109 Questions for Robert Gallo and other
"HIV/AIDS" experts:
1.
If "HIV" testing is so accurate, then why did JAMA (Journal of the
American Medical Association) publish an article a month ago that claimed that:
“Viral
load is only able to predict progression to disease in 4% to 6% of
HIV-positives studied, challenging much of the basis for current AIDS science
and treatment policy?”
(Rodriquez B, Sethi AK,
Cheruvu VK, et al. Predictive value of plasma HIV RNA level on rate of CD4
T-cell decline in untreated HIV infection. JAMA 296
(12):1498-506, 2006; Cohen J. Study says HIV blood levels don't predict immune
decline. Science 313(5795):1868, 2006). What implications does this JAMA report
have for the defendant?
"A
nationwide team of orthodox AIDS researchers led by doctors Benigno Rodriguez
and Michael Lederman of Case Western Reserve University in Cleveland are
disputing the value of viral load tests-a standard used since 1996 to assess
health, predict progression to disease, and grant approval to new AIDS drugs
after their study of 2,800 HIV positives concluded viral load measures failed
in more than 90% of cases to predict or explain immune status…”“Viral load is
only able to predict progression to disease in 4% to 6% of HIV-positives
studied, challenging much of the basis for current AIDS science and treatment
policy”
2.
If "HIV" is isolatable as an exogenous unique retrovirus, why would a
hepatitis B vaccine (Lee, D, Eby W, Molinaro, G. HIV false positivity after
Hepatitis B vaccination. Lancet 339: 1060, 1992), or flu vaccine (Simonsen L,
Buffington J, Shapiro CN, et al. Multiple false reactions in viral antibody
screening assays after influenza vaccination. Am J Epidemiol 141:1089-1096,1995; Christian, P. Erickson, Todd McNiff, Jeffrey D.
Klausner. Influenza Vaccination and False Positive HIV Results New England
Journal of Medicine,Number 13 , Volume 354:1422-1423, March 30, 2006)
cause about 2% false
positives? Do you know if the defendant had any vaccines before he was
"HIV" tested, and could prior vaccines account for his being
"HIV-positive?
A related question is, if the Center For Biologics Evaluation and
Research Advisory Committee on Vaccines and Related Biological Products claimed
in November, 1998, in a chapter regarding the Update On Reverse Transcriptase
Activity In Chicken Cell Derived Vaccines, by Dr. Arifa Khan (pages 13-15),
that:
"Initially
Boni et al. (1996) published that low level reverse transcriptase activity was
detected in ALL chicken cell derived vaccines using a highly sensitive
PCR-based reverse transcriptase assay called PERT, which can detect one to ten
virions which was reported to the WHO, and then additional studies were done by
several laboratories in Europe, as well as the U.S., including the NIBSC, the
CDC, as well as labs in the FDA to confirm this initial finding. However, after
further work, it was discovered that this reverse transcriptase activity could
be eliminated by treatment of extracts with DNAase, and that using Alu-based
EAV sequence integration studies, that no integration of anything derived from
the chicken cell supernatants was detected in Human PBMC cells."
Were/are "HIV" culture extracts also treated with DNAase
to test if reverse transcriptase activity is eliminated by DNAase treatment? A
related question is, if reverse transcriptase activity is present in all
chicken cell-derived vaccines, as the report from Khan and others (and
confirmed in several European and CDC laboratories indicate are present in all
chicken cell-derived vaccines), then is it possible that anyone injected with
measles or other vaccines derived from chicken cell-derived vaccine preparation
procedures, might also test positive for reverse transcriptase activity due to
reason that have yet to be elucidated? Was the defendant ever a recipient of a
chicken cell-derived vaccine or related product? If reverse transcriptase
activity was used to detect "HIV" in "HIV" cultures during
the early 1980's, and if reverse transcriptase is specific for "HIV,"
then why do market magazines concerning biotechnology stocks claim that reverse
transcriptase can be found in a plethora of normal
(non-"HIV"-associated) contexts (Pachez M. No need to be phased. Shares, 28-32, 2001. Papadopulos-Eleopulos E, Turner VF,
Papadimitriou J, Page B, Causer D, Alfonso H, Mhlongo S, Miller T, Maniotis A,
Fiala C. A critique of the Montagnier evidence for the
HIV/AIDS hypothesis. Med Hypotheses 63(4):597-601, 2004)?
3.
Why did the Red Cross report that even after repeated testing using different
test kits, that low-risk populations, such as blood donors (or military
recruits) will typically yield 12 (PCR) positive or 2 (ELISA) positive results
out of 37,000,000 samples, leaving potentially 10 out of 12 false positives,
depending on which test kit you believe (Stramer et al. “Detection of HIV-1 and
HCV Infections among Antibody-Negative Blood Donors by Nucleic
Acid–Amplification Testing. New England
Journal of Medicine, Volume 351:760-768, August 19, Number 8, 2004)? Is it possible that the defendant is among
these 10 out of 12 false positives, as is the woman to whom he supposedly
transmitted "HIV?"
4.
If the components of "HIV" have been isolated and are unique to
"HIV," why did Barre-Sinoussi (one of Luc Montagnier’s original group
from whom Dr. Gallo hijacked LAV, later to be called “HIV”) come out of the
closet, and say at the Toronto International AIDS festival last August that:
“It is not clear if therapeutic vaccines might
be useful, since 15 trials to date have not demonstrated definitive evidence of
improved outcomes.”
5.
Phase III trials are supposed to test the efficacy of a medical intervention
against the best current treatment in place. If the components of
"HIV" have been isolated and are immunogenic in humans, as components of an
exogenous virus would be expected to be, then why did you (Robert Gallo) say in
2004 after the failure of the AIDSVAX "HIV" trial that "a sound
rationale is needed for Phase III HIV vaccine trials?" Weren't the Phase I
and II trials based on a sound rationale? Do "HIV/AIDS" experts
advocate progressing to phase III trials even when Phase II trials are an
unmitigated failure as was the case of AIDSVAX? (Gallo and
Others. A sound Rationale needed for Phase III HIV vaccine trials.
Science, Vol 303 16
January, 2004).
6.
If the “HIV" is an exogenous virus with a unique identity, why did a group
of AIDS researchers in The Department of Microbiology, University of Minnesota
publish in The Journal of Virology, that “HIV” gene sequences can be detected
in non-infected humans, chimps, and monkeys?
“HIV-like
sequences exist in normal in human, chimpanzee, and rhesus monkey DNAs:
"Endogenous retrovirus-related sequences exist within the normal genomic
DNA of all eukaryotes…Herein we describe the first report of the presence of
nucleotide sequences related to HIV-1 in human, chimpanzee, and rhesus monkey
DNAs from normal uninfected individuals." (Horwitz MS, Boyce-Jacino MT, Faras AJ. Novel human endogenous
sequences related to human immunodeficiency virus type 1. (J
Virol. Apr;66
(4):2170-9, 1992).
7.
If "HIV" is a new virus, and if the "HIV" tests are
specific, then why did the Journal of Clinical and Diagnostic Laboratory
immunology publish an article that showed that goats and cows test positive for
"HIV" but do not develop AIDS? (Willman et al.,
Heterophile Antibodies to Bovine and Caprine Proteins Causing False-Positive
Human Immunodeficiency Virus Type 1 and Other. Enzyme-Linked
Immunosorbent Assay Results. Clinical and Diagnostic Laboratory
Immunology, p. 615-616, Vol. 6, No. 4, July 1999).
8.
What disease(s) do the following symptoms specify?
"Then
the adjacent lymph glands become swollen and rubbery, a condition known as
regional lymphadenopathy.”
“Thereafter,
the disease “matures” for up to six months" and can become characterized
by a “macular” (spotty) roseola-like rash and other skin symptoms. The regional
lymphadenopathy becomes generalized and affects the body’s whole lymphatic
system; it is a “valuable diagnostic finding” and one of the most
characteristic aspects of the early disease; the lymph nodes are “painless,”
“enlarged,” “rubbery,” “non-tender,” and “freely moveable.”
“The
patient will complain of rashes, fever, itching, sore throat, headache,
malaise, vertigo, sweating, insomnia, nausea, prostration, weight loss, loss of
hair, or aching in the bones and joints. Some have hypertension, kidney
disease, swollen liver, or swollen spleen; others have a
subacute meningitis with cranial nerve involvement. The thymus-dependent
parts of the lymphatic system deteriorate, and there is consequent decrease in
the numbers of T-lymphocytes. The T-helper cells are particularly affected by
this: there is a decline in their number and the ratio with the T-suppressor
cells is reversed."
"At
this stage, such conditions as infectious mononucleosis, iritis,
neruoretinitis, lichen planus, cancer, nephritis, dementia, lymphomas,
psoriasis and other skin eruptions, and even drug reaction… are confused with
this stage."
"Consequently,
a long-term effect of syphilis is loss of, or decline in, the system of
immunity, and lowering of the individuals capacity to defend himself against
other infectious conditions For this reason secondary syphilis is called the
great imitator” (AIDS and Syphilis-The Hidden Link, by Harris
L. Coulter, North Atlantic Books, 1987).
9. Have other medical reasons for the defendant
testing positive been excluded, including prior receipt of hemodialysis,
transfusions, gamma globulin, or immune globulin (as prophylaxis against
infections), TB or cryptic forms of that great imitator, syphilis,
malnourishment, herpes simplex I and II, arthritis, systemic lupus
erythematosus, scleroderma, connective tissue disease, dermatomyostitis,
malaria, hemophilia, hepatitis, alcoholic hepatitis, primary billiary
cirrhosis, hyperbilirubinemia, hypergammaglobulinemia, leprocy, lipemic serum,
malaria, malignant neoplasms, mycobacteriaum avium, Q-fever with associated
hepatitis, primary sclerosing cholangitis, visceral leishmaniasis, renal
failure, Stevens-Johnson syndrome, high levels of circulating immune complexes
and ERS rates (erythrocyte sedimentation rates or “sticky blood” known to be
high among Africans and other populations), free ribonucleoproteins, T-cell
leukocyte antibodies, HLA antibodies (to Class I and II leukocyte antigens),
p18, p24, p55, p12, p32, p51, p66, or gp160, gp41, gp120 antigens that may be
present in fluids obtained from patients who have warts?
10.
Patient 1, according to Montagnier, from whom he acquired the "HIV"
(LAV) isolate (that Gallo was later accused by The French, The Dingell
Commission, and The Office of Scientific Integrity at the NIH of stealing from
the Pasteur group), was said to have had herpes, 2 cases of gonorrhea, 1 case
of syphilis, cytomegalovirus, and Epstein-Barr virus. Do you think this patient
1 was a good source of your "HIV" isolate? Was the first Abbott Labs
patented test kit designed around this isolate? Why did Gallo obtain the
"LAV" isolate from the Montagnier group, and claim that he had
discovered it?
(From John Crewdson: Gallo Case, Truth Termed A Casualty Report:
Science Subverted in AIDS Dispute; Chicago Tribune (CT) - SUNDAY, January 1,
1992 from the Dingell Report):
“The violence to principles of responsible, ethical science was
just as profound. At a crucial point early in the (Gallo laboratory's) HIV
research, international politics and the technocrats committed to those
politics virtually took over that research, claiming the laboratory's putative
accomplishments as accomplishments of the United
States administration and by
extension, the United States
itself.”
“Once done, the (Gallo laboratory's) interests became the
government's interests; defending the (Gallo laboratory) scientists'
reputations and claimed accomplishments became necessary for defending the
honor of the United States.
The defense thus became a consuming effort for significant portions of the U.S.
government.”
“The result was a costly, prolonged defense of the indefensible in
which the (Gallo laboratory's) “science” became an integral element of the U.S.
government's public relations/advocacy efforts. The consequences for HIV
research were severely damaging, leading, in part, to a corpus of scientific
papers polluted with systematic exaggerations and outright falsehoods of
unprecedented proportions.”
11.
In 1956 Dr. Etienne de Harven was the first to show electron microscope images
of the Friend virus in murine (mouse) leukemia, and in 1960, to coin the word
"budding" to describe steps of virus assembly on cell surfaces. He
also delivered a speech at the 12th World AIDS Conference in Geneva
(June 28-July 3) at the session entitled, "HIV-testing: Open Questions
about Specificity."
Why did Dr. Etienne de Harven, who is now an emeritus Professor of
Pathology, University of Toronto and who worked out the ultrastructure of
retroviruses throughout his professional career of 25 years at the Sloan
Kettering Institute in New York and 13 years at the University of Toronto,
vociferously object to the standards used to claim that "HIV" viral
particles had been convincingly isolated?"
"First
the antibody.
ELISA, then Western Blot tests were hastily developed
(at sizable financial profit eagerly split between the Pasteur Institute and
the US). "Seropositivity" became synonymous
with the disease itself, plunging an entire generation into behavioral panic,
and exposing hundreds of thousands of people to 'preventive' antiviral AZT
therapy which actually hastened the appearance of severe or lethal
immunodeficiency syndrome. Appropriate controls were apparently never carried
out or were never published. Still, back in 1993 it became clear that the
so-called HIV antibody tests badly lacked specificity, (Papadopulos-Eleopulos
E, Turner VF and Papadimitnou JM, 1993. Is a positive Western Blot proof of HIV
infection? Bio/Technology 11:696-707) cross-reactivity being
observed with patients suffering from a long list of pathological conditions
including malaria, leprosy, auto-immune diseases and many more."
