THE FAUCI FILES, 3( 83): Nuremberg Code Vetoed for AZT HIV-Negative Baby Experiments

August 27, 2000

The AZT Model of Post-Partum Abortion and AIDS
Causation also appears to apply to the HIV-negative
children, not just the handful out of 100
who are "saved" from HIV infection:

   "...that the current practice of treating 
   HIV-1-positive women and their infants with
   high doses of AZT could increase cancer risk
   in the drug-exposed children when they reach
   young adulthood or middle age,"


While the proof that AZT is a cause of AIDS
in HIV+ babies born to AZT-poisoned mothers has
been establised in reproducible experiments, the silent
and not-so-silent defenders of baby killing continue
to assert The God Defense as they point to more
babies "saved" from HIV infection than are killed
by AZT "treatment".

But how do these God impersonators know if the
HIV-negative babies born to HIV-positive mothers
are really better off when only a handful out of
each 100 treated mothers are purportedly "saved"
from HIV infection by AZT? How dare they overlook
the risk of AZT long-term damage to those who would
have had healthy lives if AZT was never used on them?

Who gave these people the right to veto the
Nuremberg Code when it comes to the AZT neonate
studies in the November 1997 Journal of the
National Cancer Institute?


   "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."
    -- Agarwal & Olivero


And which of these God knock-offs can claim that ALL
the AZT-exposed HIV-negative babies -- not just the
handful "saved" from HIV infection -- are truly
better off when one considers the horrifying
outcomes of 100% deaths in the rodent genotoxicity
studies by the National Cancer Institute, which
may extend the trajectory for AZT Post-Partum
abortions into the human-equivalent range of
early adulthood, at best:


  "In utero-exposed mice "...exhibited statistically
   significant,  dose-dependent increases in tumor
   incidence and tumor multiplicity in  the lungs,
   liver, and female reproductive organs..." at 1 year.
   The same  results were not seen in AZT-exposed
   infant monkeys,but incorporation of the drug
   "...into nuclear and mitochondrial DNA was
   detected in  multiple organs..." of these monkeys,
   as well as in exposed mice, indicating genotoxicity.


As I recall, the AZT pregnancy studies only plan
to follow the HIV negative children for a few years,
certainly not long enough to determine the
scope of any harm done to these kids.

When their mother is gone and (if) they grow up, who
is there to tell them that their multiple cancers
of all kinds were the result of God Fauci's
antiviral hoax and political opportunism?

Who vetoed the Nuremberg Code?


W. Fred Shaw, Editor
THE FAUCI FILES

======

In Utero Exposure To AZT Causes Tumors In Mice

WESTPORT, Nov 05 (Reuters) - Although AZT is effective in
reducing the  incidence of maternal-fetal HIV transmission,
evidence from animal  experiments reported today suggests
that it may increase the risk of  tumors in exposed infants.

Since the studies were conducted in mice, Dr. Ofelia A.
Olivero of the  National Cancer Institute in Bethesda,
Maryland, and a multicenter team  caution in the November
5th issue of the Journal of the National Cancer  Institute
(JNCI) that the relevance "...to human exposure must be
considered in the context of dose-equivalency."

In utero-exposed mice "...exhibited statistically
significant,  dose-dependent increases in tumor incidence
and tumor multiplicity in  the lungs, liver, and female
reproductive organs..." at 1 year. The same  results were
not seen in AZT-exposed infant monkeys, but incorporation
of the drug "...into nuclear and mitochondrial DNA was
detected in  multiple organs..." of these monkeys, as well
as in exposed mice,  indicating genotoxicity.

The findings indicate "...that the current practice of
treating  HIV-1-positive women and their infants with high
doses of AZT could  increase cancer risk in the drug-exposed
children when they reach young  adulthood or middle age,"
according to the scientists. However, "The  remarkable
effectiveness of AZT in preventing fetal HIV infection
indicates that the immediate need for treatment of a
potentially fatal  disease should outweigh the potential
cancer risk." At this point, Dr.  Olivero and colleagues
recommend that pregnant women should be notified  of these
risks, and the appropriate informed consent to AZT
prophylaxis  should be documented.

Last January, the National Institutes of Health convened a
panel of  researchers to review this and other evidence of
the transplacental  carcinogenic effects of AZT, according
to Dr. Atieno A. Reggy and others  at the Centers for
Disease Control and Prevention in Atlanta, Georgia.  They
write in JNCI: "In its summary of the studies, the panel
concluded  that the known benefits of AZT in preventing
perinatal transmission far  outweigh the theoretical risk of
carcinogenesis and that, in and of  themselves, the data do
not suggest the need for changes in treatment
recommendations."

However, in light of the evidence, the "...Pediatric AIDS
Clinical  Trials Group is currently conducting a long-term
follow-up study of  children exposed to antiretroviral
therapy in clinical trials."


J Natl Cancer Inst 1997;89:1566-1567,1602-1608.

=============================

Agarwal RP, Olivero OA. 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.

Medical Oncology, University of Miami School of Medicine, FL
33136, USA.

Abstract: AZT (3'-azido-2',3'-dideoxythymidine), the first
nucleoside  analog approved for the treatment of AIDS
(acquired immunodeficiency  syndrome), induces significant
toxic effects in humans exposed to  therapeutic doses. As an
inhibitor of the HIV-1 (human immunodeficiency  virus 1)
reverse transcriptase, AZT blocks the incorporation of
nucleotides into the host's newly synthesized DNA.
Incorporation of AZT  into mammalian DNA as well as specific
localization of the drug into  telomeric DNA, has been
previously documented by immunohistochemistry.  As with
other nucleoside analogs, AZT has affinity for
polymerase-gamma,  the enzyme responsible for the
replication of mitochondrial DNA. In  order to examine the
mechanisms of toxic events induced by long-term AZT
exposure, human T-lymphocytic H9 cells were cultured with 25
microM AZT  for 7 months. In the resulting H9-AZT cells,
incorporation of AZT into  DNA was demonstrated by
radioimmunoassay and immunohistochemistry,  chromosomal
aberrations and micronuclei were scored and intracellular
lipid distribution was determined. Two pmol of AZT per
microgram of DNA  were detected by radioimmunoassay in
H9-AZT cells. Control cells showed  negative values in the
radioimmunoassay. Cytogenetic observations on  H9-AZT cells
showed an increase in chromosomal aberrations and nuclear
fragmentation when compared with unexposed H9 cells.
Electron microscopy  revealed mitochondrial damage and an
elevated accumulation of neutral  intracellular lipid
deposits probably as a consequence of a distortion  in the
beta-oxidation of fatty acids normally carried out by this
organelle. 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.