Intended for healthcare professionals

Rapid response to:

Education And Debate

The politics of AIDS in South Africa: beyond the controversies

BMJ 2003; 326 doi: (Published 01 March 2003) Cite this as: BMJ 2003;326:495

Rapid Response:

Reply to Bennett: There is no Gold Standard 'HIV' Genome

Nicholas Bennett misrepresented what I stated regarding my argument
that 'HIV' is a misinterpreted 'HERV':

"Mr Russell has missed the point. I shall re-phrase: can he supply
the Genbank Accession number and reference the sequence(s) of the HERV(s)
which he is proposing activates to create the HIV genome deposited under
accession 1906382? If such sequences are not intact (i.e. exist as
scattered fragments) can he propose a mechanism by which they would be
expressed and recombine to form the full-length sequence? If not, then I
politely suggest he has no evidence whatsoever to support his view that
HIV is a HERV!"

The 'HIV' genome model is science fiction and absurd nonsense. There
is no such thing as a definitive 'HIV' isolate to begin with – so how can
there be an 'HIV' genome? There is no 'HIV' genome. When it is alleged
that 'HIV's recovered from different parts of the same body have differing
genomes - which is the true 'HIV' genome? No two identical genomes have
ever been recovered - not even from the same individual - so what are
they talking about? Typically: viruses which cause disease have identical
genomes. There is no gold standard 'HIV' genome because there is no gold
standard 'HIV' isolate and no gold standard 'HIV' test.

Bennett concluded:

"I have pointed out previously that animal retroviruses are sexually
transmitted, and in a preferentially male to female pattern [1]. I have
also shown that barrier contraception can prevent HIV transmission, which
suggests it's an endogenous sexually transmitted retrovirus [2].

1. Portis et al J Virol. 1987 Apr;61(4):1037-44. 'Horizontal
transmission of murine retroviruses.'

2. de Vincenzi N Engl J Med. 1994 Aug 11;331(6):341-6. "A
longitudinal study of human immunodeficiency virus transmission by
heterosexual partners. European Study Group on Heterosexual Transmission
of HIV."

These references are pure supposition and speculation and do not
prove that retroviruses are sexually transmitted – they are merely assumed
to be so: hardly what constitutes concrete evidence. How does Bennett
suppose the maedi-visna virus is transmitted?

If the paper by de Vincenzi were really true we would have had
millions of heterosexual cases of 'HIV' infections in the West by now – 20
years on - but we have nothing of the kind. This alone proved that 'HIV'
has to be an endogenous epiphenomenon ('HERV') and is (re)activated in the
original 'high-risk' groups whose specific disease conditions cause 'HERV'
(aka:'HIV') expression.

Padian et. al. seemingly contradicts de Vincenzi emphasising the
insignificance of heterosexual intercourse in transmitting 'HIV'. In this
10 year study, the authors state: male-to-female transmission was
approximately eight times more efficient, than female-to-male transmission
and male-to-female per contact infectivity was estimated to be 0.00090.(1)
Inadvertantly, Padian et. al. support my thesis that 'HIV' is a 'HERV' and
not an exogenously acquired (sexually transmitted) retrovirus.

Reference:(1) Padian NS, Shiboski SC, Glass SO, Vittinghoff E.
Heterosexual transmission of human immunodeficiency virus (HIV) in
Northern California: Results from a ten-year study. Am J Epidemiol

Of interest Bennett may care to read The Perth Groups challenge to
Peter Duesberg on the putative 'HIV' genome:

Papadopulos-Eleopulos et. al. Reply to Duesberg (II); Eleni
Papadopulos-Eleopulos, Valendar F. Turner, John M. Papadimitriou &
David Causer, Continuum, February-March 1997:

We gratefully acknowledge Peter Duesberg's criticisms of our paper
'HIV Isolation: Has it really been achieved?'. (1) Before responding it
will be useful to define some terms and objectives.

1. 19 'HIV' genomes

Duesberg: "...the weakest point of the HIV-non-existentialists is
their failure to explain the origin of '19 sequences encompassing the full
-length" 10-kb-HIV-1 genome" and "19 full-length HIV genomes"…".

