Department of Medical Physics, Royal Perth Hospital, Western Australia,
F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso,
Sam Mhlongo, Todd Miller, Andrew Maniotis, Christian Fiala
Send response to journal:
Re: More responses to Christopher Noble
to Christopher Noble
his rapid response "Re: Still no proof for a correlation between the HIV PCR and
antibody tests", 11th February, Christopher Noble wrote: "The
Perth Group write "Nowhere in the text of the Owens et al paper do the authors
confirm or even mention whether any of the studies in their analysis included
controls from a "non-diseased population", "at risk for HIV infection". Under
the subtitle, "Recommendations for Study Design" they wrote: "Many of the
studies we analysed had design limitations?incomplete representation of the
spectrum of patients in the study population, insufficient sample size, and
incomplete reporting of test results. To increase the generalisability of study
results, the study sample should reflect the entire spectrum of disease
encountered in the clinical population of interest. For example, the nondiseased
population should include persons who are at risk for HIV infection and would be
candidates for testing rather than healthy controls".
What would be Christopher Noble's interpretation of the above?"
The above passage means exactly what it says no more and no less. If The Perth
Group could be bothered to read the studies that Owens et al used in their
metastudy they would indeed find that many of the studies did include
non-diseased (not HIV infected) groups that were in high risk groups. The
correlation between HIV antibody tests and HIV PCR tests remained."
Let us repeat
our request once again:
1. Of the
"many" studies could Christopher Noble please give us one which included
"non-diseased (not HIV infected) groups that were in high risk groups" and which
satisfied all the criteria set by Owens et al.
2. One study which included non-HIV/AIDS individuals but who nonetheless were
sick and which satisfied all the criteria set by Owens et al.
Noble wrote: "It is extremely obvious that it is impossible to "prove"
anything to someone that will never accept any evidence that contradicts their
problem is not that we won't "accept any evidence that contradicts" our
"dogmatic beliefs" but that we have not been given any evidence. No amount of
convincing and references (including Owens et al) would make us accept
Christopher Noble's claim that the PCR and the antibody tests are highly
specific and that a correlation exists between the "HIV" PCR and antibody tests
if he does not give us a reference which satisfies some basic scientific
principles. These include randomisation, blind performance and the use of
proper controls and a gold standard. One does not need to be a scientist to
realise that any study which does not satisfy these conditions would be flawed.
Noble wrote: “It is fruitless and pointless to even attempt to prove anything
to the Perth Group. Any paper that presents evidence that contradicts their
hypotheses will be deconstructed and "flaws" will be found. "
A response to
this accusation can be found in the rapid response: "That is a Scientist’s
Responsibility", 19th February by Mark Bartlett. We thank him for his support
and cannot improve upon his answer.
Christopher Noble wrote: "The Perth Group write "If a positive HIV-2 antibody
test was proof for HIV-2 infection and if the primers were amplifying the env
gene, then: (i) each primer pair should have given positive results with all 42
samples; (ii) all samples should have tested positive with all primer pairs."
Hughh. What are you talking about? You have previously drawn our attention to
the genetic diversity of HIV. Now you expect one PCR primer to amplify all
strains of HIV-2. The only thing that your response demonstrates is your
determination to ignore any evidence that contradicts your hypotheses."
It is true that
we have drawn Christopher Noble's attention to the genetic diversity of "HIV-1".
It was Christopher Noble who, all along in this debate, tried to convince us
that a virus can vary by more than 50% at the nucleic acid level and by more
than 81% at the amino acid level and:
1. it would still be possible to define "HIV-1" infection in molecular terms.
2. "HIV-1" infection could be diagnosed using the same antibody test. (Although
he claimed that different tests are used to prove infection with "HIV-1" group 0
he could not provide such evidence).
3. the proteins would still perform the same function.
4. it would still be possible to develop a vaccine.
Our view was, and still is, the opposite.
In particular we have claimed that, given the genetic diversity of "HIV-1", it
would not be possible to define "HIV" infection in molecular terms, that is by
hybridisation and PCR. The Damond et al findings support our claim. Although
they used a small number of patients (42) and 5 primers they could not detect
the "HIV-2" env gene in all the 42 "HIV-2" positive individuals. To detect the
env gene in all "HIV-2" positive individuals many more primers would be
necessary. If similar numbers of primers are necessary for the detection of all
the other genes the detection of the whole "HIV-2" genome would require the use
of a very large number of primers.
