the opposite direction coming from a monetary deflation? From 1996 to 1999 when you allowed the price of gold, which you once publicly recognized as the signal of a monetary inflation or deflation, to drop from $416 per ounce to $256 per ounce, you permitted a massive transfer of wealth from debtors to creditors, where those who took out loans in 1996 were forced to pay them back with more valuable dollars, in terms of gold, in 1997, 1998, 1999, 2000 and even today, in the year 2001, with a gold price of $260 per ounce.

Anyone who borrowed money in 1996 and who was forced to pay it back over the last 5 years has in effect been robbed -on just the principal portion of the loan.

Possibly no continent on earth has been hurt more by your management of US monetary policy than Africa - the continent where more of the population is dependent upon gold and other commodities than any other. There is no complicated arithmetic necessary to figure out what has happened to African commodities producers and government budgets that depend upon revenue from the produce of the earth in order to balance. Because African economies are dependent upon revenue from the export of their commodities throughout the world, the monetary deflation that hits commodities the quickest and hardest has absolutely devastated the continent. With over 40% drops in numerous commodity prices, countries that have little to no economic diversification are sentenced to unwanted budget deficits and the inability to finance badly needed social services and development projects necessary to the food, clothing and shelter of their citizens. In addition to this, every African nation saddled with an enormous external debt has seen that debt balloon even larger, as in the year 2001 it takes more of an African nation's local currency to purchase an ounce of gold or 1 US dollar than it did in 1996 - a direct result of a deflationary Federal Reserve."

Bono should care and Mr. O'Neill should think about Federal Reserve monetary policy's effects on Africa.

Day 3: Washington, D.C., The IMF

Tour Guide: Michael Camdessus w/special assistant Stanely Fischer

No tour of the reasons for Africa's economic devastation can be considered holistic unless it includes the valuable contributions to poverty made by two special men: Michel Camdessus, Managing Director of the International Monetary Fund from January 1987 to February 2000 and Stanley Fischer, First Deputy Managing Director of the International Monetary Fund from September 1994 to August 2001. From ill-advised tax increases to pressure exerted to achieve currency devaluations, no other two men, along with their international staffs could be counted on to deliver fiscal austerity, anti-economic growth policies and unnecessary privatizations and regulatory reforms - all while receiving salaries partially paid for by the taxpayers of the IMF's largest member nation, the United States of America.

But Mssrs. Fischer and Camdessus were underpaid by any measurement if impeding the progress and search for economic options and guaranteeing poverty was the objective. They went above and beyond in the call of duty. From encouraging the devaluation of the Zimbabwe dollar in 2000, to pressuring the Nigerian government to lift fuel subsidies in 2000(leading to riots), to undermining Mozambique's cashew industry in 2001, to forcing Equatorial Guinea to pay its debt before building badly-needed roads and schools in 1999, to mandating a series of tax increases in the midst of an economic downturn in Mauritius, in 1989, the IMF was unstoppable in wreaking havoc on African economies. Unfortunately both Bono and Secretary O'Neill's respective worldviews, policy prescriptions, and tour did not allow them to include an all-access review of IMF policy and its effects on the continent of 700 million.

Day 4: Fort Detrick Maryland, U.S. Army's Medical Research Institute for Infectious Diseases

Tour Guide: Dr. Len Horowitz

We have saved this day of our tour for Bono and Secretary O'Neill because it is the most difficult. This day makes for the most arduous not just because it points to a more complicated aspect of the relationship between the United States and Africa but because it, in and of itself, obliterates the cover story in both the worldviews of Bono and Secretary O'Neill that Africa largely suffers from American neglect, at worst.

It is this argument that also pulls at the heartstrings of "African-Americans" who believe that their government is "not doing enough to help Africa".

Well, after taking the tour of the Ft. Detrick military facility guided by the steady hand of Dr. Len Horowitz, it would be difficult for anyone sincerely concerned about the reality of the relationship between African suffering and the U.S. government to not question whether the problem is not the impression of benign neglect at worst but rather one of malignant attention from the U.S. government that Africa has received.