"Secondly,
'viral proteins'.
Several proteins have been identified as 'HIV markers', most frequently because
they were identified in a variety of 1.16 bands. The case of the p24
"viral" antigen is a significant example and its lack of viral
specificity has been well documented. (Todak C, Klein E, Lange M et al., 1991. A clinical appraisal of the p24 antigen test. International Conference on AIDS, vol 1, Florence, Italy)."
"Third,
reverse transcription. If reverse transcriptase activity were a unique feature
of retroviruses, it could have been an interesting molecular marker.
Unfortunately, it has been shown that reverse transcriptase is found in the
uninfected cells of yeasts, insects and mammals (Varmus H, 1987. Reverse
transcription Sci. Am. 257:48-54) and "has nothing to do with retroviruses
as such." Moreover, K. Mullis himself does not support the use - to
amplify and quantify the "HIV genome" - which is being made of the
PCR methodology he developed, which is the current method of "measuring
the viral load" in AIDS patients."
"More
disturbing is the fact that some 'markers' are searched for in the 1.16
gradient sedimenting material which is the density
where intact virions are expected to be found, but not their molecular
fragments. If lysed retrovirus particles released molecular markers, the 1.16
samples should at least initially allow investigators to demonstrate virus
particles by EM. They don't. However after 15 years of most intensive HIV
research, two independent groups finally decided to explore by electron
microscopy the ultrastructural features of the material sedimenting at the 1.16
density. Working on "HIV-1 infected T-cell" cultures supernatants,
both groups found that it contains primarily cellular debris and cell membrane
vesicles which could definitely not be identified with HIV particles and rare
"virus-like" particles (Gluschankof P. Mondor I, Gelderblom HR, and
Sattentau QJ, 1997. Cell Membrane vesicles are a major contaminant of
gradient-ennched human immunodeficiency virus type-l preparations. Virology 230:125-133; Bess JW Jr., Gorelick WJ, Bosche WJ, Henderson LE, and Arthur LO,
1997.
Microvesicles are a source of contaminating cellular proteins found in purified
HIV-I preparations. Virology 230:134-144)."
"Still,
this is the type of sample in which "viral markers" are currently
identified and used to measure the effects of anti-viral drugs in current
clinical trials."
"In
conclusion, and after extensive reviewing of the current AIDS research
literature, the following statement appears inescapable: neither electron
microscopy nor molecular markers have so far permitted a scientifically sound
demonstration of retrovirus isolation directly from AIDS patients."
12.
A few years ago, a 3 1⁄2 year-old girl named Eliza Jane Scovill died 36
hours after being prescribed amoxicillin for the first time in her life.
Commenting on the tragic death, a prominent AIDS researcher named Dr. John
Moore of Cornell Medical College who spoke at last summer's Toronto
International AIDS conference at the AIDS and Responsible Journalism session,
strongly advocated that a Salem Witch Trial for Ms. Christine Maggiore, and her
partner Robin Scovill be intensively pursued by The State and the press,
because Ms. Maggiore inconsistently tested "HIV" positive 6 times
(inconclusive, positive, inconclusive, positive, negative, and positive-with no
2 tests in a row indicating she was positive). For this reason, and perhaps to
avoid stigmatization of her children, Ms. Maggiore did not want her daughter or
son tested for "HIV." From hospital records, it was learned that the
little girl had 10,800 lymphocytes/microliter at the
time of her hospital admission, which is far more than the average number of
lymphocytes in a normal blood sample. The WHO defines AIDS as a condition in
which a person exhibits 1000 or fewer lymphocytes/microliter, and the absolute
number of lymphocytes was obtained at the hospital upon admission, and
according to "AIDS experts," they are just as predictive of
AIDS-related death in children, if not more so than CD4/CD8 ratios. In a recent
study of 3917 children, it was reported that:
“For
children older than 2 years, the 12-month risk of death and AIDS increased
sharply at values less than 1500-2000 cells per microliter, with little trend
at higher values.” (Eliza Jane's count was 10,800
cells/microliter).
“Mortality
risk was substantially higher at thresholds of total lymphocyte count
recommended by WHO than at corresponding thresholds of
CD4-cell percentage. When the markers were compared at the threshold values at
which mortality risks were about equal, total lymphocyte count was as effective
as CD4-cell percentage for identifying children before death…” (HIV Paediatric Prognostic Markers Collaborative Study. Use
of total lymphocyte count for informing when to start antiretroviral therapy in
HIV-infected children: a meta-analysis of longitudinal data. (Lancet. Nov 26;366 (9500):1868-74,
2005).
Why has Dr. Moore, and many members of
the AIDS establishment since the death of Eliza Jane claimed that this little
girl died of AIDS when her lymphocyte count was 10,800 cells/microliter? Is Dr.
Moore correct in his assertion that AIDS is a disease of too many lymphocytes
rather than too few lymphocytes?
13.
Have you (Gallo or "HIV" expert) or anyone you work with ever written
a letter of apology to the kin of the dentist, Dr. David Acer, for his
committing suicide on the basis of mistaken charges that he spread “HIV” to his
patients, which the CDC later exonerated him of doing (after he committed
suicide), because the CDC could "find
no evidence the dentist's HIV-positive patients contracted their infections
from him because their virus' DNA did not match his, and also concluded the
dentist's patients did not contract the virus from one another -- in effect,
that unclean dental implements did not act as conduits." Ted Anthony.
STUDY: HIV not contracted from dentist. Associated Press, Thursday, December 1, 1994. ww2.aegis.org/news/ap/1994/AP941233.html
14.
Why have so many studies which begun even at the beginning of the AIDS era, and
that have followed exposure of health care workers to "HIV" through
sharps, or other injuries, found no transmission of AIDS (Hirsch MS, Wormser
GP, Schooley RT, Ho DD, Felsenstein D, Hopkins CC, Joline C, Duncanson F,
Sarngadharan MG, Saxinger C et al. Risk of nosocomial infection with human T-cell
lymphotropic virus III (HTLV-III).N Engl J Med. Jan 3;312(1):1-4, 1985)?
15.
If you are a cancer researcher, and you don't believe, for example, that the
deregulation of the p53 oncogene completely, or even
partially explains cancer, you are not considered a Holocaust denier, or worse
perhaps, a flat-earther, irresponsible, or criminal. Instead, other hypothesis are permitted,
tolerated, and even funded. Why is it that alternate hypotheses of AIDS
pathogenicity, such as the redox hypothesis of the Perth Group, the Multiple
Antigen Mediated Autoimmunity hypothesis advanced by Robert Root-Bernstein, the
illicit and pharmaceutical-drugs-AIDS hypothesis advanced by government
researcher Harry Haverkos and NAS member Peter Duesberg, not been pursued or funded
in 25 years? As a related question, why have the following letters and articles
from just one group of researchers (The Perth Group) been repeatedly rejected
from scientific journals? Are they poorly written? Are they filled with what
you would consider to be dangerous ideas?
Gallo's experiments and a plea for clarification
Perth Group reponse to Nature and its Durban Declaration
gp120 and HIV infection 8K
Commentary on the Ho and Wei Nature papers
Concerning TB in Africa
Commentary on AZT
Anti-HIV antibodies, ARVs and informed consent
HIV transmission from chimpanzees
A critical analysis of HIV serology does not affirm a retroviral
infection
A critical appraisal of the evidence for the existence of HIV
Commentary on the Gallo/Montagnier HIV as the cause of AIDS paper
Response to Declan Butler
Letter to Lancet in response to the WHO
Letter to NEJM July 2004
Letter to BMJ
Letter to Nature Medicine
Letter to Lancet
Letter to Structure
16.
How are the chimps who were injected with AIDS-patient
sera more than 20 years ago and who never developed any AIDS-indicator diseases
doing in their retirement community? (The New York Times, January 7, 2003 "For Retired Chimps, a Life of Leisure," by Sheryl Gay
Stolberg).
17.
Why does the CDC still maintain that the average course of "HIV/AIDS"
is from 5-10 years, while Dr. Bruce R. Schackman, chief of health policy at
Weill Cornell Medical College in New York and lead author of a paper appearing
in Medical Care in 2006, a journal published by the American Public Health
Association claim that "...patients
can live average 24 years, if they pay $385,000," while David Ho,
Daniel Douck, Ronald Desrosiers, have claimed that "HIV" destroys the
gut lymphoid tissue of "recently infected people," and essentially “wipes clean" the lymphoid tissue lining
the gut shortly after infection?
18.
When the FDA recalls defective "HIV" tests or statistics package
software, how long does it take the medical community to respond to the typical
recall? For instance, are testing labs
immediately provided with the lot numbers of defective testing merchandise in a
timely manner, and are patients who received these tests quickly notified about
the recall of the test they were subjected to? A few recent cases may here be illustrative:
Recall of HIV p24 Antigen Test Kit
Globus Media REcall HIV test
ORTHO Antibody to HBsAg ELISA Test FDA recall Ortho HBsAG System
Recall of Antibody to Human Immunodeficiency Virus Type 1 p24
Antigen Test Kits
Recall lancets for HIV kit
FDA Recall of NucliSens HIV test kit
FDA Recall of HCV EIA 2.0 Test Kit
Market Withdrawal of HIV-1 - HCV Assay, FDA recall Procleix
FDA Recall HIV-1 - HIV-2 Plus O EIA
Testing Software
Recall of HIV Types 1 &2 (Synthetic Peptide)
FDA Recall of Amplicor HIV test kit
19.
Why did Dr. Alfred Hässig, Emeritus Professor in Immunology at the University
of Bern, former Director Swiss Red Cross blood banks: Director of the Swiss Red
Cross Transfusion Service, and President of the Board of Trustees of the
International Society of Blood Transfusion (who, with colleagues, formed the
Study Group for Nutrition and Immunity), claim the following:
“The
sentence of death accompanying the medical diagnosis of AIDS should be
abolished.” (Sunday Times (London) 3 April 1994).
“In
the virological research, so much money is invested, and the research people
want to stay in that area because if you deviate to research in other
directions probably other people come in and must be funded.” (Meditel 1992).
“Virologist
have nothing new to offer. They keep coming up with
excuses, they find constant growth and change in the virus structure, it
evades, attacks, strange things, but none of them has the courage to explain
properly how these things could possibly be so.” (Continuum Jan/Feb 1996)
“AZT
(anti-viral AIDS medicine) has, in countless cases, brought about the
inevitable and slow asphyxiation of the patient's body cells. The doctors
wrongly diagnose the fatal consequences of AZT medication as AIDS following a
prior HIV infection. Treatment with AZT and allied toxic substances may be
equivalent to joining a suicide squad with a time fuse.”
“It
is the duty of every doctor to preserve life at any cost -- and not death-curse
people based on any test so they are so frightened they kill themselves. I am
sad to say that these voodoo methods were practiced despite there never being
any proof that the detected antibodies are an indication of mortality in all
diagnosed people. I consider it medical malpractice to push patients into dying
by prophesying an early death. We are medical scientists, not prophets!”
Did
Dr. Hassig mean here when he said, “The
sentence of death accompanying the medical diagnosis of AIDS should be
abolished,”
that, with increased testing of all pregnant women and more aggressive
treatment regimens with AZT and other antiretrovirals, that AIDS might some day
be abolished? Or is he saying that the
AIDS establishment has mistakenly confused the side effects of AZT and other
antiretroviral treatments with the destruction imagined to be brought on by
“HIV,” before they appreciated that failed anticancer chemotherapy drugs like
AZT could “do all those bad things” to the human body?
20.
Why did Dr. Heinrich Kremer, MD, Medical Director of the Federal Clinics for
Juvenile and Young Adult Drug Offenders for five German counties, including
Berlin, Bremen, and Hamburg, and author of the book, 'The Silent Revolution of
the AIDS- and Cancer-Medicine.' From AIDS: DEATH BY PRESCRIPTION, Continuum, July/Aug. 1996 claim that:
“The
advertising drums are beaten hard all over the world today. The same doctors
are calling for obedient candidates for their experiments and holding out the
same promise of a cure who have poisoned countless
AIDS patients by administering the DNA blocker AZT for the past ten years in an
attempt to hunt down the phantom HIV virus.
“The
same doctors are now trying to conjure up a substance from the test tube under
the magic name of 'protease inhibitor' and to market it as having a limitless
cure potential, although nobody in fact knows what long-term reactions this
molecule, which has never been tested on man, may cause in the living
organism.”
“The
victims and perpetrators have only recently come to realise that AZT (also
known as Zidovudine or Retrovir) has, in countless cases, brought about the
inevitable and slow asphyxiation of the patient's body cells, which are in
particular need of oxygen and hence the equally inevitable death by poisoning
of those persons who are stigmatized as HIV-positive or diagnosed as suffering
from “AIDS” and who trust their doctors. Despite that realization, new test
candidates are already being sought who will be voluntarily prepared, through
fear of death suggested by the medical profession, not only to swallow AZT in
combination with allied toxic substances, but in addition to take an inhibitor
which has an incalculable impact on cell metabolism.”
“A
guarantee of success is secured in advance, as with AZT, because any fatal
'secondary effects' of the mixture are described as an outcome of the phantom
HIV infection. These are the selfsame laboratory doctors and clinical
practitioners who for years abused the confidence of anxious AIDS patients with
the assertion that AZT would reliably, and with total certainty, prevent the
proliferation of their 'phantom' HIV.”
