THE FAUCI FILES: 1995 Prophecy: "The Fat Lady Is Singing"

[fred]

As prophesied in the July 30, 1999 issue of THE FAUCI FILES: Elton John
Edition, Harold Varmus became history as the ex-Director of the NIH on
October 7, 1999. The second part of the prediction will now complete
that prophecy as the diminutive Anthony "Mussolini" Fauci is poised to 
become the next direktor of that LARGE agency as he struggles to
compensate for his vertical handicap.

Dangerous small men aside, let's review some of the prophecy by my
research associates from BEFORE the foisting of the 1996 Fauci HAART 
Treatment Hoax upon which the current 1999 Fauci IL-2 Kure Hoax now 
rests, along with the tens of thousands who died -- and WILL die --
in the IL-2 Human Experiment meat grinder, which continues to this 
day on an even greater -- and much more lethal -- scale. 

Fauci's victims will not rest in peace. It is our responsibility to see
that this little monster Fauci doesn't either... not to mention his
murderous sellout Quizzlings of the Larry Kramer, TAG, Projekt
MisInform and decomposing ACT UP corpses of the "I Love Toni" set.

The Wellcome Committee in Hell awaits ALL of these murderers!

fred
==========

           The Fat Lady Is Singing! (July, 1995)
          by Charles R. Caulfield and Billi Goldberg

The old saying is that it's not over until the fat lady starts singing. 
Well, now she's screaming her siren song to the point of shattering 
glass and hanging her head in shame. What's criminal about this sorry 
state of affairs is that her requiem for the dead and dying continues to
fall upon deaf ears.

All of the institutionalized and scientific dogma about AIDS has now 
been proven wrong--it was never right! Yet the medical myths which have 
resulted in the horrible and tragic deaths of a quarter of a million 
Americans are tenaciously guarded by the AIDS scientific-medical- 
pharmaceutical complex. These "Doctors of Death" continue to sneer at 
any and all dissenters while they continue to assault their patients 
with toxic and horrific immunosuppressive "therapeutic agents." 

In the article, "Agenda for U.S. AIDS research is due for a complete 
overhaul," published in the April 4, 1994 The Scientist, Robert S. 
Root-Bernstein calls for a re-evaluation of all theories of pathogenesis
and treatments for AIDS. He states "Identifying the sources and types of
our medical ignorance thus becomes our highest research priority." In 
discussing the role of the newly formed National AIDS Task Force, 
Root-Bernstein cautions that "The useful function that the Task Force 
can play is to make sure that the utmost reaches of our ignorance are 
quickly and efficiently identified. We will not do that by staying in 
the rut that has been gouged out during the past decade, but rather by 
deviating from it."

How could anyone disagree with this sobering assessment of the current 
state of knowledge regarding AIDS in light of recent discoveries in 
immunology and recently published journal articles? We all know who will
disagree: the scientists and doctors of AIDS Inc. who have made livings,
royalties, and careers by ignoring these advances in science. And the 
death machines continue to roll along.

It's evident that every single theory how AIDS is caused and how it 
should be treated have been proven wrong during recent years. The truth 
about AIDS rather than the dogma is as follows: (1) HIV does not cause 
AIDS by killing T4 cells; (2) CD4 (T4) cells are an invalid surrogate 
marker for disease progression; (3) CD8 (T8) cells and the DTH Multitest
are valid surrogate markers; (4) antibody-based vaccines are worthless; 
(5) antiretrovirals not only don't work, they kill people; (6) 
prophylaxis drugs are immunosuppressive, toxic and don't stop people 
from dying (except for PCP prophylaxis which extends survival); (7) 
there is no latency period in AIDS; (8) all AIDS opportunistic 
infections are intracellular in nature; and (9) activating the cellular 
immune response (Th1) is the only way to control HIV and intracellular 
infections. (For further insights on the hopelessness of the past and 
present focuses, see Bernard N. Field's article "AIDS: time to turn to 
basic science" in the May 12, 1994 Nature; and Flossie Wong-Staal's 
"AIDS Research: A Five-Year Prospective" in the May, 1994 The Journal of
NIH Research.)