Given that the "HIV-1" genome is more diverse than that of "HIV-2" and that many
more people are infected with "HIV-1" the number of primers needed to detect the
whole "HIV-1" genome in all "infected" individuals, that is, to define "HIV-1”
infection in molecular terms in these individuals, would be prohibitory.
Christopher Noble wrote: "The Perth Group write: "However, after repeated
questioning he [Montagnier] admitted that reverse transcriptive activity is not
specific to retroviruses and thus, indirectly, that he did not isolate HIV"
Montagnier has not, directly or indirectly, admitted that he did not isolate
HIV. This is purely your spin, your interpretation and your lies."
response to this accusation can be found in the rapid response: "Re: Re: Still
no proof for a correlation between the HIV PCR and antibody tests", 14th
February by Murali Mohan. We thank him for his response and are unable to offer
any improvement to his reply.
Christopher Noble wrote: "The Perth Group write: "Repeat, although maybe not
to his liking, we have honestly answered all Christopher Noble's questions. If
he wishes he may repeat them and we will answer them again."
Half a year ago I asked you to provide a citation for your claim that "the
genomes of the most variable RNA viruses do not differ by more than 1%". So far
you have not done so. You have repeatedly cited a paper that says nothing of the
In the study we
have cited the authors even gave several reasons, based on sound biological
principles, why the variability of the viral genomes cannot be much larger than
1%. In fact, to avoid any misinterpretation we have repeatedly quoted these
Noble wrote: "It is imperative in science that you accurately report the
contents and findings of the papers you cite.
Once again you do exactly the opposite.
You write: "The largest, longest, best designed and executed studies conducted
in the USA and Africa show that HIV is not heterosexually transmitted.24-27"
The first reference you give is 24. Gray RH, Wawer MJ, Brookmeyer R, et al.
Probability of HIV-1 transmission per coital act in monogamous heterosexual,
HIV-1 discordant couples in
Lancet 2001; 357:1149-1153."
It is a blatant lie to claim that this study shows that HIV is not
means 4 references. Christopher Noble claims that ref. 24 does "not show that
HIV is not heterosexually transmitted". Does it mean that he agrees with us
that the other 3 references show "that HIV is not heterosexually transmitted"?
Secondly, the only way to obtain epidemiological evidence for heterosexual
transmission is to follow a large number of discordant couples in prospective
studies where other confounding, non-sexual routes of transmission are excluded.
No such studies have been published from Africa. The claims of heterosexual
transmission are based on the prevalence of "HIV-1" seropositivity and the equal
number in men and women, or at best, in cross-sectional studies.
In the Gray et al community based study, "174 monogamous couples in which one
partner was HIV-1 positive, were retrospectively identified from a population
cohort" of 15,127 individuals aged 15-59 years of age in a period of 4 years.
Like in the Padian et al cross-sectional part of the study, in the Gray et al
study non-sexual routes of transmission cannot be totally excluded. Neither did
the authors exclude anal intercourse.
The estimated infectivity for male-to-female transmission was the same in both
studies, 0.0009 per sexual contact. According to this estimate, it would take
770 or 3333 sexual contacts respectively to reach a 50% or 95% probability of
becoming infected. If sexual contacts were to take place repeatedly every three
days this would require a period of 6.3 and 27.4 years respectively. Padian
estimated that male-to-female transmission was "approximately eight-times more
efficient than female-to-male", while Gray et al estimate that the probability
of transmission per sexual contact for female-to-male was 0.0013. Again,
assuming sexual contact occurs on average once every three days, according to
the Padian estimates would require 51 and 222 years to reach a probability of
50% and 95% respectively and to Gray's et al estimates 4.4 and 19.5 years .
Gray et al concluded: "The probability of HIV transmission per sex act in Uganda
is comparable to that in other populations, suggesting that infectivity of HIV
subtypes cannot explain the explosive epidemic in Africa". If: (i) there is no
more heterosexual transmission in Africa than anywhere else; (ii) in the Padian
prospective study the transmission was zero;
then in Africa, like anywhere else, "HIV" is not sexually transmitted.
If only for this fact it is imperative to discover the reason(s) for the very
high level of seropositivity in Africa.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, et al. Mother to Child
Transmission of HIV and its Prevention with ATZ and Nevirapine. pp 204.
Perth: The Perth Group, 2001.
The Perth Group