The question of where AIDS came from and why it so uniquely devastates Blacks in Africa, in particular, is one for which neither Mr. O'Neill or Bono have the public stomach. It is certainly much easier to hug and hold beautiful African babies in your arms than it is to ask a legitimate political and scientific question, in light of the documented sinister and covert action that the U.S. government has directed toward African leaders and African people.

That is why we have enlisted the help of Dr. Horowitz, who better than just about any person we know of, has adequately contemplated the reality of a continent ravaged by AIDS, the activity of the U.S. military industrial complex, and the mysterious and sudden appearance of HIV and AIDS, all in the light of medical and scientific evidence.

Any scientist and medical professional who would accompany Bono and Secretary O'Neill or anyone else who has been led to believe that human AIDS viruses arose innocently from African green monkey viruses should feel comfortable questioning Dr. Horowitz, whose, findings we partially provide below.

It is time for Black people in the Diaspora, not Bono and Secretary O'Neill, to make a real tour of why Africa is suffering as she is today.

Cedric Muhammad
June 10, 2002


(The following manuscript is a revised version of the scientific paper Dr. Leonard G. Horowitz and coauthors presented at the XI International Conference on AIDS in Vancouver, BC Canada on July 10, 1996. For more information contact 208-265-2575
, and see "Emerging Viruses: AIDS & Ebola--Nature, Accident, or Intentional?" [Tetrahedron Press, 1996; $29.95] by Dr. Horowitz)


This article reviews scientific and U.S. Government documents that show AIDS-like viruses were developed by National Cancer Institute researchers along with military biological weapons contractors between 1962 and 1974 during the "Special Virus Cancer Program." The possibility of this research giving rise to contaminated experimental hepatitis B (HB) vaccines, and thus, the simultaneous emergence of acquired immunodeficiency syndrome (AIDS) in New York City and Central Africa in 1978 is advanced.


Contrary to widespread speculations that human AIDS viruses arose from African green monkey viruses that naturally jumped species, in 1971, National Cancer Institute (NCI) researchers noted that "only one virus [of 27 then known retroviruses] which contains reverse transcriptase, does not seem to be oncogenic", the simian foamy virus (SFV).(1)

Indeed, during the early days of cancer virus and viral vaccine research, simian viruses were common experimental contaminants. Could they have somehow mutated giving rise to the human immunodeficiency viruses (HIV-1 and 2) and AIDS?


The theory that viruses played a major role in carcinogenesis was most actively investigated by researchers at the NCI during the 1960s to mid-1970s. On the eve of Nixon's "war on cancer," NCI investigators explained how retrovirus related cancers such as lymphoma, leukaemia, and sarcoma might develop following virus infections. Twelve years later, in 1984, Dr. Robert Gallo and other esteemed NCI researchers advanced an essentially identical theory to explain AIDS.(1-10)

During the late 1960s and early 1970s, cell tumor biology researchers determined that synthetic RNA and feline leukaemia virus (FELV) "template" added to "human type C" viruses--those associated with cancers of the lymph nodes increased the rate of DNA production (and subsequent provirus and virus reproduction) as much as thirty times.(1) Such hybrid viruses, these researchers reported, may cause many cancers besides leukaemias and lymphomas, including sarcomas. Other NCI and Litton Bionetics teams reported modifying the fortieth discovered simian virus (SV40) by infusing it with nucleic acids from other species including FELV RNA, avian (i.e., chicken) myeloblastosis virus (AMV) RNA, associated with leukemia and sarcoma development, and mouse sarcoma RNA to: 1) make them carcinogenic, 2) prompt extreme immunosuppression in primates,(2,4,11) and 3) study RNA-dependent DNA polymerase (i.e., reverse transcriptase) and its relationship to human carcinogenesis,(6,11-14) For example, early work in viral engineering in relation to human carcinogenesis examined the activity of reverse transcriptase in normal versus acute immature leukaemic lymph cells (i.e., lymphoblasts). To do so, researchers evaluated the single stranded "70S RNA retrovirus" found in chickens which caused white bood cell (WBC) dysfunction, sarcomas, progressive wasting, and death--all prominent features of AIDS.(13)