Is Dr. Kramer is saying here that “beating of the advertising
drums” for the use of AZT and HAART, must be non-ceasing, and unabashedly
banged yet ever louder for the use of AZT and now other antiretrovirals?
21.
Why did Dr. Michael Lange, MD, Head of AIDS Programme, St. Lukes Hospital,
New York, claim that:
“We
do not know the pathogenesis of this disease. And we were very early forced
into a very dogmatic view: namely, that somehow HIV kills the T-cells.”
(Spin April 1991).
“I
was very upset…The cause of AIDS was discovered by government fiat...I had been
working with the Pasteur Institute for six months, but then that [Gallo]
announcement was made at the press conference. As far as I’m concerned, from
that point on AIDS research turned into seedy, criminal politics, and it
remained that way.” (Spin, June, 1992).
“I
was far from convinced by the data they had then and I’m still not convinced.
We were all forced into a very dogmatic and simplistic view of what caused
AIDS. Today, I think even the greatest proponents of HIV no longer believe that
it does all that damage to the immune system by itself. There have to be other
factors involved. And because of the HIV hypothesis, there’s been little or no
research done on what those other factors may be.”
(Spin June 1992).
“I
personally do not prescribe AZT unless a patient insists. I have continued to
find that patients survive longer without it.” (Spin, April 1991).
A related issue is why is Dr. Michael Lange, MD, Head of AIDS
Programme, St. Lukes Hospital, New York, being quoted in Spin Magazine,
Continuum, Synapse or other popular magazines, rather than in The New England
Journal of Medicine, Science, Nature, JAMA, or other high profile science or
medical journals? Same question regarding Dr. Hassig, Dr. Kramer, and other
high profile directors involved directly on the front lines of AIDS?
22.
Why did Dr. Donald Abrams, Professor of Medicine, San Francisco General
Hospital, and one of the first AIDS physicians, claim that (Synapse Vol 4,
pages 1 and 5 (1996):
"In contrast with many of my colleagues,
I am not necessarily a cheerleader for anti-retroviral therapy. I have been one
of the people who's questioned, from the beginning,
whether or not we're really making an impact with HIV drugs and, if we are
making an impact, if it's going in the right direction."I have a large
population of people who have chosen not to take any antiretrovirals. They've
watched all of their friends go on the antiviral bandwagon and die, so they've
chose to remain naive [to therapy]. More and more, however, are now succumbing
to pressure that protease inhibitors are 'it.'
We are in the middle of the honeymoon period, and whether or not this is
going to be an enduring marriage is unclear to me at this time."
23.
Why are antiretrovirals called "life-saving" or "life
extending" when a report in The New England Journal of Medicine by The Veterans Affairs Cooperative Study Group reported that:
"AZT disproportionately harmed Blacks and Hispanics, and provided
no benefit to the quelling of advancing immune suppression in Caucasians"
(JD Hamilton et. al. and the Veterans Affairs Cooperative Study Group. A controlled trial of early versus late treatment with zidovudine
in symptomatic human immunodifficiency virus infection" New England
Journal of Medicine, 326: 437-434, 1992)?
24.
Although there were many problems with record keeping, and the Boston Arm of
the trail was supposed to be thrown out, the 1987 Fischl AZT trial won AZT FDA
approval after 4 months when the trial was terminated for "compassionate
reasons." Why are antiretrovirals still called "life-saving" or
"life extending" when there was little, if any difference between the
outcome of either AZT treated versus AZT-untreated groups after 1 year, and,
and despite the fact that The Concorde study (that was much larger, longer, and
better designed trial than The Fischl trial) concluded:
"The
results of Concorde do not encourage the early use of zidovudine in
symptom-free HIV-infected adults. They also call into question the uncritical
use of CD4 cell counts as a surrogate endpoint for assessment of benefit from
long-term antiretroviral therapy" (Seligmann et al.,
Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and
deferred zidovudine in symptom-free HIV infection. Concorde
Coordinating Committee. Lancet, Apr 9;343(8902):871-81,
1994)?
25.
Why are antiretrovirals called "life-saving" and "life
extending" when it has been more than 7 years since it was published in
The Journal, AIDS, that children born to ZDV-treated mothers:
"are
more likely to have a rapid course of HIV-1 infection compared with children
born to untreated mothers, as disease progression and immunological
deterioration are significantly more rapid and the risk of death is actually
increased during the first 3 years of life"
(de Martino et al., Rapid disease progression in HIV-1 perinatally infected
children born to mothers receiving zidovudine monotherapy during pregnancy.
(AIDS. 13 (8): 927-933, May
28, 1999. The Italian Register for HIV
Infection in Children. AIDS, 13:927-933, 1999)?
“Results: Comparison of HIV-1-infected
children whose mothers were treated with ZDV with children whose mothers were
not treated showed that the former group (AZT
group) had a higher probability of developing severe disease [57.3% (95% CI 40.9-74.3) versus 37.2% (95% CI 30.0-45.4);
log-rank test 7.83, P=0.005; adjusted hazard ratio 1.8 (95% CI 1.1-3.1)] or severe immune suppression [53.9% (95% CI 36.3-73.5) versus 37.5% (95% CI 30.0-46.2);
log-rank test 5.58, P=0.018; adjusted hazard ratio 2.4, (95% CI: 1.3-4.3)] and a lower survival [72.2% (95% CI 50.4-85.7) versus 81.0% (95% CI 73.7-86.5); log-rank test
4.23, P=0.039; adjusted hazard ratio of death 1.9 (95% CI 1.1-3.6)]..“
Why did these authors conclude that:
"Findings
may suggest a need to hasten HIV-1 diagnosis in infants of ZDV-treated mothers
and undertake an aggressive antiretroviral therapy in those found to be
infected."
Were these claims plagued with
typographical errors? Shouldn't the report have read:
"Children
born to ZDV-treated mothers are more likely to have a slow course of HIV-1 infection compared with children born
to untreated mothers, as disease progression and immunological deterioration
are significantly more reduced
and the risk of death is actually decreased
during the first 3 years of life,”
and not:
“Children born to ZDV-treated mothers “are
more likely to have a rapid course of HIV-1 infection compared with
children born to untreated mothers, as disease progression and
immunological deterioration are
significantly more rapid and the risk of death is actually increased during the first 3
years of life?”
26.Why
are antiretrovirals called "life-saving" and "life
extending" when it has come to National attention that research directors
such as Edmond Tramont, who was/is still the government's chief of AIDS
research, rewrite safety reports on a U.S.-funded drug studies of nevirapine
(the controversial HIVNET 012 clinical trial) to change its conclusions and
delete negative information, and later order that research resumed over the
objections of his staff and trial safety officer, Jonathan Fishbein, who was
fired because he blew the whistle on this dangerous study, and even after the company withdrew its trial in the U.S.
because of reports of excessive toxicity? How often do AIDS
researcher change scientific data to conform to political or financial
pressures?
27.
Why are antiretrovirals called life-saving when Lockman et al. with Max Essex
just reported last month (1/2007) in the New England Journal of Medicine that
nevirapine increased drug resistant "HIV" progression to AIDS over
controls by 41.7 % in women
(euphemistically called virological failure or drug resistant "HIV"),
and that a single dose of nevirapine (one each to mother and infant) as
compared with placebo, was associated with significantly
higher rates of virologic failure and
smaller CD4+percentage increases in response to subsequent nevirapine-based
antiretroviral treatment?"
“Nevirapine
remains central to the prevention of mother-to-child transmission of human
immunodeficiency virus type 1 (HIV-1) and to combination antiretroviral
treatment throughout much of the developing world. Nevirapine administered as
one dose to the mother and one to the newborn reduces mother-to-child
transmission of HIV-1 by 41 to 47%, and well over 875,000 women and infants have received a single dose of
nevirapine. A single dose of nevirapine is the cornerstone of the regimen
recommended by the World Health Organization (WHO) to prevent mother-to-child
transmission among women without access to antiretroviral treatment and among
those not meeting treatment criteria.
However, nevirapine resistance is detected (with the use of standard genotyping
techniques) in 20 to 69% of women and 33 to 87% of infants after exposure to a
single, peripartum dose of nevirapine.
Among 60 women starting antiretroviral treatment within 6 months after
receiving placebo or a single dose of nevirapine, no women in the placebo group
and 41.7% in the nevirapine group had virologic failure (P<0.001). Women
who had received a single dose of nevirapine had significantly higher rates of
virologic failure on subsequent nevirapine-based antiretroviral treatment than
did women who had received placebo. This apparently deleterious effect of a
single dose of nevirapine was concentrated in women who initiated
antiretroviral treatment within 6 months after receiving a single dose of
nevirapine…Among the 30 HIV-infected
infants, a single dose of nevirapine (one each to mother and infant) as
compared with placebo was associated with significantly higher rates of
virologic failure and smaller CD4+percentage increases in response to
subsequent nevirapine-based antiretroviral treatment”
(Lockman S. et al., Response to
Antiretroviral Therapy after a Single, Peripartum Dose of Nevirapine. The New
England Journal of Medicine 356 january 11, 2007).
A related question is, if "HIV" has 10 genes that are
essential for its pathogenicity, and if it is constantly mutating any
nucleotide comprising any of these 10 genes, how does "HIV" maintain
its biological identity or its pathogenicity?
28.
Why are antiretrovirals called "life-saving" or "life
extending" when it was published in The Journal of Virology that severe
toxicity of saquinovir and other protease inhibitors are frequently observed in
patients receiving this class of drugs (Estaquier et al., Effects of
Antiretroviral Drugs on Human Immunodeficiency Virus Type 1-Induced CD4+ T-Cell
Death Journal of Virology, June, p. 5966-5973, Vol. 76, No. 12, 2002)?
29.
Why are antiretrovirals called "life-saving" or "life
extending" when Mark Harrington, a member of The Treatment Action Group
(TAG-a radical group in favor of drugging everybody with antiretrovirals) summoned
"the power of prayer" over
"HIV" mutability, and discussed "The Chinese Menu Approach" in a description of a meeting he
attended on developments regarding anti-retrovirals that included AIDS leaders
such as Marc Wainberg, Director, McGill AIDS Centre,
and this summer's Chair of The Toronto International AIDS Conference-who
possesses several "HIV" drug patents such as lamivudine (3TC), and
grants from GlaxoSmithKlein, Bristol-Myers Squibb and Boehringer-Ingelheim.
Also present at the meeting was Emilio Emini, Tufts
University's John Coffin, Roche's Noel Roberts, the CDC's Harold Jaffe,
Chiron's David Chernoff, the ACTG's Robert ("Chip") Schooley and John
Mellors (developer and champion of the viral load tests now known to be
invalid), as well as treatment activist Dawn Averitt-Doherty of Atlanta-based
Woman's Information Service and Exchange (WISE)?
"During the coffee break, I (Harrington) joined three
activists outside to share nicotine and despair. What was the point of quitting
smoking if we were still all passengers on the speeding train heading for the
cliff? The Birmingham resistance data were wrenching. Our fears of
multiple cross-resistance, from November 1995's 3TC
and saquinavir FDA approval hearings, reared their ugly heads. Several months of
post-Vancouver euphoria crumbled in a moment as it became clear that many of
those who developed resistance to ritonavir and indirovine-as thousands clearly
would-might have no protease inhibiting options ahead of them. Today's
resistance news made for a toxic cocktail. As I left the auditorium I bumped
into Emilio Emini."
"Harrington: So what do you do if you fail Crixivan?"
"Emini: [sighs] We don't know what
to do."
"Harrington: Take two new nucleosides and nevirapine?"
"Emini:
Yeah. And pray."
"No
one had yet assessed the healing effects of prayer on viral load. This was what
we'd come to. I rushed into the lobby of the Interior Department and ran into a
colleague, who was wild with fear and disappointment."
"Sometimes the gap between how the researchers felt and how
we felt became an abyss. They were excited about the endless possibilities
opened up by the research advances of 1996; we were terrified about the limited
treatment options facing people who had exhausted most of the current arsenal
of antiretroviral therapy. What to do with those whose viral load refused to go
undetectable? What to do with those who added a protease inhibitor to a failing
two-drug regimen and appeared doomed to develop resistance, most of
it-especially with ritonavir and indinovir-cross-resistant to all other
protease inhibitors? What to do with those who jumped aboard last year's
bandwagon, AZT+3TC, and now appeared likely to have developed 3TC resistance
and, with it, cross-resistance to ddI, ddC and possibly 1592? The Chinese menu approach to antiretroviral
treatment suddenly looked much less appetizing, and
much less nourishing" (TAGline/Volume
4 Issue 2 February 1997).
30.
Why are antiretrovirals called "life-saving" or "life
extending" when a registry has been established to monitor adverse fetal
outcomes born to women exposed to the AIDS drug, efavirenz" (FDAMedWatch 6/10/2005)?
31.
Why are antiretrovirals called "life-saving" and "life
extending" when Olivero OA et al., in “3'-azido-3'-deoxythymidine (AZT)
transplacental perfusion kinetics and DNA incorporation in normal human
placentas perfused with AZT” (Mutat Res Fundam Mol Mech Mutagen. Jul 16;428(1-2):41-7, 1999),
reported that:
“Incorporation
of ZDV into DNA was detected in most of the samples from ZDV-exposed adults and
infants. Therefore, the biologic significance of ZDV-DNA damage and potential
subsequent events, such as mutagenicity, should be further investigated in
large cohorts of HIV-positive individuals?”
