Unanswered scientific questions about "AIDS", sent to the American experts.
These questions were sent on December 1 2007 by Lambros Papantoniou, journalist and Greek press correspondent in Washington, to the experts of the National Cancer Institute (NCI), a part of the American Department of Defense (DOD) which seems to be the top level for the AIDS subject.
Beforehand, he received an official e-mail by Mrs Brooke Hardison Wand, on November 29 2007, who came to the knowledge that he was asking for an interview with an NCI expert about HIV/AIDS. The same day, the journalist called her and was urged to send written questions and they would reply. On December 1 2007, the questions were sent via e-mail.
December 5 2007, the journalist called again and it was Richard Folkern who then picked the phone. He introduced himself as the director of the Public Relations office and asked the interview and any follow-up to be given in written form, not recorded. The journalist accepted it.
On 19 December 2007, the journalist called again but Mr Folkern was not there so he left a message on the phone machine. It was never answered.
On 20 December 2007, the journalist called, Mr Fokern picked the phone and said that the answers were about to be sent in 10 days the most, as there are several scientists working on them. Again never did they arrive.
On 15 January 2008, the journalist called again, Mrs Wang picked the phone and told him that she could not understand the reason of such a delay and she would ask Dr Giorgos Pavlakis about it in order to give an answer. She also said that the answer could be negative, that they wouldn't answer his questions. The journalist answered "No problem, but I need to know so that I can go on with it, as I absolutely want those questions to be answered. She promised to call again, but never did.
On 31 January 2008, the journalist called, it was Mr. Anthony Beal who picked the phone, he didn' t know about the case. After being given full
report on the phone, he said that both Mr. Folkern and Mrs. Wang are not there and he will be glad to leave them a message and they would call back.
On February 1 2008, the journalist found a message on the phone machine by a lady who didn't leave her name but was informing him that the NCI is not interested in answering his questions, because that is the way Dr Giorgos Pavlakis advised them now. She named Dr Pavlakis and also said that he suggested the journalist to address to other offices.
The unanswered questions so far are in the following message:
-------------------------------------------------------------
Ms.
Brooke Hardison Wang, M.P.H.
NCI,
DOD Laboratory
Washington,
D.C.
Dear
Ms. Wang,
As
per your request, dated November 29, 07, I'm sending my questions
for an interview with a scientist of NCI to be published in Greece,
regarding vaccines against the virus "HIV":
1.
Can you state in words that the average person will understand what
the MOLECULAR mechanism is that this vaccine will be based upon to
outwit the wily HIV?
2.
Will a person given this vaccine generate any antibodies against HIV?
3.
Will any of the antibodies generated by the vaccine be against p18,
p24, p39, p55, p32, p53, p68, gp41, gp120 or gp160?
4.
Can you explain why both the Merck vaccine and the 2004 GP120 vaccine
of VAXGEN failed to
immunize anybody against “HIV,” as there were only 20 people in
the vaccinated group who seroconverted in response to vaccination and
even less who seroconverted in the non-vaccinated group?
5.
In the African arm of the Merck trial, why did only about 20 persons
of more than 700 persons that were vaccinated seroconvert, while only
9 seroconverted in the non-vaccinated group? Assuming that the
vaccine isn’t causing more “HIV” than the placebo group
acquired through sex, then how do you explain these extremely low
rates of seroconversion if the antigens of “HIV” were indeed
given in the vaccine? Wouldn’t you expect most of the vaccinated
group to seroconvert like they would if given a hepatitis B vaccine,
or any other vaccine?
6.
If “HIV” is a “retrovirus”
that integrates its genome through a process called “reverse
transcription, then how can you
immunize against “HIV” if
“HIV” is hidden from the
immune system inside the genomes of infected cells?
In other words, if the “HIV” virus can spread through direct
cell-to-cell contact, avoiding ”immune activation,” then how do
you expect the vaccine to protect against it?
7.
Are the antibodies generated by this vaccine enough to cause one or
more bands to show up on the WESTERN blot?
8.
If a person had an indeterminate western plot before vaccination,
missing only one band, would they potentially be positive after
vaccination?
9.
Which of the following will be measured as end points of the trial:
A)
Development of antibodies or other signs of successful vaccination ,
B)
Lower risk of becoming HIV-Positive,
C)
Lower risk of disease,
D)
Lower risk of death?
10.
How long will participants be monitored for? And what outcomes will
be monitored long term?
11.
Will the trial be halted as the Merck trial was if it is found that
more vaccine recipients begin to test positive for “HIV” than the
non-vaccinated?
12.
Why do the HIV antibody
tests used since 1986 continue to carry an alarming disclaimer?
“At
present, there is no recognized standard for establishing the
presence or absence of antibodies to HIV-1 and HIV-2 in human blood.”
And
why do the package inserts accompanying viral load tests still say
they are:
“Not
intended to be used as a screening test for HIV or as a diagnostic
test for confirm the presence of HIV infection (HIV-1/HIV-2
EIA/ELISA, Abbot Laboratories; OraQuick Rapid HIV-1 Antibody Test,
Abbot Diagnostics; Amplicor HIV-1 Monitor Test, Roche)?
13.
A vaccine was promised at the first announcements in 1984, on what
basis should people believe that a vaccine is possible in the near
future after so many failures? How do explain those failures for a
vaccine against HIV for 25 years now, since you are claiming that
your DOD Laboratory isolated the virus 1984?