(a) Let us repeat that the claim of the existence of "19 sequences
encompassing the full length, 10-kb-HIV-1 genome", "19 full-length HIV
genomes" is not one of our making but that of the HIV experts we quote.
The same experts accept that of the "19 full-length HIV genomes", no two
are the same either in sequence or even in length;
(b) The question we set out to answer in our critique was not what is the
origin of the 19 full-length HIV-1 sequences but does the presently
available data prove that these sequences represent the genome of a
unique, exogenous retrovirus, HIV? The answer, we repeat, is NO.
Nonetheless, although it was not our task to determine the origin of these
sequences, we did present a number of alternative mechanisms that science
offers as a "rational origin for such sequences" in addition to "viruses
or other infectious agents".

2. Odds of assembly

"Remember the odds of coming up with even one nucleotide sequence of
9150 bp by chance are astronomically low namely, 1 in 49150 which is very
close to 0."

It is apparent that we and Peter Duesberg are referring to two
entirely different systems, one completely random and the other heavily
biased by cell and culture conditions. True, the probability of assembling
a particular sequence of RNA (DNA) of 9150 bases randomly selecting each
of the four nucleotides is one in 49150 However, this statistical
reasoning bears no resemblance to how nucleic acid polymers are assembled
either in vivo or in vitro and thus on the probability of finding a
particular unique sequence. That this is the case is best illustrated by
Spiegelman’s minivariant, a 220-nucleotide stretch of RNA of unique length
and sequence which was discussed in our Continuum paper. The probability
of assembling such a unique RNA stretch by chance is 1 in 4220, also "very
close to 0"" yet, under certain conditions in the laboratory, the
Spiegelman minivariant is frequently produced indicating that the assembly
of nucleotides is anything but a random process. Furthermore, the 19
unique sequences do not have to be assembled from the four, individual
nucleotides. They may result, for example, by recombination of:

(a) stretches of pre-existing cellular DNA sequences;

(b) stretches of DNA sequences of endogenous retroviruses which form
1% of the cellular DNA, a phenomenon accepted to take place quite
frequently and to result in the assembly of novel genomes. It is also
accepted that the conditions affect the recombination both qualitatively
and qantitatively.

It is significant that as far back as 1985 both Gallo and Montagnier
accepted that it is not possible to generate "HIV" and the effects
attributed to it unless the cells are activated (stimulated) and that this
year Chermann and his colleagues showed that the infected cultures contain
fragments of the "HIV genome" but after PHA stimulation there is an
increase in the "full-length genome" and a concomitant decrease in the
fragments. (2) Whatever the odds may be of obtaining by chance the
conditions necessary to generate "even one nucleotide sequence of 9150
bp", it is certain not 1 in 49150.

3. Viral genome

Duesberg: "The non-HIV-existentialists also fail to realize that
available isolation efforts have already adequately identified the 9150
bases as the genome of a virus".

ln our extensive search of the HIV literature we could not find even
one reference, (although it is possible we may have missed some), in which
the HIV genome was reported to of 9150 nucleotides. The closest length was
reported Montagnier’s group who, in 1984, reported it to be 9.1 to 9.2
kbases and, in 1985, as 9193 bases. (3,4) lf the 9150 base DNA is the
genome of a virus then an absolutely necessary but not sufficient
condition is that the virus in all infected individuals will have a length
of 9150 bases. Yet, two HIV genomes of the same length have yet to be
reported. More importantly, the length of an RNA (DNA) fragment, no matter
how often such a fragment is detected, provides no information regarding
its origin. The only way to prove it belongs to a unique virus is to
isolate a viral particle and demonstrate it has a genome of 9150 bases.
This has not been done and the"available isolation efforts" do not contain
even suggestive evidence let alone proof that a 9150 base long RNA is a
constituent of a particle, any particle much less a viral particle.

Competing interests:
None declared

Competing interests: No competing interests

02 April 2005
Alexander H Russell