32.
Why are antiretrovirals called "life-saving" and "life
extending" when Lallemant et al., in an article entitled, "A trial of
shortened zidovudine regimens to prevent mother-to- child transmission of human
immunodeficiency virus type 1" (NEJM. 2000 Oct 5;343(14):982-91) reported
that:
“[Table
3 shows that congenital abnormalities occurred in 7% of infants when both
mother and child had the long course of AZT (long-long), and only 1% when both
had the short course (short-short). Neutropenia and leukopenia occurred in 7%
of infants on the long-long course and 2% on short-short. Infections or other
HIV-related events occurred in 43% on long-long and 33% on short-short.
Neonatal or other obstetrical events occurred in 22% on long-long and only 14%
on short-short. Number of deaths, severe anemia were similar (although severe
anemia occurred significantly less (0%/1%) in the long-short and short-long
treatment arms). Mothers who received the long AZT treatment had a higher rate
of stillbirth (8% vs. 4%), severe anemia (7% vs 4%), infection or other HIV
events (20% vs 17%), events related to pregnancy or delivery (24% vs 17%) than
mothers who received the short course, although fewer died" (3% vs 8%)?
33.
Why are antiretrovirals called "life-saving" and "life
extending" when Kuhn L et al. in "Disease Progression and Early Viral
Dynamics in Human Immunodeficiency Virus Infected Children Exposed to
Zidovudine during Prenatal and Perinatal Periods" (Journal of Infectious
Diseases, 2000 July;182:104-11) reported that:
“In
a multicenter observational cohort study of 325 HIV-infected children born
during 1986-1997, clinical progression was compared among infected children
exposed or unexposed to Zdv [AZT] during prenatal and perinatal periods. Zdv
exposure was associated with 1.8-fold (95% confidence interval, 1.02-3.11)
increased risk of progressing to AIDS or death after adjusting for year of
birth, maternal CD4 cell count, maternal AIDS diagnosis, and subsequent
antiretroviral therapy of the child. Mean
log10 viral copies at 712 weeks were higher among Zdv-exposed children"
(P = .004)?
34.
Why are antiretrovirals called "life-saving" and "life
extending" when Newschaffer et al. in “Prenatal Zidovudine Use and
Congenital Anomalies in a Medicaid Population. JAIDS.
2000 Jul 1;24(3):249-256) reported that:
“Children
of study women who were prescribed ZDV [AZT] had increased adjusted odds of any
anomaly (adjusted odds ratio [OR], 1.55; 95% CI, 1.01-2.29) [i.e. more than
one-and-one-half times the risk of a birth anomaly than the HIV+ population
being studied in general"]?
35.
Why are antiretrovirals called "life-saving" and "life
extending" when de Souza RS et al., in an article entitled, "Effect
of prenatal zidovudine on disease progression in perinatally HIV-1-infected
infants" ( JAIDS. 2000 Jun 1;24(2):154-161) reported that:
“After adjusting for prematurity and maternal
clinical characteristics, RPD [rapid disease progression] was three times more likely to occur in infants born to [mothers]
treated [with AZT] compared with findings in untreated mothers" (RR=2.8; p
= .021)?
36.
Why are antiretrovirals called "life-saving" and "life
extending" when Kumar et al., in “Zidovudine Use in Pregnancy: A Report on
104 Cases and the Occurrence of Birth Defects” (JAIDS.;7:1034-9, 1994) reported that:
“In
reviewing the frequency of birth defects in this population [of HIV+ women
taking AZT during pregnancy] we noted eight birth defects (10%) out of 80 live
births?”
These
included:
1. Two male infants with the "minor abnormalities" of
"low-set ears, retrognathia [a mis-aligned jaw], prominent epicanthal
folds [i.e., unexpected skin flaps above the eye, which can be a sign of mental
retardation], hirsutism [abnormal hairiness], triangular facies with blue
sclera [a triangular-shaped face with abnormally blue eyes], hyperpigmented
skin macules, and prominent sacral dimple [a pronounced indentation at the
bottom of the spinal cord]."
2. A female infant was born with extra fingers on both hands (the
report doesn't say how many "extra digits" grew on each hand).
"There was no similar family history," Kumar and co-workers noted.
3. One child was diagnosed as having "fetal alcohol
syndrome," although there was no evidence that the mother consumed
alcohol.
4. A male infant was born with a serious congenital heart defect
("asymptomatic atrial septal defect") and "pectus
excavaatum," a depression or actual hole in the chest. This child died at
the age of five months.
5. A male infant was born with an abnormally small brain
(microencephaly) and chorioretinitis (a condition that rapidly results in
blindness, due to lesions on the retina).
6. Another male infant was born with the same type of hole in his
chest as the previously described child ("pectus excavatum").
7. A female was born with albinism (no pigmentation) and
congenital ptosis, a condition in which the upper eyelid droops uncontrollably
(which interferes with eyesight) because of nerve damage.
37.
Why are antiretrovirals called "life-saving" and "life
extending" when Panther et al. published a paper entitled, "Genital
tract human immunodeficiency virus type 1 (HIV-1) shedding and inflammation and
HIV-1 env diversity in perinatal HIV-1 transmission"
( Journal of Infectious
Diseases 2000 Feb;181:555-63) claiming
that:
“All women [in this study] received oral
zidovudine [AZT] prior to delivery and/or intravenous zidovudine at
delivery...Of 42 subjects...24 had a CVL [cervicovaginal lavage] taken...Of
these 24 women, 7 transmitted HIV-1 to their infants and 17 did not...In the
CVL samples, 41% yielded culturable HIV-1, 67% were PCR positive for proviral
HIV-1 DNA, 30% were positive for cell-free HIV-1 RNA and 45% were positive for
cell-associated HIV-1 RNA. Peripheral
CD4 cell counts did not correlate with levels of HIV-1 in the CVL by DNA or RNA
PCR or by amount of genital tract inflammation...Although all subjects in
our study received zidovudine therapy in the third trimester, the high rate
(29%) of HIV-1 perinatal transmission in this data set does not agree with the
largest prospective, randomized study addressing this question, ACTG 076 [in
fact, this rate is higher than the transmission rate in the placebo arm of ACTG
076]?”
38.
Why are antiretrovirals called "life-saving" and "life
extending" when Smith et al. in, "Timing of perinatal human immunodeficiency
virus type 1 infection and rate of neurodevelopment" (Pediatr Infect Dis
J. 2000;19:862-71) reported that:
“Infants
with early positive HIV-1 cultures demonstrated a notable decrement in neurodevelopmental functioning within the
first 30 months of life. They achieved motor developmental scores that were
increasingly and significantly discrepant [worse]
both from the average and from scores achieved by late HIV-1-positive children
over the course of the study period. Those children with early HIV-1-positive
cultures also demonstrated a trend toward a similar decline in mental
functioning over time...The mothers of infants with early [HIV] positive
cultures were more likely to receive ZDV [AZT] treatment during pregnancy, and
their infants were more likely to receive ZDV treatment prophylactically during
the first 6 weeks of life...Because antiretroviral therapy has been shown to
improve neurodevelopmental function in children whose CNS has been affected by
the HIV-1 virus...Infants with early HIV-1 culture positivity should be treated
with multiple drugs with well-established CNS penetration to reduce the
likelihood that resistance will develop in the CNS compartment?"
Why did the authors of this study, for some reason, ignore the
fact that early positive HIV-1 cultures equate with infants who have been on
AZT the longest, and advance the idea that hitting the infants aggressively
with multiple drugs will block "HIV's" destruction of brain tissue.
Why do they conclude this?
39.
Why are antiretrovirals called "life-saving" and "life
extending" when Blanche et al. in "Persistent mitochondrial
dysfunction and perinatal exposure to antiretroviral nucleoside
analogues," (Lancet, 1999 Sep 25) conclude that:
“We analysed observations of a trial of
tolerance of combined zidovudine [AZT] and lamivudine and preliminary results
of a continuing retrospective analysis of clinical and biological symptoms of
mitochondrial dysfunction in children born to HIV-1-infected women in France....Findings: Eight children had mitochondrial
dysfunction. Five, of whom two died,
presented with delayed neurological symptoms and three were symptom-free but
had severe biological or neurological abnormalities. Four of these children
had been exposed to combined zidovudine and lamivudine, and four to zidovudine
alone. No child was infected with
HIV-1..."
" Our
findings support the hypothesis of a link between mitochondrial dysfunction and
the perinatal administration of prophylactic nucleoside analogues. Current
recommendations for zidovudine monotherapy should however be maintained[!].
Further assessment of the toxic effects of these drugs is required!”
40.
Why are antiretrovirals called "life-saving" and "life
extending" when Neenyah Ostrom (07/12/2000) reviewed the Blanche
study in the following way:
"The
French study, led by Stephane Blanche at the Necker Hospital in Paris, was published in The Lancet. Of 1,754
mother-child pairs exposed to AZT during the mother's pregnancy (or just after
birth, for the child), Blanche and colleagues discovered eight children whose
mitochondria didn't function properly. The mitochondria are our cells' energy
producing organelles; if they malfunction, neurological development is delayed,
and the result can be fatal. Four of the children with mitochondrial
dysfunction had been exposed to a combination of AZT and another anti-HIV drug,
lamivudine; the other four had been exposed to AZT alone. "No child was infected with HIV-1," Blanche and
co-workers pointed out."
"Five
of the eight children developed "delayed" neurological symptoms
(meaning they weren't present at birth, but became obvious later); two of these
children died. The other three children "were symptom-free but had severe
biological or neurological abnormalities," according to the French scientists."
"One
of the two children with neurological symptoms who
died, Patient A, was partially blind. When Patient A was 4 months old, an MRI
showed that the child had demyelinating lesions in the brainstem (a primitive
part of the brain that controls basic life functions). Over time, these lesions
-- which were really just areas of dead brain tissue -- spread throughout the
child's brain. Patient A's growth was "abnormal," according to the
doctors, and the child vomited frequently. At 13 months of age, Patient A died
from heart and lung disorders."
"Patient
B died at the age of 11 months. At 4 months old, Patient B developed epilepsy
as well as suffering severe deterioration of cognitive and motor abilities.
This child, too, was found to have "diffuse demyelinating lesions
associated with massive cortical necrosis," that is, widespread brain
tissue death."
"The
other children who developed symptoms of mitochondrial dysfunction had
seizures, heart dysfunction, brain lesions (one child with, and one without,
brain tissue death), blindness associated with a too-small head
("microencephaly" a problem identified earlier in babies treated in
utero with AZT), and numerous biochemical abnormalities (including abnormal
liver and pancreatic enzyme levels, among others).
"In
their discussion of how AZT probably contributed to the illness and deaths of
these children, Blanche and colleagues noted that researchers at the US
National Cancer Institute have demonstrated that AZT crosses the placenta from
mother to fetus. In monkey fetuses, AZT is incorporated into the mitochondrial
DNA. Fetal monkeys dosed with AZT for periods of time and with doses similar to
those used for pregnant women developed mitochondrial dysfunction after birth,
Blanche and co-workers pointed out. They added, 'The experimental [monkey]
model does not show whether the toxic effects are reversible after birth. Also,
it gives no insight into the possible clinical impact of this type of
dysfunction throughout a tissue, especially a long time after the drug is
stopped…. As with other drug-induced toxic effects in mitochondria, these
lasting abnormalities may be associated with a symptomless constitutional
dysfunction.' In other words: Many more children exposed to AZT in utero may
have mutations in their mitochondria that we don't detect because they don't
immediately produce identifiable symptoms. The type of mitochondrial illness
observed in these eight children (out of 1,754 French children treated with
AZT) was found in only 21 children out of 12 million studied in the United Kingdom."
"We
are aware that the suggestion that antiretroviral drugs are toxic raises
delicate issues," the French scientists wrote, concluding that "the current recommendations for
zidovudine [AZT] monotherapy prophylaxis should be maintained." They
added, however, "Pregnant women should be informed of the potential
effects associated with these treatments during pregnancy."
41. Why are antiretrovirals
called "life-saving" and "life extending" when The UK's
Committee on Safety of Medicines in Perinatal AZT: New warning on potential
risk to infants. www.aidsmap.com. 1999 Jul 21, http://www.aidsmap.com/namsearch.htm/news/07jul99/story6.htm
issued a warning to doctors about the risk of mitochondrial dysfunction in
infants born to HIV infected mothers treated with zidovudine (AZT) to prevent
vertical transmission."
The warning came in advance of the publication of data from a
French study in which it was discovered that 8 out of approximately 200 infants
developed mitochondrial dysfunction following exposure to zidovudine, with or
without 3TC treatment, for the prevention of vertical transmission of HIV
infection.
42.
Why are antiretrovirals called "life-saving" and "life
extending" when Olivero et al. in an article entitled,
"3'-azido-3'-deoxythymidine (AZT) transplacental perfusion kinetics and
DNA incorporation in normal human placentas perfused with AZT" ( Mutat Res
Fundam Mol Mech Mutagen. 1999 Jul 16;428(1-2):41-7) reported that:
“The
data show that AZT crosses the human placenta and becomes rapidly incorporated
into DNA of placental tissue in a dose-dependent fashion, suggesting that even
short exposures to this drug might induce fetal genotoxicity and might also
inhibit maternal-fetal viral transmission?”