Take CD4s for example. An immunologic parameter so revered by physicians
and researchers that just over a year ago they were adopted as 
"AIDS-defining" by the CDC, are now discredited by the very pioneers in 
using this prognostic marker. Paul Volberding, MD, of San Francisco 
General Hospital and the godfather of the early and deadly use of AZT in
asymptomatics, states in the February 2, 1994 Journal of the American 
Medical Association, "Much more controversial, however, has been using 
CD4+ cell counts as an acquired immunodeficiency syndrome (AIDS)-
qualifying diagnosis, and CD4+ cell number has been disappointing as a 
surrogate marker of the clinical benefits of antiretroviral drugs." 

Clinical benefits of AZT? ddI? ddC? d4T? 3TC? Protease Inhibitors? TAT 
Inhibitors? Hydroxyurea? Sounds like HIV-negative dementia or knowing 
where your money is coming from. The latest spin from the AIDS, Inc. is 
to use HIV plasma viremia levels as a new surrogate marker to try and 
prove that antiretrovirals work. Of course, they have not been able to 
correlate these levels with clinical benefits or lack of disease 
progression or lymphoid tissue viral infection since they have not yet 
figured out how HIV causes AIDS.

Mounting evidence of the importance of CD8 T-lymphocytes as protective 
and predictive elements has been largely ignored by physicians in 
clinical practice. We still hear of patients having difficulty in 
obtaining absolute CD8 counts from their physicians because the doctors 
either think they're unimportant or in high numbers, deleterious. Yet 
Florence Buseyne and Yves Riviere of the Pasteur Institute in their AIDS
1993 (v7-suppl 2) journal article, "HIV-specific CD8+ T-cell immune 
responses and viral replication," state that "These CD8 T-cells may help
to maintain a low viral load in vivo, thus allowing a long asymptomatic 
period of infection." 

Jay M. Schlumpberger's group provides substantiation for the importance 
of CD8s in the January, 1994 Journal of Family Practice. Based on the 
evaluation of 133 PWAs for a period of one year, the researchers 
conclude that "Our study suggests that an urgent need for new surrogate 
markers of AIDS progression for use in evaluating novel therapies might 
be partially addressed by the use of CD8 counts as surrogate markers in 
patients with advanced HIV infection, and that potential therapies 
directed at increasing CD8 counts might prove beneficial in patients 
with advanced HIV infection." This determination was drawn from the 
observation that ". . . for every 100 cell decline in the enrollment CD8
count, the risk of death increased by 16%." The researchers identify the
CD8 "danger-zone" for serious opportunistic infections as 400 CD8s.

Whatever microbial agents and environmental factors cause the cluster of
diseases we know as AIDS, becomes a moot point in light of this current 
research. CD8 lymphocytes only proliferate in adults in response to 
specialized cells presenting antigens to the immune system. The 
impairment of the function of these antigen presenting cells has been 
linked to the lack of proliferative responses in all T-cell subsets. 
NIAID's Anthony Fauci, in AIDS 1993 (v7-suppl 2), states "The loss and 
the impaired function of antigen presenting cells, (i.e. follicular 
dendritic cells, dendritic cells and macrophages) are presumably the key
events over time that are responsible for the transition from the state 
of immune activation associated with early stage disease to the state of
immunosuppression, invariably associated with advanced stages of 
disease." Fauci has been the ultimate disbeliever, until recently, of 
the involvement of antigen presenting cells in the pathogenesis of AIDS.

As of yet, we might add, only one therapeutic agent has been developed 
which restores and modulates the activities of dendritic cells. This is 
the skin sensitizing agent DNCB. But, as we all know, DNCB's low cost 
and ready accessibility provide no financial incentive for trials of its
effectiveness, leaving its results relegated to the scrap heap of 
"unsubstantiated" and "anecdotal" by the powers of AIDS Inc. 