Human WBCs were injected with this AMV RNA to determine if the cells were prompted to produce proteins and new viruses called for by the virogene.(14) Another team evaluated the human cancer-causing effects of the single-stranded 70S RNA reverse transcriptase enzyme. They used FELV and Mason-Pfizer monkey viruses to deliver these carcinogens to normal human lymphocytes.(15)

During parts of these experiments, NCI and Bionetics investigators even mixed RNA and DNA from chickens and cats with human WBC fractions including human lymphocyte DNA polymerases to induce cancer type and AIDS-virus-like reactions (see fig. 1).(15)

Other Gallo publications detailed the steps involved in creating immune-system-destroying cancer-causing viruses by adapting monkey, rat, and bird leukemia and tumor viruses for experimental use in a human (NC-37) cell line.16 One team discussed the synthesis of new RNA tumor viruses induced by 5-iodo-2'-deoxyuridine (IdU), a constituent of RNA in rodent cell cultures, and noted that chemical treatment might be used to halt the reverse transcriptase-linked viral reproduction cycle.(17)

In another report NCI researchers isolated a virus-like particle from human acute leukemic WBCs which had a specific density of 1.16-1.17g/ml, which allowed it to be repeatedly recovered without being destroyed by physical handling. Moreover, it was capable of producing the principal rapidly growing cancers seen in AIDS, including leukemias, sarcomas, and carcinomas.(19)

Defense Industry Interest

On April 4 and 5, 1969, at Fort Detrick, Maryland--America's premier biological weapons testing facility, a controversial symposium on the entry and control of foreign nucleic acids into human cells was held.(10) That year the National Academy of Sciences-National Research Council informed Department of Defense (DOD) officials that "synthetic biological agents" that caused treatment resistant immunosupression could be developed "over the next five years" at a cost of $10 million.(9) A year later, NCI researchers described the experimental entry of bacterial RNA into human WBCs before a special symposium sponsored by the North Atlantic Treaty Organization (NATO). Their paper, published in the Proceedings of the National Academy of Sciences, discussed several possible mechanisms prompting the entry of foreign nucleic acids into lymphocytes.(2) Soon thereafter, the NCI acquired the lion's share of Fort Detrick's facilities.(10)

According to a 1970 Congressional Record, Bionetics Research Laboratories, a subsidiary of Litton Industries, Inc., was sixth on the list of U.S. Army biological weapons (BW) contractors.(20) Later Congressional Records showed that Bionetics's affiliate--Litton Systems, Inc., another subsidiary of Litton Industries, Inc.--was among the most frequently contracted companies involved in BW research and development between 1960 and 1970.(21)

The Litton Industries, Inc. 1977-1978 annual reports stated,

"In June, [1976] Litton Bionetics won the fourth renewal of its contract to manage the operations of the National Cancer Institute's Frederick (Md.) Cancer Research Center."(22)

Later, Litton sold Bionetics Research Labs to Medpath--a subsidiary of Dow Corning--among the largest medical laboratories in the United States, yet continued to administer the lion's share of NCI's Frederick operations funding to the time of this writing.

Furthermore, NCI staff reports revealed that Litton Bionetics had been granted the service contract to supply all NCI researchers, worldwide, with virtually every primate cancer research material requested, including seed viruses and viral hybrids, experimental reagents, and colony born monkeys, including M. mulatta, associated with the major monkey AIDS virus outbreaks in California's Davis Lab, and the 1967 Marburg virus outbreaks in three European vaccine production facilities and the African green C. aethiops.(24-26) Furthermore, from these publications, a list of the viruses and virus recombinants that Bionetics researchers developed, tested, and supplied to other NCI researchers during the 1960s and early 1970s was developed (see fig. 2).