43.
Why are antiretrovirals called "life-saving" and "life
extending" when Olivero OA et al., in a presentation entitled,
"3'-azido-3'-deoxythymidine (AZT) transplacental perfusion kinetics and
DNA incorporation in normal human placentas perfused with AZT” (Third
Conference on Environmental Mutagens in Human Populations. 1999 Feb 18) claimed
that:
“transplacental exposure studies demonstrated that AZT is a
moderate to strong transplacental carcinogen in mice...Since AZT-DNA
incorporation in human placenta occurs rapidly by 2 hr of AZT perfusion,
infants exposed to AZT even for short periods of time during gestation may
sustain genotoxic damage. In previous studies AZT has been shown to produce both,
large scale DNA damage and point mutations...the consequences of any fetal
exposure to a nucleoside analog, in utero, remain unknown”
44.
Why are antiretrovirals called "life-saving" and "life
extending" when an article in Reuters. (1999 Feb 2) stated that HIV drugs
may show adverse effects in babies:
“…these
two [HIV+ babies taking AZT+3TC] died of an extremely rare disease caused by
genetic damage to the mitochondrial DNA - which is found in the cell body
rather than in the nucleus with the genes. One died at 11 months and one died
at 13 months, both from severe brain damage. Blanche [of the French medical
research institute INSERM] told the meeting that there was no proof the drugs
caused the damage. But he said there was also no evidence the babies had
inherited abnormalities, and HIV drugs are known to cause mitochondrial
damage.”
45.
Why are antiretrovirals called "life-saving" and "life
extending" when Bennett and Foster concluded in an article entitled,
"Mandatory testing of pregnant women and newborns: a necessary evil? Realistic alternatives to breastfeeding in the HIV/AIDS era.
(AIDS Information Exchange. 1998) reported that:
“At
present, data regarding the effects of ZDV use on vertical transmission rates
are inconclusive and incomplete. In addition, the long-term effects of ZDV use
during pregnancy and after birth on the woman and any resulting child are yet
to be discovered…the possibility has not yet been ruled out that this
‘risk-reducing’ measure may not be effective and may prove detrimental to the
health of both mother and child.”
46.
Why are antiretrovirals called "life-saving" and "life
extending" when Lorenzi et al. wrote an article entitled,
"Antiretroviral therapies in pregnancy: maternal fetal and neonatal
effects" (AIDS.
1998;12:F241-247) which concluded that:
"In
HIV-infected pregnant women treated with two RTI [nucleoside analogs, of which
AZT was the most common] with or without protease inhibitors, one or more
adverse events occurred in 29 out of 37
women and in 14 out of 30 babies.”
47.
Why are antiretrovirals called "life-saving" and "life
extending" when Patterson et al. in an article entitled, "Transplacental pharmacokinetics
and fetal distribution of azidothymidine, its glucoronide, and phosphorylated
metabolites in late-term rhesus macaques after maternal infusion" (Drug Metab Dispos. 1997;25(4):453-459)
reported that:
“The
authors selected six patients who were HIV positive and who had requested
termination of pregnancy to study the passage of zidovudine through the
placenta...1 gram of zidovudine [AZT] was given in five doses of 200 mg each
orally...At a mean age of 17.5 weeks [into the pregnancy], samples were taken
from the mothers’ blood, from the amniotic fluid and from the fetal blood...The
concentrations of [AZT] in the [amniotic fluid] and in the fetal blood were
higher or equaled those found in the maternal blood...The drug remains
contra-indicated in pregnancy.”
48.
Why are antiretrovirals called "life-saving" and "life
extending" when McKinney et al., in an article entitled, "A multicenter trial of oral zidovudine
in children with advanced human immunodeficiency virus disease" (NEJM.
1991 Apr 11;324(15):1018-25) reported that:
“Children treated with zidovudine continued to
have bacterial and opportunistic infections. The effect of the drug on the
frequency of these events could not be assessed because of the lack of control
groups...One or more episodes of hematologic toxicity occurred in 54 children
(61 percent)anemia (hemoglobin level, <75g per liter)
in 23 children (26 percent) and neutropenia (neutrophil count, <0.75X10^9
per liter) in 42 (48 percent).
49.
Why are antiretrovirals called "life-saving" and "life
extending" when Gerschenson et al., in an article entitled, "Fetal mitochondrial heart and skeletal
muscle damage in Erythrocebus patas monkeys exposed in utero to
3'-azido-3'-deoxythymidine" (AIDS Res Hum Retroviruses. 2000 May
1;16(7):645-44) reported that:
“3'-azido-3'-deoxythymidine
(AZT) is given to pregnant women positive for the human immunodeficiency virus
type 1 (HIV-1) to reduce maternal-fetal viral transmission. To explore fetal
mitochondrial consequences of this exposure, pregnant Erythrocebus patas
monkeys were given daily doses of 1.5 mg (21% of the human daily dose) and 6.0 mg
(86% of the human daily dose) of AZT/kg body weight (bw),
for the second half of gestation. At
term, electron microscopy of fetal cardiac and skeletal muscle showed abnormal
and disrupted sarcomeres with myofibrillar loss. Some abnormally shaped
mitochondria with disrupted cristae were observed in skeletal muscle myocytes.
Oxidative phosphorylation (OXPHOS) enzyme assays showed dose-dependent
alterations. At the human-equivalent dose of AZT (6 mg of AZT/kg bw), there was
an approximately 85% decrease in the specific activity of NADH dehydrogenase
(complex I) and three- to sixfold increases in specific activities of succinate
dehydrogenase (complex II) and cytochrome-c oxidase (complex IV). Furthermore,
a dose-dependent depletion of mitochondrial DNA levels was observed in both
tissues. The data demonstrate that transplacental AZT exposure causes cardiac
and skeletal muscle mitochondrial myopathy in the patas monkey fetus.”
50.
Why are antiretrovirals called "life-saving" and "life
extending" when Ha et al., in an article entitled, "Fetal, infant, and maternal
toxicity of zidovudine (azidothymidine) administered throughout pregnancy in
Macaca nemestrina," (JAIDS, 1998 May 1;18(1):27-38) reported a study
showing that:
“The
AZT animals [Macaques given AZT during pregnancy] developed an asymptomatic
macrocytic anemia, but hematologic parameters returned to normal when AZT was
discontinued. Total leukocyte count decreased during pregnancy and was further
affected by AZT administration. AZT-exposed infants were mildly anemic at
birth. AZT caused deficits in growth,
rooting and snouting reflexes, and the ability to fixate and follow near
stimuli visually?”
51.
Why are antiretrovirals called "life-saving" and "life
extending" when Diwan et al., in "Transplacental carcinogenicity of
3'-azido-3'-deoxythmidine (AZT) in mice” (Proc Am Assoc Cancer Res. 1998;39:21) reported that:
“CD-1
mice exposed prenatally to 12.5 and 25.0 mg of AZT...had statistically significant increases in numbers of liver, lung and
female reproductive tract tumors. These observations have been extended to
offspring at 2 years of age...there was a 2- to 3-fold increase in the
incidence (from 20% in controls to 55-60% in AZT groups) and
multiplicities of lung tumors in AZT-exposed mice. The incidence of hepatocellular adenomas in the female mice exposed to
prenatal AZT increase from 0 in the control group to 20% in the high dose AZT
group, and hepatocellular carcinomas mestastasizing to lungs were observed only
in AZT-treated mice. Prenatal administration of AZT also increased the
incidence of neoplasms of reproductive tract, female mammary gland epithelium
and squamous cell epithelium of forestomach. AZT...significantly reduced the
incidence of hematopoietic tumors?”
52.
Why are antiretrovirals called "life-saving" and "life
extending" when Olivero OA et al., in "Transplacental effects of
3'-azido-2',3'-dideoxythymidine (AZT): tumorigenicity in mice and genotoxicity
in mice and monkeys" (J Natl Cancer Inst. 1997 Nov 5;89(21):1602-8)
reported that:
“At
1 year of age, the offspring of AZT-treated mice exhibited statistically
significant, dose-dependent increases in tumor incidence and tumor multiplicity
in the lungs, liver, and female reproductive organs...AZT is
genotoxic in fetal mice and monkeys and is a moderately strong transplacental
carcinogen in mice examined at 1 year of age?”
53.
Why are antiretrovirals called "life-saving" and "life
extending" when Olivero OA et al., in "AZT is a Genotoxic
Transplacental Carcinogen in Animal Models" (JAIDS. 1997 Apr 1;14(4):A29) reported that:.
“…in
adult mice, lifetime AZT administration induces vaginal tumors at a 10-20% incidence...In newborn monkeys
and mice, AZT was incorporated into DNA of many fetal tissues...AZT appears to
be a moderately-strong transplacental carcinogen [i.e. it crosses the
placenta and may cause cancer in the fetus]?”
54.
Why are antiretrovirals called "life-saving" and "life
extending" when Ha et al., in "Fetal toxicity of zidovudine
(azidothymidine) in Macaca nemestrina: preliminary observations" (JAIDS.
1994;7(2):154-7) reported that:
“Hemoglobin
dropped significantly in the AZT-treated animals [Macaques] after treatment
began and remained low until the end of the study...Postnatal weight increase
was significantly lower in AZT-exposed infants...Infant hematocrits taken at
time of birth were lower in the AZT-exposed group...AZT-exposed infants took
three times as many sessions as controls to meet criterion on Black-White
Learning, a simple discrimination task...It took significantly more matings to
achieve the six AZT pregnancies than the six control pregnancies?”
55.
Why are antiretrovirals called "life-saving" and "life
extending" when Olivero OA et al., in "Vaginal epithelial DNA damage
and expression of preneoplastic markers in mice during chronic dosing with
tumorigenic levels of 3'-azido-2',3'-dideoxythymidine (AZT)" (Cancer Res.
1994;54:6235-42) reported that:
“we have found positive correlations between the dose of AZT
administered to female CD-1 mice, the incorporation of AZT into vaginal DNA,
the hyperproliferation of the vaginal epithelial basal layer, and the aberrant
expression of alpha-6 integrin toward the epithelial suprabasal strata of the
vagina, a target organ for carcinogenesis in mice. These results suggest that
there is an ordered progression of abnormal events leading to tumorigenesis in
vaginal epithelial tissues?”
56.
Why are antiretrovirals called "life-saving" and "life
extending" when Toltzis et al., in "Zidovudine-associated embryonic
toxicity in mice" (Journal of Infectious Diseases, 1991;163:1212-8)
reported that:.
“Mice
receiving AZT during gestation yielded fewer fetuses…and greater numbers of
resorptions…Exposure to AZT was highly correlated with failure to develop to
the blastocyst stage…These data indicate that AZT has a direct toxic effect on
the developing mouse embryo?”
57.
Why are antiretrovirals called "life-saving" and "life
extending" when Mansuri et al., in "Comparison of In Vitro Biological
Properties and Mouse Toxicities of Three Thymidine Analogs Active against Human
Immunodeficiency Virus" (Antimicrobial Agents and Chemotherapy.
1990;34(4):637-641) reported:
“[in
mice] AZT had a profound effect on the number of erythrocytes [mature red blood
cells] and a small effect on the number of leukocytes [white blood
cells]…anemia was seen in all the
mice tested at 1,000 mg/kg per day?”
58.
Why are antiretrovirals called "life-saving" and "life
extending" when Zietz et al., in "An unusual cluster of cases of
Castleman's disease during highly active antiretroviral therapy for AIDS" (NEJM. 1999
Jun 17;340:1923-4) reported:
"Recently,
we observed an unusual cluster of cases of rapidly progressing multicentric
Castleman's disease. Fever, weakness, generalized enlargement of lymph nodes,
and marked polyclonal gammopathy developed in three patients with AIDS...Two of
these patients died within one week after the diagnosis, with generalized
involvement of the lymphatic system, liver, and bone marrow at autopsy. A
fourth patient with AIDS who died equally rapidly after the diagnosis of
multicentric Castleman's disease had been seen in our hospital 14 months
earlier... symptoms of multicentric
Castleman’s disease started after the initiation of highly active
antiretroviral therapy in these three patients?”
59.
Why are antiretrovirals called "life-saving" and "life
extending" when Sussman et al., in a presentation entitled, "Mutagenicity
of AZT in the human lymphoblastoid cell line, TK6" (2nd National AIDS
Malignancy Conference 1998) reported:
“Perinatal
treatment with 3'-azido-3'-deoxythymidine (AZT) has been found to reduce the
rate of maternal-infant transmission of HIV; however, AZT is clastogenic at
therapeutic doses in adult patients and induces cancers in the offspring of
mice treated in utero. The purpose of the present study was to investigate the
mutagenicity of AZT at the hypoxanthine-guanine phosphoribosyltransferase
(hprt) locus of the human lymphoblastoid cell line, TK6, following in vitro
exposures. ..There was a significant increase over background in hprt Mfs
[mutation frequencies] in TK6 cells exposed to 300mM AZT for 3 days (1.8-fold
increase). In cells exposed for 6 days, there was a decrease in...cell survival. These
preliminary results indicate that AZT treatment is mutagenic and produces large
deletions in human cells?”
60.