14.
Will the vaccine be tested in people who are ill or malnourished?
If
not, how can we be sure that significant adverse reactions in those
groups are not likely? And
15.
Why your Federal Agency does not accept any question for the HIV
virus itself- as you told me over the phone, November 29- since the
entire effort universally- as I understand- is to fight the virus,
as soun as possible for the benefit of the humanity? Why you should
be keep secret any information to this effect? What do you mean that
any discussion on HIV is classified? Is there any specific reason?
16. Why
didn’t the Merck vaccine prevent “HIV” infection in volunteers
who received at least one dose of the three-dose vaccine series, and
why were 24 cases of HIV infection were observed in the 741
volunteers who received vaccine and why were 21 cases of HIV
infection observed in the 762 participants in the placebo group?
17.
In the subgroup who had received at least two vaccinations and who
were HIV negative for at least the first 12 weeks of the trial, why
were there 19 cases of “HIV infection” or seroconversion were
observed in the 672 volunteers who received vaccine and 11 cases were
observed in the 691 volunteers who received placebo. How could there
be less seroconversions in the placebo group than in the vaccinated
group?
18.
In addition, why didn’t the Merck vaccine not reduce the amount of
virus in the bloodstream of those who became infected; HIV RNA levels
approximately 8 to 12 weeks after diagnosis of infection were similar
in the vaccine and the placebo arms. Why was the ”HIV” RNA levels
in the blood of infected individuals more than in the non-vaccinated
group (40,000 copies/mL in the vaccine group and approximately 37,000
copies/mL in the placebo group)?
19.
Why in 1995, did the conclusions of The Office of Technology
Assessment Book (1995 Congress of the United States: Office of
Technology assessment. Adverse Reactions to HIV Vaccines: Medical,
Ethical, and Legal Issues. Roger C. Herdman, Director) were presented
to the 1995 Congress of the United States in 1994 by the AIDS
Research Advisory Committee (ARAC) of the National Institute of
Allergy and Infectious Diseases (NIAID) recommend that Phase III
clinical trials with enveloped vaccines should not proceed in the
United States because of scientific, political, and ethical issues,
and the significant level of scientific uncertainty about the wisdom
of immediate trials.
20.
Why did some of the conclusions specifically state, and I quote:
“Vaccines
may cause a false-positive HIV screening testing test resulting in
discrimination against vaccine recipients in, for example, military
service, health insurance, life insurance, employment, and travel?”
“Participation
in an HIV vaccine trial, itself, may result in stigmatization, as
others may assume that all vaccine trial participants are members of
groups, such as injection drug users and men who have sex with men,
who are at increased risk for HIV infection?”
“Vaccines,
relying on the protection afforded by an experimental vaccine, may
engage in behaviors that increase their risk for HIV infection?”
“There
is the potential for the viruses to be inadequately attenuated, for
an adequately attenuated viral vaccine to cause disease in
immunocompromised individuals (Read AIDS patients), and for an
adequately attenuated virus to revert to virulence. There is also
concern that a live attenuated vaccine could induce tumors.” Are
people who are immune compromised at increased risk of acquiring
“HIV” and if so, why immunize people at risk?
21.
At the end of the Congressional document, why is the term “original
antigenic sin” used to describe:
A)
When a vaccinated individual is exposed to a non-cross- reactive
strain of HIV that induces the production of antibodies specific for
the vaccine strain that are unable to neutralize the newly
encountered strain (in other words when a vaccine doesn’t work)?
B)
The fixing of an immune response in a non-adaptive pattern? What is a
non-adaptive pattern? Does this mean that an adaptive pattern is when
the vaccine evokes antibodies?
C)
When vaccinated individuals may be no worse off than unvaccinated
individuals because unvaccinated individuals also have a lag in
generation of antibody to HIV because their immune response has not
been “primed” by vaccination. Why should vaccinated individuals
be no worse off than unvaccinated individuals? Why bother
vaccinating?
22.
Why did the Office of Technology Assessment in 1995 state that:
“The
major factor influencing vaccine development is the
expected return on investment or profitability,
and the major obstacles to developing an HIV vaccine are scientific?”
Why are the major obstacles “scientific” according to the
congressional report?
23.
From Page 10 of the Office of Technology report presented to Congress
in the section entitled: “ADVERSE REACTIONS TO HIV VACCINES”
cont.),” it states that “as
of May 1994, 10 neoplasms (tumors) were observed among participants
in 9 vaccine trial protocols. One of the neoplasms was benign.”
Does this mean that the rest were malignant, and why
do you think that cancer was
only seen in 10 out of 9 trials?
24.
Will this vaccine be tested against an inert placebo, or will
adjuvants such as squalene be added to evoke a non-specific T-cell
response?
25.
If an adjuvant such as squalene is added, how do you explain the fact
that this adjuvant is used by scientists to cause rheumatoid
arthritis and other autoimmune diseases in experimental animals, but
was used in previous vaccine trials in humans?
I
am ready for the interview and the follow-ups whenever you are ready,
any day,
any place, any time.
In
expectation of your reply, I thank you very much.
Sincerely
yours,
Lambros
Papantoniou
Greek
Correspondent
202
675 0697
Washington,
D.C., December 1, 07
|