A 1971 Litton Bionetics research report noted that "highest priority was given to the search for human leukemia viruses resembling the type-C viruses causing chicken and mouse leukemias" beginning as early as 1962.(23) Bionetics researchers, who received approximately $2 million annually for this work, reported:

"Several of the Type C viruses are established as the causative agents in leukemias, lymphomas, and sarcomas of chickens, mice, cats and hamsters. Many of these can infect and produce malignancies in other species (e.g., a sarcoma virus of the cat produces tumors in marmoset monkeys). Furthermore, some of these viruses can cause malignant transformation to occur in animal and human cells grown in the laboratory (e.g., cat leukemia and sarcoma viruses alter embryonic human cells). Type C virus particles have been found in association with malignancies of a spectrum of animal species including nonhuman primates, rats, cattle, wooley monkeys, gibbons, and man. . . ."(24)

Though some contemporary investigators have argued that HIV-1 and 2 are not type-C viruses,(27) more recently, researchers noted they go through a stage of type-C morphogenesis during replication and look and behave similar to the type-C viruses. "Although not classified as type-C viruses, lentiviruses follow a similar assembly strategy, by which capsid [shell] formation and budding [of the virus from the infected cell] occur simultaneously."(28)

Perhaps not coincidentally, during the metamorphosis of HIV, researchers found "a reproducible peak of viral protein in the fraction corresponding to a density of approximately 1.15 to 1.16g/ml . . . in gradients of gag HIV," that is, the gene that codes for the inner shell, capsid-like structure, of the AIDS virus.28 It may be recalled that Gallo et al. reported this number also, but in 1973, after repeatedly recovering the same density "virus-like particle" from human leukemic cells that was capable of producing the principal rapidly growing cancers seen in AIDS.19 Moreover, Kyle noted the United States Food and Drug Administration (FDA) Bureau of Biologics found a similar characteristic in the "adventitious virus" found in some live polio vaccine approved by and released in 1977.(29)

It is known that RNA viruses in general, and type-C and D lentiviruses in particular, "undergo extensive genetic variation as a result of error-prone replication and recombination such that they are considered to exist as 'quasispecies,'" that is, a population of relatives with similar genes.30 One researcher noted "the exceptional ability of HIV-1 to mutate results in rapid development of quasispecies which evade host defenses and become resistant to various antiviral" agents.(31)

Bionetics/NCI researchers went on to report that, "Reactions between Type C viruses causing leukemias and sarcomas (solid tumors)," were a major area of interest for cancer prevention studies including the detection of cancer viruses, and viral vaccine experiments. The investigators wrote:

"When inoculated into appropriate cell cultures, type C sarcoma viruses of chickens, mice and cats produce foci [cancerous growths] of altered cells. This fundamental discovery provides a readily visible indicator reaction for the detection of sarcoma viruses. On the other hand, leukemia viruses grown in tissue culture do not cause foci or other detectable changes. The finding that leukemia viruses can either inhibit or enhance focus formation by sarcoma viruses of the same species has led to the development of methods for the detection and quantitation of leukemia viruses indirectly.

Certain of the chicken, cat and mouse sarcoma viruses are "defective" in that they do not produce foci in cell cultures or tumors in animals in the absence of a co-infecting, 'helper' leukemia virus. [Note the researchers called carcinogenic viruses "defective" if they were unable to produce cancers without the help of other factors including chemicals, radiation, and here leukemia viruses.] Further, in the presence of a defective sarcoma virus the helper action of leukemia viruses can be used as a specific indicator for their detection and quantitation. It is now believed that defective sarcoma virus leukemia virus interactions may be more widespread in nature than originally thought and that similar systems may be found in man. A mouse leukemia virus which has been adapted to grow in human cells is now available to search for defective human sarcoma viruses, if they exist."(24)

In continuing this effort, they developed an "alternative approach" for the detection of possible human leukemia viruses that employed recombinant cat and mouse leukemia and sarcoma viruses engineered to cross species.

"A defective mouse sarcoma virus and its leukemia virus helper can be made to form tight functional aggregates, which behave as one virus. Using a mixture of mouse sarcoma virus and cat leukemia virus, a hybrid aggregate which could be grown continuously in cat cells was produced. [As Gallo et al. also reported.(14,15)] Because the aggregate is defective, it requires the simultaneous presence of a cat leukemia virus for producing altered foci in cat cells. Thus, a focus forming sarcoma virus of the mouse, artificially changed to one possessing infectivity for cat cells, can now be used in cultures for the detection of cat leukemia viruses.