Why are antiretrovirals called "life-saving" and "life
extending" when Agarwal et al., in "Genotoxicity and mitochondrial
damage in human lymphocytic cells chronically exposed to
3'-azido-2',3'-dideoxythymidine" (Mutat Res. 1997 May 23;390(3):223-231)
reported that:
“AZT … induces significant toxic effects in
humans exposed to therapeutic doses...Cytogenetic observations on H9-AZT cells
showed an increase in chromosomal aberrations and nuclear fragmentation when
compared with unexposed H9 cells...The toxicities explored here suggest that
the mechanisms of AZT induced cytotoxicity in bone marrow of the patients
chronically exposed to the drug in vivo may involve both chromosomal and
mitochondrial DNA damage?”
61.
Why are antiretrovirals called "life-saving" and "life
extending" when Lewis W. Dalakas in "Mitochondrial toxicity of
antiviral drugs" (Nat Med. 1995 May;1(5):417-22)
claimed that:
“Clinical
manifestations of ANA [Antiviral Nucleoside Analogs, such as AZT] toxicity: It
is self-evident that ANAs, like all drugs, have side-effects. However, the
prevalent and at times serious ANA mitochondrial toxic side-effects are
particularly broad ranging with respect to their tissue target and mechanisms
of toxicity: … Haematalogical toxicity [anemia, and other
blood disorders] … Myopathy [muscle disorders] … Cardiotoxicity [heart
disorders] … Hepatic toxicity [liver disorders] … Peripheral neuropathy [nerve
damage]?”
62.
Why are antiretrovirals called "life-saving" and "life
extending" when an article appearing in Neurology (1994;44:1982-1900)
suggested that:
“among
the subjects with CD4+ [immune system] cell counts < 200/mm3, the risk of developing HIV dementia among
those reporting any antiretroviral use (AZT, ddI, ddC, or d4T) was 97% higher
than among those not using this antiretroviral therapy...In addition, the
findings of our analysis seem to confirm previous observation of a neurotoxic
effect of antiretroviral agents.”
63.
Why are antiretrovirals called "life-saving" and "life
extending" when Fischl MA et al. in "Prolonged zidovudine therapy in
patients with AIDS and advanced AIDS-related complex" (JAMA. 1989;262(17):2405-10) in a
follow-up study to the 1987 study which ushered AZT through FDA approval concluded:
“58% of all subjects with AIDS and
AIDS-related complex receiving zidovudine experienced granulocytopenia of grade
3 or higher...Serious anemia occurred in 32%
of all subjects receiving zidovudine...and could be typically managed by dose
attenuation, temporary dose interruption of zidovudine therapy and/or red blood
cell transfusions...12% of subjects...had an episode of thrombocytopenia [low
platelet count] after the initiation of zidovudine therapy...Ten patients had
liver enzyme levels elevated...and were managed with dose attenuations or
interruptions of zidovudine therapy...One report of a grand mal seizure, two
events associated with cardiac dysfunction, and five reports of myopathy were
the only new serious potentially drug-related adverse events reported during
extended periods of zidovudine administration?”
64.
Why are antiretrovirals called "life-saving" and "life
extending" when Dournon et al., in "Effects of zidovudine in 365
consecutive patients with AIDS or AIDS-related complex" (Lancet. 1988 Dec 3;2:1297-1302)
concluded that:
“AZT
was started at full dose in 260 patients, 64 with ARC and 196 with AIDS. In 58
of these patients, AZT had to be stopped at least once for a minimum of 7 days.
In 142 other patients, dosage was reduced by half because of leucopenia (79),
leucopenia and anaemia (32), anaemia (20), rash (3), vomiting (3), headaches
and insomnia (2), myalgia (2), or hepatitis (1). 3 patients reduced the dose
with no medical reason. Later on, progression of toxicity led to suspension of
AZT (for at least 7 days) in 85 of the 142 patients whose treatment had been
reduced to half dose. Thus AZT was stopped at least once in 143 (55%) patients
who began the full-dose regimen. Because of their initial haematological status
105 (28.8%) patients were treated from the start with half-dose AZT - toxicity
led to cessation of treatment in 71 (67.6%) cases?”
65.
Why are antiretrovirals called "life-saving" and "life
extending" when Mocroft A et al., in "Anaemia is an independent
predictive marker for clinical prognosis of HIV-infected patients from across Europe"
(AIDS. 1999;13:943-50) reported:
“We
found that 78.2% of the patients
with mild or severe anaemia at baseline had received zidovudine [AZT]”
66.
Why are antiretrovirals called "life-saving" and "life
extending" when Hymes et al., in "The Effect of Azidothymidine on
HIV-related Thrombocytopenia" (NEJM. 1998 Feb 25;318(8):516-7)
reported:
"The
hematocrit [red blood cell count] decreased in the same patients...with three
of eight patients requiring red-cell transfusion by the fourth week of
treatment?”
67.
Why are antiretrovirals called "life-saving" and "life
extending" when the advertisement for PROCRIT, 1997 solicited that:
“While
effective drug therapy is continued in zidovudine [AZT]-treated HIV-infected
patients…PROCRIT Reduces Transfusion Requirements and Helps Lift the Burden of
Anemia?”
68.
Why are antiretrovirals called "life-saving" and "life
extending" when Fischl MA et al., in "A randomized controlled trial
of a reduced daily dose of Zidovudine in patients with the Acquired
Immunodeficiency Syndrome" (NEJM. 1990;323(15):1009-14)
reported that:
“178
subjects (34%) had a hemoglobin concentration below 5 mmol per liter
[anemia]...A greater proportion of subjects in the standard-treatment [high
dose AZT] group had a first episode of severe anemia earlier in the study, as
compared with the proportion in the low-dose group. 134 subjects (26%) received
red-cell transfusions (65 in the standard-treatment group and 69 in the low-dose
group)...230 subjects(44%) had a [low] neutrophil
[infection fighting white blood cells] count...134 (51%) in the
standard-treatment group and 96 (37%) in the low-dose group...22 subjects (4%)
had a [low] platelet [blood clotting cells] count?”
69.
Why are antiretrovirals called "life-saving" and "life
extending" when Mir et al., in "Zidovudine and Bone Marrow" (Lancet. 1988
Nov 19;1195-6) reported:
“Zidovudine
is well known to produce haematological toxicity in vitro and in some
patients...It is worrying that bone marrow changes in patients on zidovudine
seem not to be readily reversed when the drug is withdrawn…These findings have
serious implications for the use of zidovudine in HIV positive but symptom-free
individuals?”
70.
Why are antiretrovirals called "life-saving" and "life
extending" when Dainiak et al., in "3’-Azido-3’-deoxythymidine (AZT)
inhibits proliferation in vitro of human haematopoietic progenitor cells"
(British Journal of Haematology, 1988;69:299-304)
claimed:
“nearly one half of patients treated with AZT
for [HIV]-associated disease develop transfusion-dependent anaemia due to bone
marrow depression”
The good news of course is that half of patients don’t experience hematotoxicity!
71.
Why are antiretrovirals called "life-saving" and "life
extending" when Costello., in
"Haematological abnormalities in human immunodeficiency virus (HIV)
disease" (J Clin Pathol. 1988;41:711-5) reported that:
“Blood
transfusion is often necessary in patients with AIDS, especially in those
receiving AZT, a drug which produces severe anaemia in a proportion of
recipients. Forty nine (36%) of 138 patients treated with AZT
… required blood transfusion at least once?”
72.
Why are antiretrovirals called "life-saving" and "life
extending" when Walker et al., in "Anemia and erythropoiesis in
patients with the acquired immunodeficiency syndrome (AIDS) and Kaposi sarcoma
treated with zidovudine" (Ann Int Med. 1988;108:372-6)
reported:
“In
the current study, transfusion-dependent
anemia occurred in 6 of 15 patients with AIDS and Kaposi sarcoma who were
receiving zidovudine therapy. All 6 affected patients required their first
blood transfusion between 3 and 9 weeks after starting zidovudine therapy, and
each required 4 to 14 units of packed erythrocytes to maintain a hemoglobin
level above 100 g/L over a 12-week study.”
73.
Why are antiretrovirals called "life-saving" and "life
extending" when Gina Kolata of the New York Times health desk wrote:
"Imminent marketing of AZT raises problems; marrow suppression hampers AZT
use in AIDS victims." (Science. 1987 Mar 20;235:1462-3)
where she argued that:
“more than half of all AIDS patients may not
benefit from the drug because it is more toxic for them than their AIDS
infection. The most serious side effect of AZT is to suppress the bone
marrow, leaving patients highly vulnerable to bacterial infections?”
74.
Why are antiretrovirals called "life-saving" and "life
extending" when Richman et al., in "The Toxicity of Azidothymidine
(AZT) in the Treatment of Patients with AIDS and AIDS-Related Complex"
(NEJM. 1987;317:192-197) reported that:
“Anemia…developed
in 24% of AZT recipients and 4% of placebo recipients (P<0.001). 21% of AZT
recipients and 4% of placebo recipients required multiple red-cell transfusions
(P<0.001). Neutropenia (<500 cells per cubic millimeter) occurred in 16%
of AZT recipients, as compared with 2% of placebo recipients (P<0.001)?”
75.
Why are antiretrovirals called "life-saving" and "life
extending" when Gill PS et al., in "Azidothymidine Associated with
Bone Marrow Failure in the Acquired Immunodeficiency Syndrome (AIDS)" (Ann
Int Med. 1987;107:502-505) reported that:
“Four patients with [AIDS], and a history of
Pneumocystis carinii pneumonia developed severe pancytopenia [marked decrease
in all types of blood cells]…12 to 17 weeks after the initiation of
azidothymidine (AZT) therapy…Partial bone marrow recovery was documented
within 4 to 5 weeks in three patients, but no
marrow recovery has yet occurred in one patient during the more than 6 months
since AZT treatment was discontinued?”
76.
Why are antiretrovirals called "life-saving" and "life
extending" when P. Chariot, and R. Gherardi ., in
"Partial cytochrome c oxidase deficiency and cytoplasmic bodies in
patients with zidovudine myopathy” (Neuro muscul Disorders. 1991;1:357-363)
reported:
“Long
term therapy with [AZT] can induce a toxic myopathy associated with
mitochondrial changes?”
77.
Why are antiretrovirals called "life-saving" and "life
extending" when Hayakawa
et al., in "Massive conversion of guanosine to
8-hydroxy-guanosine in mouse liver mitochondrial DNA by administration of
azidothymidine, Biochem Biophys Res Commun. 1991;176:87-93)
reported that:
“typical
mitochondrial myopathy has been reported to be expressed among many patients
with AIDS treated with long-term azidothymidine (AZT) therapy" and
"for AIDS patients, it is urgently necessary to develop a remedy
substituting this toxic substance, AZT?”
78.
Why are antiretrovirals called "life-saving" and "life
extending" when Coker R et al., in "Exacerbation of HIV-associated
myopathy by zidovudine, AIDS, 1991;5(2):229-31)
claimed that:
“A
clinically significant myopathy that precedes
the development of zidovudine associated mitochondrial myopathy has been a rarity in our experience?”
79.
Why are antiretrovirals called "life-saving" and "life
extending" when Dalakas et al., in "Mitochondrial myopathy caused by
long-term zidovudine therapy. NEJM. 1990;322(16):1098-1105) wrote:
“Before
1986, when zidovudine (formerly called azidothymidine [AZT]) was introduced…the
number of patients with HIV-associated myopathy was small, and myopathy [muscle
disorders] was considered a rare complication of HIV infection. During the past
two years [1988-1989], an increasing number of patients receiving long-term
zidovudine therapy have had myopathic symptoms such as myalgia (in up to 8
percent of patients), elevated serum creatine kinase levels (in up to 15
percent), and muscle weakness. These symptoms generally improve when zidovudine
is discontinued...We conclude that
long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy,
which... is indistinguishable from the myopathy associated with primary
HIV infection?”
80.
Why are antiretrovirals called "life-saving" and "life
extending" when M. Till , and K.B. MacDonnell, in
"Myopathy with Human Immunodeficiency Virus type 1 (HIV-1) infection:
HIV-1 or zidovudine?" (Ann Int Med.
1990;113(7):492-4) reported that:
“In
our review of our clinic patients who have received zidovudine therapy for more
than 6 months, 16% (14 of 86 patients) have had persistently elevated creatine
kinase values. Six percent of these patients (5 of 86) developed symptomatic
myalgia and objective proximal muscle weakness. These 5 symptomatic patients
had received zidovudine for an average of 45 weeks and had had creatine kinase
elevations for several weeks before onset of symptoms. Of these 5 patients, 4 had creatine kinase values return to normal and
symptoms resolve after zidovudine was withdrawn...Three patients were
rechallenged with zidovudine: each had recurrent creatine kinase elevations at
a dose of 600 mg/d. The zidovudine dose was increased to 1200 mg/d in 2
patients: after a few days, both developed recurrent muscle symptoms that again
responded to dose reduction. ...Results of quadriceps muscle biopsies done
on our patients who responded to zidovudine withdrawal showed severe myopathic
changes without evidence of inflammatory infiltrates. Electron microscopy
revealed many ultrastructural changes, including destruction of the sarcomere
profile with z-band change in the form of streaming and rod bodies. Muscle
mitochondria showed wide variation in size, swelling, degeneration and laminar
bodies. ...There have been 40 case reports [to 1990] of patients who have
developed myopathy while taking zidovudine (including our 5 symptomatic
patients). Zidovudine therapy was discontinued in 34 of these patients and 26
improved?”