The cell-mediated cascade (Th1) of the immune system is initiated by 
contact sensitization and weekly use of topically-applied DNCB according
to scientific studies. It is known that this systemic response, 
utilizing the antigen presenting capability of dendritic cells and 
macrophages, activates cytotoxic T lymphocytes, cytotoxic macrophages, 
and natural killer cells. According to Sergio Romagnani of Italy, an 
acknowledged expert in immunology, "In general, the activation of Th1 
cells leads to several effector functions causing cytotoxicity, and so 
progression of an immune response toward a Th1 pathway would probably be
the most appropriate for dealing with intracellular organisms and 
viruses." In the same issue of Annual Review of Immunology 1994 and in 
the January 28, 1994 Cell, William E. Paul, Director of the Office of 
AIDS Research, supported and expanded on the importance of Th1 in 
controlling intracellular infections.

Timothy R. Mosmann, discoverer of the TH1/TH2 cytokine patterns, wrote a
brilliant and elegant perspective, "Cytokine Patterns During the 
Progression to AIDS," in the July 9, 1994 issue of Science. He closes by
stating "TH1-like cells may resist direct HIV infection and also be more
able to induce destruction of infected cells. . . . It is conceivable 
that we could live with HIV infection provided the immune system could 
contain the infection, in the same way that infection by some herpes 
viruses can be life-long, yet cause minimal symptoms unless the immune 
system is suppressed. If a TH1-like, cell-mediated, non-antibody 
response can control HIV, this has enormous importance for the design of
vaccines and strategies for treating HIV-infected patients."

Conversely, activation of the antibody response (Th2) appears to result 
in suppression of the protective cell-mediated cascade (Th1). In the 
May, 1994 issue of AIDS Research and Human Retroviruses, Romagnani 
expresses this danger by stating "Evidence is also accumulating to 
suggest that HIV-infected subjects who mount Th2-type responses, due 
either to their genetic background (e.g., individuals with atopic 
allergy) or to environmental conditions (e.g., individuals living in 
helminth-infested areas), may undergo more severe and active HIV 
replication and therefore progress faster to AIDS." 

When Dr. Raphael B. Stricker, principal investigator in a small pilot 
study of DNCB users, observed a decrease in viral burden in addition to 
increases in cytotoxic CD8 T-cells and natural killers cells, he was 
forbidden by HRI Research Corporation of Concord, California, the owners
of the polymerase chain assay he was using in the study, to publish his 
data. The letter from HRI to Stricker includes the hypocritical 
statement "Upon initial conversation with our patent counsel, there is 
some concern that the observation of a reduction of viral load by DNCB 
may be viewed as a 'discovery' and therefore patentable subject matter. 
. . I am sorry that we have to take the position not to disclose in 
writing at this time." The communique was signed by George D. Cimino, 
PhD, Vice-President of HRI. 

Of course, the maverick and controversial Stricker disclosed his 
findings during the International Conferences on AIDS in Amsterdam, 
Berlin, and Yokohama, along with publishing the results in Immunology 
Letters. (1993;36:1-6) and the Journal of the American Academy of 
Dermatology  (1994;31:462-6).

Stricker's findings were confirmed and expanded in a "pure-and-simple" 
Brazilian DNCB study done by Dr. Ari Traub and presented at the 1994 
10th International Conference on AIDS in Yokohama (PB0304). During the 
study period (11/93-7/94), the results were as follows: (1) all of the 
14 patients in the study used DNCB; (2) none of the patients developed 
an opportunistic infection or malignancy; (3) all of the patients gained

weight; (4) all of the CD4 counts remained stable or had a slight 
increase (p=0.002); (5) all of the CD8 counts were significantly 
increased (p<0.0001); (6) there were no side-effects other than mild 
eczema; and (7) none of the patients were using antiretrovirals, 
prophylaxes, or alternative treatments.

Let's face it. Clinical trials of drugs are never designed to 
demonstrate efficacy, but rather to bring their drugs to market. This 
costs the companies hundreds of millions of dollars per drug; money they
have every intention of not only retrieving, but at a maximum profit. 
Billions of industry dollars would be lost if DNCB was accepted by the 
mainstream as a viable treatment for AIDS. Therefore, the focus of 
research becomes higher-tech, more worthless, and less accessible to the
majority of people in the world suffering from this disease.