This hybrid virus, as well as the cat leukemia virus, will also grow in human embryonic cells in tissue culture. If sufficient amounts of the Type C particles found in association with human leukemia can be obtained, the possibility exists that the cat-adapted mouse sarcoma virus can be hybridized with the human agent to produce an indicator system for the detection of human leukemia viruses. [Figure 3 presents a graphic description of this work.](24)

The NCI staff went on to explain their work elucidating: 1) the "biochemical pathways of tumor virus infection and replication," 2) reverse transcriptase activity "in cells of patients with acute lymphoblastic leukemia . . . sarcomas, Burkitt's lymphoma and breast cancer," 3) experiments with Type B viruses thought to be associated with breast cancer, 4) Herpes-type viruses "associated with some forms of chronic leukemia, lymphoma, and postnasal carcinoma," and 5) Epstein-Barr viruses extracted from Burkitt's lymphomas and postnasal carcinomas. Vaccines, the NCI researchers explained, were expected to be developed from these efforts to help prevent and treat human cancers as coordinated "through the International Agency for Research on Cancer (IARC) in the West Nile District of Uganda."(24)

A Possible Iatrogenic Cause of AIDS

In May 1942, George W. Merck was commissioned by President Franklin D. Roosevelt to direct the War Research Service overseeing America's biological weapons industry.(32) Since then, the Merck company, in collaboration with the U.S. Public Health Service, provided ongoing expertise to the U.S. Army and its contractors "to bolster ongoing projects in fields in which it has an independent interest."20

A service contract awarded Merck and Company, Inc., under the "Special Virus Cancer Program (SVCP)," called for "oncogenic virus research and vaccine development." The chief objective of this work was reported as being "of fundamental importance to the goals of SVCP." Their proposed course of study included “work towards development of a feline leukemia-sarcoma virus vaccine and a herpesvirus type 2 vaccine [to] be continued as rapidly as possible."(33)

This grant description revealed that simian viruses (SV40)--currently suspected as being an AIDS virus progenitor29—and their "tumor cell ghosts" were prepared and used as principle carcinogenic triggers against which "non-protective SV40 tumor cell vaccines" were tested.33 This work was done at the same time Merck's chief vaccine developer, tumor cell virologist Maurice Hilleman collaborated with Hepatitis B (HB) vaccine pioneer Dr. Saul Krugman of New York University Medical Center, another documented Army biological weapons contractor,(20) and Robert Purcell of the National Institute for Allergies and Infectious Diseases (NIAID) to develop and test the first "4 lots of vaccine that would amount to perhaps 200,000 human doses" by 1974.(34-36)

Bionetics military supplied rhesus monkeys and chimpanzees were used to develop these vaccines during this "initial limited clinical test for establishing safety and measuring antibody response [in human subjects]." This work was based on pilot investigations conducted between 1967 and 1971 with "heat-inactivated hepatitis B vaccine" in animals and high risk human subjects in New York and Central Africa.(34)

At this time Dr. A. M. Prince, charged with overseeing the Laboratory of Virology at the New York Blood Center, wherein the non-human primates were housed, reported a major biohazard and containment problem. Prince admitted, "I would say more than 70%" of the animals became environmentally infected with hepatitis B (and likely other viruses) during their captivity.(34)

In 1974, Purcell reported failed attempts to grow the HB seed viruses, needed for these vaccines, in cell cultures. Willowbrook State School (Staten Island, NY) mentally retarded children, rhesus monkeys, and chimpanzees, he announced, were successfully used instead to culture the viruses subsequently inoculated into high risk human subjects (e.g., Willowbrook children, Central African villagers, and apparently New York's gay men as well) to develop the various vaccine subtypes.(35) "Cross-challenge experiments, and evaluation of various aspects of passive and active immunization against hepatitis B infection," Purcell explained, then proceeded in collaboration with the FDA.