81.
Why are antiretrovirals called "life-saving" and "life
extending" when Helbert et al., in "Zidovudine-associated
myopathy" (Lancet, 1988 Sep 17;2:689-90) claimed
that:
“A
severe proximal myopathy, predominantly affecting the legs, seems to be a
significant complication of long-term zidovudine therapy, even at reduced
doses; it affected 18% of our patients
who had received treatment for more than 200 days. Other drugs could not be
implicated. The pathogenesis is obscure;
the myopathy resolves on cessation of zidovudine, but not on dose-reduction,
though there is then a risk of rebound encephalitis?”
82.
Why are antiretrovirals called "life-saving" and "life
extending" when D.V. Havlir and P.F. Barnes., in "Tuberculosis in
patients with human immunodeficiency virus infection" (NEJM. 1999 Feb 4;340:367-73) reported that:
“Antiretroviral
therapy may be initiated early during antituberculosis therapy in HIV-infected
patients with tuberculosis. After
initial clinical improvement, paradoxical worsening of disease developed in up
to 36 percent of these patients, characterized by fever, worsening chest
infiltrates on radiograph, and peripheral and mediastinal lymphadenopathy...In
contrast, only 7 percent of patients
who received antituberculosis therapy but not antiretroviral therapy had
paradoxical reactions?”
83.
Why are antiretrovirals called "life-saving" and "life
extending" when Kelleher et al., in "Immunological effects of
antiretroviral and immune therapies for HIV" (AIDS, 1997;Vol
11 (suppl A):S149-155) reported that:
“[AZT
may] unmask silent opportunistic infections...Lack of strong evidence exists for sustained immune reconstitution by
current therapies...If [immune reconstitution] does not occur with time,
despite prolonged viral suppression, then the case for immunorestorative
strategies...could be justifiably explored?”
84.
Why are antiretrovirals called "life-saving" and "life
extending" when The Canadian Pharmaceutical Association Compendium of
Pharmaceuticals & Specialities (1997;1357-61)
recommended that:
“The long-term consequences of in-utero and infant exposure to
zidovudine [AZT] are unknown. The long-term effects of early or short-term use
of zidovudine in pregnant women are also unknown...The incidence of adverse
reactions [to AZT] appears to increase with disease progression, and patients
should be monitored carefully, especially as disease progression occurs. [i.e. AZT does not prevent progression to AIDS]?”
85.
Why are antiretrovirals called "life-saving" and "life
extending" when The Physicians Desk Reference, (Mosby-Year Book Inc..
1996, http://www.virusmyth.com/aids/data/pdrazt.htm)
claimed:
“[in these clinical trials] it was often difficult to
distinguish adverse events possibly associated with administration of Retrovir
from underlying signs of HIV disease or intercurrent illnesses [i.e. AZT can
cause AIDS-defining illnesses]?”
86.
Why are antiretrovirals called "life-saving" and "life
extending" when Sperling et al., in "Maternal viral load, zidovudine
treatment and the risk of transmission of human immunodeficiency virus type 1
from mother to infant" (NEJM. 1996;335(22):1621-9)
reported that:
“Overall,
zidovudine treatment was associated with only a small reduction in circulating
levels of plasma RNA...Explanations need
to be considered for the apparent lack of association between the observed RNA
levels and the effect of zidovudine treatment [i.e. lower rates of
transmission from mothers on zidovudine to their children cannot be due to
lower levels of virus!]?”
87.
Why are antiretrovirals called "life-saving" and "life
extending" when Bacellar et al., in "Incidence of clinical AIDS
conditions in a cohort of homosexual men with CD4+ cell counts < 100/cubic
mm" (JID. 1994;170:1284-7) reported that:
“The median CD4 lymphocyte count did not differ in the 3 groups:
54 for the group receiving neither antiretroviral nor P. carinii pneumonia
prophylaxis, 53 for the group receiving only antiretroviral therapy, and 52 for
the combined treatment group. There were also no major differences in the median CD8 lymphocyte
count of the 3 groups...Other illnesses now have elevated incidence rates among
persons receiving P. carinii pneumonia prophylaxis [and AZT or didanosine]: M.
avium complex, nonretinitis cyomegalovirus disease, cytomegalovirus retinitis,
candida esophagitis, and wasting syndrome?”
88.
Why are antiretrovirals called "life-saving" and "life
extending" when Sheppard et al., in "Viral burden and HIV
disease" ( Nature. 1993 Jul 22;364(6435):291-2)
reported that:
“the high level of plasma virus observed by Piatak et al, was
about 99.9 per cent non-culturable,
suggesting that it was either neutralized or defective. Therefore, rather than
supporting a cytopathic model, this observation actually may help explain the
relatively slow dissemination of the infected cell burden and thus the relative ineffectiveness of therapy
with nucleoside analogues which target this process?”
89.
Why are antiretrovirals called "life-saving" and "life
extending" when The National Institute of Allergy and Infectious Diseases
State-of-the-Art Panel on Anti-Retroviral Therapy for Adult HIV-Infected
Patients, in "Anti-retroviral therapy for adult HIV-infected patients.
Recommendations from a state-of-the-art conference" (JAMA. 1993;270:2583-9) concluded that:
“Some
HIV-infected individuals have remained healthy for more than 15 years following
seroconversion. Lower numbers of CD4+ peripheral blood lymphoctyes have
generally been found to indicate the advancement of HIV disease... [but] The CD4+ cell counts vary from day to day and laboratory
to laboratory, and similar levels do not necessarily reflect the same disease
status in all patients. For example, very low CD4+ cell counts (less than
0.05x10**9/L (50/microL)) usually indicate advanced disease; however, some
patients with these levels remain asymptomatic for extended periods of time
while others succumb rapidly...While knowledge of the clinical use of
zidovudine has increased during the last several years, the panel was concerned
overall by the drug’s limited effectiveness and durability of response?”
90.
Why are antiretrovirals called "life-saving" and "life
extending" when Lu et al., in "Similar replication capacities of
primary human immunodeficiency virus type 1 isolates derived from a wide range
of clinical sources" (J Virol. 1992 Jan;66(1):334-340)
concluded that:
“Replication
curves and cytopathic effect of a standard inoculum (1 ng of p24) of 66 primary
HIV-1 isolates were similar regardless of the clinical stage of the patient...There was no difference between viruses
derived from patients sensitive to zidovudine and those derived from patients
resistant to zidovudine?”
91.
Why are antiretrovirals called "life-saving" and "life
extending" when Reinvang et al., in "Only temporary improvement in
impaired neuropsychological function in AIDS patients treated with
zidovudine" (AIDS. 1991;5(2):228-9) reported
that:
“Doubts
may be raised about the long-term beneficial effects of zidovudine treatment on
AIDS-related cognitive impairments?”
92.
Why are antiretrovirals called "life-saving" and "life
extending" when In 1990, Fischl MA et al. in NEJM (1990;323(15):1009-14)
reported that:
“thirteen subjects of 146 tested who were
negative for HIV antigen before treatment later had detectable levels of
antigen during the 128 weeks of treatment"!
How
does AZT make you test HIV-positive?
93.
Why are antiretrovirals called "life-saving" and "life
extending" when Phillips et al., in "Viral load and combination
therapy for Human Immunodeficiency Virus" (NEJM. 1997 Mar 27;336(13), www.nejm.org/content/1997/0336/0013/0958.asp)
suggested that:
“Extended
follow-up of patients in one [AZT] trial, the Concorde study, has shown a significantly increased risk of
death among the patients treated early...where is the evidence that for a
patient with a CD4 count of 450 cells per cubic millimeter and a low plasma
viral level, it would not be better to wait before initiating therapy?...In
1990...a patient with a CD4 count of 450 cells per cubic millimeter would have
been advised to start monotherapy with zidovudine. We now tell such a patient
that, in fact, follow-up data for up to
4.5 years since that time have shown no survival benefit?”
94.
Why are antiretrovirals called "life-saving" and "life
extending" when White et al., in "Impact of treatment changes on the
interpretation of the Concorde trial” (AIDS, 1997;11:999-1006)
suggested that:
“participants
of open-label ZDV [AZT] still had four to five times the incidence of
ARC/AIDS/death of participants on blinded therapy [of which approximately half
were on AZT and half on placebo]...The
unadjusted hazard of ARC/AIDS/death was 4.6 times higher for participants [in
the deferred group] who had received ZDV...after adjustment for latest CD4 this
became 1.6...There was a suggestion of a benefit in terms of [slower]
progression to ARC, AIDS or death [with AZT], no effect on progression to AIDS
or death, and a suggestion of an
increase in mortality?”
95.
Why are antiretrovirals called "life-saving" and "life
extending" when Chaisson et al., in "Sex, race, drug use and
progression of human immunodeficiency virus disease" (NEJM.
1995;333(12):751-6) reported that.
“The mortality rate was significantly higher
among [a group of 1372] patients who had received antiretroviral therapy
[principally AZT] before enrollment in the clinic?”
96.
Why are antiretrovirals called "life-saving" and "life
extending" when Buchbinder et al., in "Long-term HIV-1 infection
without immunologic progression" (AIDS, 1994; 8:1123) reported that:
“Only
38% of the HLP [Healthy long-term
positives] had ever used
zidovudine [AZT] or other nucleoside analogues, compared with 94% of the progressors?”
97.
Why are antiretrovirals called "life-saving" and "life
extending" when Pluda et al., in "Development of Non-Hodgkin Lymphoma
in a Cohort of Patients with Severe Human Immunodeficiency Virus (HIV)
Infection on Long-Term Antiretroviral Therapy" (Ann Int Med.
1990;113:276-282) claimed that AZT caused cancer?
“after starting antiretroviral treatment...the estimated
probability of developing lymphoma ...by 36 months, [was] 46.4% (CI, 19.6% to 75.5%)...a direct role of therapy itself cannot
be totally discounted...Zidovudine can
act as a mutagen.”
98.
Why are antiretrovirals called "life-saving" and "life
extending" when Costello (1988) reported in the Journal of Clinical
Pathology that, “Blood transfusion is
often necessary in patients with AIDS, especially in those receiving AZT, a
drug which produces severe anaemia in a proportion of recipients. Forty nine (36%) of 138 patients treated
with AZT required blood transfusion at least once?”
99.
Why are antiretrovirals called "life-saving" and "life
extending" when Harrison's
Principles of Internal Medicine states: “[AZT], used for treating [HIV], often causes severe megaloblastic anemia caused by impaired DNA synthesis?"
100.
Writing in the journal Palliat Med. (1997 Mar;11(2):152-8),
Kelleher et al. published a paper entitled, "HIV infection: the spectrum
of symptoms and disease in male and female patients attending a London
hospice," in which they concluded that:
“Lack
of strong evidence exists for sustained immune reconstitution by current
therapies [comprising AZT and other drugs], and AZT may unmask silent
opportunistic infections. Not only can AZT unmask silent opportunistic
infections, it can exacerbate clinically conspicuous ones.”
101.
Why are antiretrovirals called "life-saving" and "life
extending" when AZT has some of the following caveats on the AZT package
insert printed in bold and
CAPITALIZED type?
“WARNING:
RETROVIR (ZIDOVUDINE, AZT) MAY BE ASSOCIATED WITH HEMATOLOGIC TOXICITY
INCLUDING GRANULOCYTOPENIA AND SEVERE ANEMIA PARTICULARLY IN PATIENTS WITH
ADVANCED HIV DISEASE.” (underline is mine).
“PROLONGED
USE OF RETROVIR HAS BEEN ASSOCIATED WITH SYMPTOMATIC MYOPATHY SIMILAR TO THAT
PRODUCED BY HUMAN IMMUNODEFICIENCY VIRUS. RARE OCCURRENCES OF LACTIC ACIDOSIS
IN THE ABSENCE OF HYPOXEMIA, AND SEVERE HEPATOMEGALY WITH STEATOSIS HAVE BEEN
REPORTED WITH THE USE OF ANTIRETROVIRAL NUCLEOSIDE ANALOGUES, INCLUDING
RETROVIR AND ZALCITABINE, AND ARE POTENTIALLY FATAL.”
“Persistent
headaches lasting longer than 1 month, anemia, dementia, diarrhea,
muscle wasting, candidiasis, non-specific oral
lesions, severe fatigue,
enlarged liver and liver failure, heart failure,
diabetes, unmasking of opportunistic
infections
including CMV retinitis, spontaneous bleeding in hemophiliacs, lymphoma, severe
skin rashes, Stevens-Johnson syndrome, and other toxic reactions, back pain,
body odor, chest pain, chills, edema of the lip, fever, flu syndrome,
hyperalgesia, syncope, vasodilation, bleeding gums, constipation, dysphagia,
edema of the tongue, eructation, flatulence, mouth ulcer, rectal hemorrhage,
lymphadenopathy, arthralgia, muscle spasm, tremor, twitch, anxiety, confusion,
depression, dizziness, emotional lability, loss of mental acuity, nervousness,
paresthesia, somnolence, cough, dyspnea, epistaxis, hoarseness, pharyngitis,
rhinitis, sinusitis, acne, changes in skin and nail pigmentation, pruritus,
rash, sweat, urticaria, amblyopia, hearing loss,photophobia, taste perversion,
dysuria, polyuria, urinary frequency, urinary hesitancy.”