Gene therapy? Recombinant cytokines? Clonal expansion? Lymphocyte 
infusion? Baboon bone marrow transplants? Yeah, right! Even if these and
other new hair-brained treatment schemes had a chance of working, they'd
be years away in the future, and exclusionary of the third world, the 
poor in the industrialized world, and minorities, with deaths 
conceivably in the hundreds of millions if we continue on the present 
course. Staring right in our faces is a treatment which thousands of 
people with AIDS have gained immune reconstitution, increased quality of

life, and survival. When does this preponderance of anecdotal and 
scientific evidence warrant attention? Obviously, it will always be 
ignored by the antiretroviral lobby. Anecdotal evidence is from and 
about real people, and real people have no place in the "big picture" 
except as guinea pigs in clinical trials for treatments that are 
immunologically and rationally doomed to fail.

The best example to date about the failure of the scientific-medical- 
pharmaceutical complex is in a recent article by Dennis Osmond and 
collaborators in the April 13, 1994 Journal of the American Medical 
Association. The authors determined that, for individuals at the time 
their CD4 counts were 200, survival was 40.1 months from 11/86 to 11/88.

At the beginning of the AIDS pandemic, survival was 28.4 months from 
10/83 to 11/86. Presently(11/88 to 11/93), the survival time from having

a CD4 count of 200 is 38.1 months. This increased survival time was not 
due to antiretroviral therapy, alternative therapies, or better drugs 
for prophylaxis against opportunistic infections. It was due solely to 
prophylaxis against Pneumocystis carinii pneumonia (PCP) which became 
common in 1986. Drs. Sonnabend, Conant, and Volberding recommended its 
use in the early eighties and were ignored!

Where do we go from here? Will Root-Bernstein's proposals be accepted 
and evaluated by the National AIDS Task Force. Of course not. These 
"Doctors of Death" can never admit their errors and responsibility for 
the deaths of thousands. Survival, then, depends on individuals fighting

for their own lives in spite of and against AIDS, Inc. But, along with 
our criticism and attack on the scientific-medical-pharmaceutical 
complex, we have offered a safe, cheap, and non-toxic treatment 
alternative that boosts cellular immunity.

Convincingly, the brilliant UCSF retrovirologist, Jay A. Levy, in the 
June 24, 1995 issue of Lancet, delineates the critical importance of 
activating cellular immunity in an article titled "HIV research: a need 
to focus on the right target." Elegantly, Dr. Levy undercuts the AIDS, 
Inc. focus on the virus and trying to stop de novo infection of new 
cells by stating ". . . focusing only on the virus is akin to treating 
the symptoms but not the cause." He underscores this misdirection by 
adding "In both vaccine development and therapy, not enough attention 
has been given to approaches that can kill virus-infected cells or 
suppress virus replication by these cells." In his comparisons between 
AIDS and cancer, he adds "Both diseases can remain latent for long 
periods. Maintaining tumour dormancy or HIV latency may be, in fact, a 
viable clinical objective, easier to attain than the long-sought cure." 

There is no more we can do. Treatments for AIDS are a matter of personal
choice; the ball is now in your hands to do what you will. And, lest you
forget, the fat lady is still singing her siren song for the dead and 
dying.

___________________________________________________________

This is the last article of Charles R. Caulfield. He swore that he would
not die from the HIV virus and he didn't. He passed away on Sunday, July
17, 1994 from an accidental fall. His activism, altruism, compassion, 
and writings have left a legacy that will live forever. In his memory, 
The Fat Lady is Singing! has been updated to the present. This has 
resulted in minimal additions that have provided more support for the 
article's thesis: The failure of the establishment. The Anarchist AIDS 
Medical Formulary (1993 North Atlantic Books: Berkeley, CA) is his 
magnum opus. I have lost a dear friend. May he rest in peace. -- b.g.