Thus, simian viruses, and/or Bionetics engineered viral hybrids, infecting chimpanzees during this work might have infected humans and given rise to HIV-1 or its immediate progenitor(s). As Shultz explained, "a lentivirus isolated from chimpanzees (SIVcpz)" is "the closest primate relative of HIV-1."(27) Given, Bionetics's involvement in primate cancer virus and animal supply to these New York/Bethesda/Uganda investigators, SIVcpz might have evolved because the chimps had likely been among the first creatures to be exposed to man-made retroviruses by way of direct inoculation or experimental monkey cohabitation.

It is also possible, even if Merck's human experimental HB vaccine hadn’t included contaminated chimpanzee serum, only serum taken from New York's children and/or gay men, live viruses injected around 1970 could have combined with the simian viruses (e.g., SV40, SIVagm, or SFV) the donors may have carried following vaccination with Merck's polio vaccines administered during the previous decade.(29)

These facts provide additional background for evaluating Hilleman's 1986 published comments of having imported AIDS into North America by way of African green monkeys destined for use in Merck's viral and vaccine research. In an effort to reduce laboratory and vaccine contamination, Hilleman reported, "I brought African greens in. I didn't know we were importing AIDS virus at the time."(37)

Summary and Conclusions

This article reviews scientific literature and U. S. government documents that provide additional insight into the iatrogenic theory of AIDS. All it may have taken was one monkey used to develop the initial pilot HB vaccine lots, administered virtually simultaneously in New York City and Central Africa by 1974, carrying iatrogenically evolved or genetically engineered simian sarcoma-leukemia virus hybrids, to have started the AIDS epidemic.(38) This knowledge is important for at least three reasons: 1) the guilt and stigma attached to the victims of AIDS, homophobia, and racism, may ease in light of these findings; 2) new therapies might evolve from this knowledge; and 3) a thorough independent investigation and analysis of the aforementioned facts may help to prevent future outbreaks and epidemics.(39)

This work additionally supports others who have called for careful PCR analyses of suspected vaccine lots allegedly in safe keeping at the FDA.(38) Furthermore, as this report unearths evidence linking Willowbrook State School children, and apparently other high risk groups in New York City and Central Africa, to possibly contaminated experimental HB vaccines developed in chimpanzees, look-back studies of AIDS cases among those who received these early vaccines is clearly warranted.