“Zidovudine was administered orally at three
dosage levels to separate groups of mice and rats (60 females and 60 males in
each group). Initial single daily doses were 30, 60, and 120 mg/kg/day in mice
and 80, 220, and 600 mg/kg/day in rats. The doses in mice were reduced to 20,
30, and 40 mg/kg/day after day 90 because of treatment- related anemia, whereas
in rats only the high dose was reduced to 450 mg/kg/day on day 91 and then to
300 mg/kg/day on day 279.”
“In
mice, seven late-appearing (after 19 months) vaginal neoplasms (5
nonmetastasizing squamous cell carcinomas, one squamous cell papilloma, and one
squamous polyp) occurred in animals given the highest dose. One late-appearing
squamous cell papilloma occurred in the vagina of a middle dose animal. No
vaginal tumors were found at the lowest dose.”
“In
rats, two late-appearing (after 20 months), non-metastasizing vaginal squamous
cell carcinomas occurred in animals given the highest dose. No vaginal tumors
occurred at the low or middle dose in rats. No other drug-related tumors were
observed in either sex of either species.”
“It
is not known how predictive the results of rodent carcinogenicity studies may
be for humans. At doses that produced tumors in mice and rats, the estimated
drug exposure (as measured by AUC) was approximately 3 times (mouse) and 24
times (rat) the estimated human exposure at the recommended therapeutic dose of
100 mg every 4 hours.” “ In the presence of metabolic
activation, the drug was weakly mutagenic at concentrations of 1000 A?g/ml and
higher. In an in vitro mammalian cell transformation assay, zidovudine (AZT)
was positive at concentrations of 0.5 ug/ml and
higher. In an in vitro cytogenetic study performed in cultured human
lymphocytes, zidovudine induced dose-related structural chromosomal
abnormalities at concentrations of 3 ug/ ml and higher.”
“In
two in vivo micronucleus studies (designed to measure chromosome breakage or
mitotic spindle apparatus damage) in male mice, oral doses of zidovudine 100 to
1000 mg/kg/day administered once daily for approximately 4 weeks induced
dose-related increases in micronucleated erythrocytes. Similar results were
also seen after 4 or 7 days of dosing at 500 mg/kg/day in rats and mice.”
Nothing wrong with a few micronucleated cells or mitotic spindle damage.
“In
a study involving 11 AIDS patients, it was reported that the seven patients who
were receiving Retrovir (1200 mg/day) as their only medication for 4 weeks to 7
months showed a chromosome breakage frequency of 8.29ug/ml2.65 breaks per 100
peripheral lymphocytes. This was significantly (P< 0.05) higher than the
incidence of 0.5ug/ml 0.29 breaks per 100 calls that was observed in the four
AIDS patients who had not received Retrovir.
102.
Why are antiretrovirals called "life-saving" and "life
extending" when Brinkman et al., reported that "Mitochondrial
toxicity induced by nucleoside-analogue reverse transcriptase inhibitors is a
key in the pathogenesis of antiretroviral-related lipodystrophy." (Lancet.
1999 Sep 25;354:1112-15.1999), and concluded that:
“Highly
active antiretroviral therapy (HAART) can induce a characteristic lipodystrophy
syndrome of peripheral fat wasting and central adiposity. HIV-1 protease
inhibitors are generally believed to be the causal agents, although the
syndrome has also been observed with protease-inhibitor-sparing regimens. Here,
we postulate that the mitochondrial toxicity of the nucleoside-analogue
reverse-transcriptase inhibitors plays an essential part in the development of
this lipodystrophy, similar to the role of mitochondrial defects in the
development of multiple symmetrical lipomatosis?”
103.
Why are antiretrovirals called "life-saving" and "life
extending" when Estaquier, et al., reported in an article entitled,
"Effects of Antiretroviral Drugs on Human Immunodeficiency Virus Type
1-Induced CD4+ T-Cell Death" (Journal of Virology, Vol. 76, No. 12, p.
5966-5973, June 2002) that:
"We
treated PBMC from HIV-seronegative
healthy donors with increasing concentrations of IDV, SQV, or ddI for 3
days and monitored T-cell proliferation and cell death. Both IDV and SQV decreased T-cell proliferation mediated by CD3 MAb in
three independent experiments performed with healthy donor cells with a mean
decrease for SQV of 53% ± 15% and a mean decrease for IDV of 48% ± 12%
(Fig. 4A). Moreover, in the absence of T-cell activation, we observed that 10
µM IDV and SQV induced a loss in membrane mitochondrial potential (m) as
assessed by flow cytometry using DiOC6."
104.
Why are antiretrovirals called "life-saving" and "life
extending" when Martinez et al., in "Risk of lipodystrophy in HIV-1
infected patients treated with protease inhibitors: a prospective cohort
study" (Lancet. 2001;357(9256):592-8, 2001),
suggested that:
“Clinical
research on lipodystrophy has usually rested on the idea that it was merely a
complex adverse event related to individual antiretroviral agents or families of drugs...Our study suggests that the risk of
lipodystrophy is mainly related to the total exposure to HAART and only to a
lesser degree to specific antiretroviral drugs.”
105.
Why are antiretrovirals called "life-saving" and "life
extending" when Tsiodras et al., also described the "Effects of
Protease Inhibitors on Hyperglycemia, Hyperlipidemia, and Lipodystrophy"
(Arch Intern Med. 2000 Jul 10;160(13):2050-6, 2000),
where they suggested that:
“Our
study reports an independent association between PI [protease inhibitors] use
and ... lipodystrophy, on the basis of a 5-year cohort study that encompassed the pre-PI and post-PI therapeutic eras. Although these
metabolic changes were occasionally observed in patients not exposed to PIs,
they were much more frequent after initiation of PI therapy.”
106.
Why are antiretrovirals called "life-saving" and "life
extending" when
Bica et al (2001) stated:
“In
1998-1999, 11 (50%) of 22 deaths were due to end-stage liver disease [a common side
effect of AIDS drugs]... End-stage liver
disease is now the leading cause of death in our hospitalized HIV-seropositive
population.”
107.
Why are antiretrovirals called "life-saving" and "life
extending" when Lederman MM, Valdez H. (2000), published a study that
claimed:
“Of
recent HIV-related deaths occurring in the University Hospitals of Cleveland although
OIs [Opportunistic Infections] constituted less than 25% of deaths in 1999,
end-organ failures [which could well be caused by medication] constituted
nearly half. Importantly, the median CD4 cell count among the patients who
died in our clinic has risen, and about
20% of recent deaths have occurred among patients with plasma HIV RNA levels
below the limit of detection?”
108.
If antiretrovirals such as AZT or combinations such as HAART are indeed
"life-saving" and "life extending," then why has there been
the need to make so many of them? Here is a more or less complete list of
"the life saving drugs that have been improperly called or considered as
"antiretrovirals" that are aggressively peddled by the pharmaceutical
giants in collusion with
the current Public Health Service administrations (eg. Agenerase (amprenavir), GlaxoSmithKline; Combivir, (lamivudine
and zidovudine), GlaxoSmithKline;
Crixivan, (indinavir, IDV, MK-639), Merck;
Emtriva, (FTC, emtricitabine), Gilead
Sciences; Epivir, (lamivudine, 3TC Epzicom, abacavir) GlaxoSmithKline; Fortovase, (saquinavir), Hoffmann-La Roche; Fuzeon, (enfuvirtide, T-20), Hoffmann-La Roche & Trimeris; Hivid,
(zalcitabine, ddC, dideoxycytidine), Hoffmann-La
Roche; Invirase, (saquinavir mesylate, SQV), Hoffmann-La Roche; Kaletra, (lopinavir and ritonavir), Abbott Laboratories; Lexiva,
(Fosamprenavir Calcium), GlaxoSmithKline;
Norvir, (ritonavir, ABT-538), Abbott
Laboratories; Rescriptor, (delavirdine, DLV), Pfizer; Retrovir (zidovudine, AZT, azidothymidine, ZDV) GlaxoSmithKline; Reyataz, (atazanavir sulfate), Bristol-Myers
Squibb; Sustiva, (efavirenz),
Bristol Myers-Squibb; Truvada, (tenofovir disoproxil/emtricitabine), Gilead Sciences, Inc.; Videx EC, (enteric coated didanosine), Bristol Myers-Squibb; Videx, (didanosine, ddI, dideoxyinosine), Bristol Myers-Squibb; Viracept,
(nelfinavir mesylate, NFV), Agouron
Pharmaceuticals; Viramune, (nevirapine, BI-RG-587), Boehringer Ingelheim; Viread, (tenofovir disoproxil fumarate), Gilead; Zerit, (stavudine, d4T) Bristol Myers-Squibb; Ziagen (abacavir)
GlaxoSmithKline.
109.
Why do some AIDS researchers such as Gisselquist et al. who have studied Africa
and African AIDS extensively, claim that "HIV/AIDS" is caused mostly
by doctors, and are now advocating that this is how the Tripoli Six infected
more than 400 children in a Libyan hospital, and who are said to be soon
executed by firing squad! The reasons in
support of the Gisselquist et al. claims have been published repeatedly in the
International Journal of STD’s and AIDS (Gisselquist D, Friedman E,
Potterat JJ, Minkin SF, Brody S. Four policies to reduce HIV transmission
through unsterile health care. Int J STD AIDS. 2003 Nov;14(11):717-22;
Gisselquist D, Potterat JJ, Brody S, Vachon F. Let it be sexual: how health
care transmission of AIDS in Africa
was ignored. Int J STD AIDS. 2003 Mar;14(3):148-61; Brewer DD, Brody S, Drucker
E, Gisselquist D, Minkin SF, Potterat JJ, Rothenberg RB, Vachon F. Mounting
anomalies in the epidemiology of HIV in Africa: cry the beloved paradigm. Int J
STD AIDS. 2003 Mar;14(3):144-7; Gisselquist D, Potterat JJ, Epstein P, Vachon
F, Minkin SF. AIDS in Africa. Lancet. 2002 Nov
2;360(9343):1422-3; author reply 1423-4; Gisselquist D, Rothenberg R, Potterat
J, Drucker E. HIV infections in sub-Saharan Africa not explained by sexual or
vertical transmission. Int J STD AIDS. 2002 Oct;13(10):657-66)
include the following types of reasons for the claim that “HIV/AIDS” is caused
by doctors (a synopsis can be obtained at Editorial
with Gisselquist, statistics quoted from: International Journal of STD &
AIDS Royal Society of Medicine, October 2002 Africa HIV/AIDS through unsafe
medical care. Also available: Africa Policy E-Journal.
www.africaaction.org/docs02/hiv0210t.htm):
"An expanding body of evidence challenges
the conventional hypothesis that sexual transmission is responsible for more
than 90% of adult HIV infections in Africa.
Differences in epidemic trajectories across Africa do not correspond to differences in sexual
behavior. Studies among African couples find low rates of heterosexual
transmission, as in developed countries. Many studies report HIV infections in
African adults with no sexual exposure to HIV and in children with HIV-negative
mothers. Unexplained high rates of HIV incidence have been observed in African
women during antenatal and postpartum periods. Many studies show 20%-40% of HIV
infections in
African adults associated with injections (though direction of causation is
unknown). These and other findings that challenge the conventional hypothesis
point to the possibility that HIV transmission through unsafe medical care may
be an important factor in Africa's
HIV epidemic. More research is warranted to clarify risks for HIV."
"The assumption that historic and
continuing high rates of epidemic increasesamong African adults are almost
exclusively due to sexual transmission requires much higher rates of
heterosexual transmission in Africa
than in the developed world. However, a recent study of HIV incidence in
serodiscordant couples in Africa (only 1.2% reported consistent condom use)
estimated a rate of transmission per coital act of only 0.0011,(23) comparable to rates of 0.0003-0.0015 from similar studies in the US and Europe [22].
"A study in Kinshasha in 1985 found 39% (17
of 44) of HIV-positive inpatient andoutpatient children 1-24 months old to have
HIV-negative mothers; only five of 16 (with information) had been transfused...
In a later report from Rwanda, 7.3% (54 of 704) of mothers of children with
AIDS were HIV-negative; transfusions were identified as the risk factor for 22
of the 54 children… rates of unexplained incidence among African women are
comparable to rates of maternal mortality from puerperal fever of 6% to 16%
observed by Semmelweis during 1841-46 in the First Clinic at the University of
Vienna's obstetric department. "
"Starting in the 1950s Africans experienced
a massive increase in medical injections associated with mass injection
campaigns targeted at yaws, with introduction and spread of parenteral
therapies to treat other diseases, and with plummeting prices for antibiotics
and injection equipment. For example, UNICEF administered 12 million injections
for yaws in Central
Africa
alone during 1952-57. From the 1950s into the 1980s, unsafe injections may have
contributed to the silent spread of HIV in Africa in much the same way that unsafe injections for
schistosomiasis and other treatments in Egypt established hepatitis C as a major blood-borne
pathogen, infecting about 15% to 20% of the general population at the end of
the 1990s."
"Our observations raise the serious
possibility that an important portion of HIV transmission in Africa may occur through unsafe injections and other
unsterile medical procedures."
The author wishes to thank Dr. Andrew Maniotis,
College of Medicine, University of Illinois at Chicago for his work in developing these questions and his permission to use them on this website.