1. Gallo RC, Sarin PS, Allen PT, Newton WA Priori ES, Bowen JM and Dmochowski L. Reverse transcriptase in type C virus particles of human origin. Nature New Biology 1971;232:140-142; see also Gallo RC. Transfer RNA and transfer RNA methylation in growing and "resting" adult and embyonic tissues and in various oncogenic systems. Cancer Research 1971;31:621-29.
2. Herrera F, Adamson RH and Gallo RC. Uptake of transfer ribonucleic acid by normal and leukemic cells. Proc Nat Acad Sci 1970;67;4:1943-1950. This paper was presented before NATO scientists at the "International Symposium on Uptake of Informative Molecules by Living Cells, Mol, Belgium, 1970," the year in which $10 million in funds were appropriated by the Department of Defense for the development of AIDS-like viruses.
3. Gallo RC, Perry S and Breitman RT. The enzymatic mechanisms for deoxythymidine synthesis in human leukocytes. Journal of Biological Chemistry 1967;242;21:5059-5068.
4. Gallo RC and Perry S. Enzymatic abnormality in human leukaemia.Nature 1968;218:465-466.
5. Gallo RC and Breitman TR. The enzymatic mechanisms for deoxythymidine synthesis in human leukocytes: Inhibition of deoxythymidine phosphorylase by purines. Journal of Biological Chemistry 1968;243;19:4943-4951.
6. Gallo RC, Yang SS and Ting RC. RNA dependent DNA Polymerase of human acute leukaemic cells. Nature 1970;228:927-929.
7. Gallo RC and Longmore JL. Asparaginyl-tRNA and resistance of murine leukaemias to L-asparaginase. Nature 1970;227:1134-1136.
8. Horowitz LG. Deadly Innocence: The Kimberly Bergalis Case: Solving the Greatest Murder Mystery in the History of American Medicine.
Rockport, MA: Tetrahedron, Inc., 1994, p. 14.
9. Department of Defense Appropriations For 1970: Hearings Before A Subcommittee of the Committee on Appropriations House of Representatives, Ninety-first Congress, First Session, H.B. 15090, Part 5, Research, Development, Test and Evaluation, Dept. of the Army. U.S., July 1, 1969, Government Printing Office, Washington, D.C., pg. 79 and page 129 of supplemental record obtained through the Freedom of Information Act.
10. Washington Correspondent. Relief of Fort Detrick. Nature 1970;228:803; regarding controversial conference see: Boffey PM. Detrick birthday: Dipute flares over biological warfare center. Science April 19, 1968;171;285-288.
11. Gallaher RE, Ting RC and Gallo RC. A common change aspartyl-tRNA in polyoma and SV transformed cells. Biochimica Et Biophysica Acta 1972;272:568-582.
12. Fujioka S and Gallo RC. Aminoacyl transfer RNA profiles in human myeloma cells. Blood 1971;38;2:246-252.
13. Smith RG and Gallo RC. DNA-dependent DNA polymerases I and II from normal human-blood lymphocytes. Proceedings of the National Academy ofSciences 1972;69;10:2879-2884.
14. Bobrow SN, Smith RG, Reitz MS and Gallo RC. Stimulated normal human lymphocytes contain a ribonuclease-sensitive DNA polymerase distinct from viral RNA-directed DNA polymerase. Proceedings National Academy of Sciences 1972;69;11:3228-3232.
15. Robert MS, Smith RG, Gallo RC, Sarin PS and Abrell JW. Viral and cellular DNA polymerase: Comparison of activities with synthetic and
natural RNA templates. Science 1972;176:798-800.
16. Gallo RC, Abrell JW, Robert MS, Yang SS and Smith RG. Reversetranscriptase from Mason-Pfizer monkey tumor virus, avian myeloblastosis
virus, and Rauscher leukemia virus and its response to rifamycin derivatives. Journal of the National Cancer Institute 1972;48;4:1185-1189.
17. Wu AM, Ting RC, Paran M and Gallo RC. Cordycepin inhibits induction of murine leukovirus production by 5-iodo-2’-deoxyuridine. Proceedings of the National Academy of Sciences 1972;69;12:3820-3824.
18. Gillespie D, Gillespie S, Gallo RC, East J and Dmochowski L. Genetic origin of RD114 and other RNA tumor viruses assayed by molecular hybridization. Nature New Biology 1973;224:52-54.
19. Gallo RC, Miller NR, Saxinger WC and Gillespie D. Primate RNA Tumor Virus-Like DNA Synthesized Endogenously by RNA-Dependent DNA Polymerase in Virus-like Particles from Fresh Human Acute Leukemic Blood Cells. Proceedings National Academy of Sciences 1973;70;11:3219-3224.
20. Department of Defense Appropriations For 1970: Hearings Before A Subcommittee of the Committee on Appropriations House of Representatives, Ninety-first Congress, First Session, H.B. 15090, Part 5, Research, Development, Test and Evaluation, Dept. of the Army. U.S. Government Printing Office, Washington, D.C., 1969, p. 689; see also Congressional Record, August 8, 1969, p. 23073, and for U.S. Public Health Service involvement and funding see page 23079.
21. Committee on Human Resources, United States Senate. Hearings before the Subcommittee on Health and Scientific Research, Biological Testing Involving Human Subjects by the Department of Defense, 1977: Examination of Serious Deficiencies in the Defense Departments Efforts to Protect the Human Subjects of Drug Research. Washington, D.C.: U.S. Government Printing Office, May 8 and May 23, 1977, pp. 80-100.
22. Litton Industries, Inc. Annual Report[s] to the Securities and Exchange Commission for Fiscal Year Ended July 31, 1977 [and 1978]. Commission file number 1-3998. Securities and Exchange Commission, Office of Reports, October 31, 1977 [and October 30, 1978].
23. NCI staff. The Special Virus Cancer Program: Progress Report #8 [and #9].Office of the Associate Scientific Director for Viral Oncology (OASDVO). J. B. Moloney, Ed., Washington, D. C.: U. S. Government Printing Office, 1971 [and 1972]. Note: This is a very hard publication to find. Few library data bases have it listed, including the NCI Library at Fort Detrick. It is available through the Davis Library, The University of
North Carolina, Chapel Hill, Government Documents Department Depository, Reference # HE 20.3152:V81.
24. Ibid., 15-19; 20-26.
25. Ibid., 187-188; and in 1972 Progress Report #9, pp. 273-289.
26. Fine DL and Arthur LO. Prevalence of natural immunity to Type-D and
Type-C Retroviruses in primates. In: Viruses in Naturally Occurring
Cancers: Book B. Myron Essex, George Todaro and Harald zur Hausen, eds.,
Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1980, Vol. 7,
pp. 793-813; see also Gallo RC, Wong-Staal F, Marhkam PD, Ruscetti R,
Kalyanaraman VS, Ceccherini-Nelli L, Favera RD, Josephs S, Miller NR
and Reitz, Jr MS. Recent studies with infectious primate retroviruses:
Hybridization to primate DNA and some biological effects on fresh
human blood leukocytes by simian sarcoma virus and Gibbon ape leukemia
virus. Ibid.. 793-813.
27. Shultz TF. Origin of AIDS (letter to the editor). The Lancet 1992;339:867.
28. Sakalian M, Parker SD, Weldon RA and Hunter E. Synthesis and assembly of retrovirus gag precursors into immature capsids in vitro.
Journal of Virology 1996;70;6:3706-3715.
29. Kyle WS. Simian retroviruses, poliovaccine, and origin of AIDS. The Lancet 1992;339:600-601; Personal communication from Walter Kyle, May 19, 1996.
30. Drew L, Lichtenstein, Issel CJ and Montelaro RC. Genomic quasispecies associated with the initiation of infection and disease in ponies
experimentally infected with equine infectious anemia virus. Journal of Virology 1996;70;6:3346-3354.
31. Shaheen F, Duan L, Zhu M, Bagasra O and Pomerantz RJ. Targeting human immunodeficiency virus type 1 reverse transcriptase by intracellular expression of single-chain variable fragments to inhibit early stages of the viral life cycle Journal of Virology 1996;70;6:3392-3400.
32. Covert NM. Cutting Edge: A history of Fort Detrick, Maryland 1943-1993. Fort Detrick: United States Army Garrison, 1993, pp. 17-19.
33. NCI staff. Op cit. p. 111; and in 1972 Progress Report #9, pp. 139-141.
34. Krugman S. Viral hepatitis type B: Prospects for active immunization. In: International Symposium on Viral Hepatitis, Milan, Dec. 1974.
Develop. biol. Standard. Vol. 30, Munich: S. Karger Basel, 1975, pp. VI; 363-367; the General Discussion can be found on pp. 375-379.
35. Purcell RH. Current understanding of hepatitis B virus infection and its implications for immunoprophylaxis. In: Antiviral Mechanisms: Perspectives in Virology IX, The Gustav Stern Symposium. New York: Academic Press, 1975 pp. 49-76.
36. Krugman S, Giles JP and Hammond J. Infectious hepatitis: Evidence for two distinctive clinical, epidemiological, and immunological
types of infection. JAMA 1967;200;5:366-373(96-103).
37. Shorter E. The Health Century: A companion to the PBS televisioneries. New York: Doubleday, 1987, pp. 67-69; 195-204. Maurice Hilleman
was interviewed by Edward Shorter on February 6, 1987. A copy of the audiotaped interview is held in the archives of the National Library
of Medicine, History Division, Washington, D.C.
38. Horowitz LG. Emerging Viruses: AIDS & Ebola, Nature, Accident or Intentional? Rockport, MA: Tetrahedron Publishing Group, 1996 p. 481.
39. Stricker RB and Elswood BF. Origin of AIDS (letter to the editor). The Lancet 1992;339:867.

Monday, June 10, 2002

To discuss this article further enter The Deeper Look Dialogue Room

The views and opinions expressed herein by the author do not necessarily represent the opinions or position of or Black Electorate Communications.

Copyright © 2000-2002 BEC