Response to CNOB: Part 1

This is the first part of a reponse to points made by Dr Chris Noble. Posted on the HIV/AIDS Alternative Views forum on 15/10/02:

My position is that HIV has never been proven to be exogenous, it is harmless anyway and the antibody tests can prove nothing more than antibody production above an arbitrary threshold level.

You state:

"Each test uses the serum dilution that gives the best balance between sensitivity and specificity. There is nothing fishy about dilution."

"Different Anti-HIV tests do work at a variety of serum dilutions from 1:2 to 1:400. In each case the amount of antigens and the optical density cut-off value is given for that particular serum dilution. If you do not use the correct serum dilution for that particular test then the test will not work at the specified sensitivity and specificity."

The amount of antigen is independent of the serum dilution. Antigen is not diluted, it is laid down in the microtiter wells prior to adding diluted serum. What you appear to be saying is that the amount of antigen applied varies in accordance with the extent of serum dilution. Can you expound upon the rationale for doing this? Why should this be more accurate than always using the same amount of antigen and the same dilution factor? The optical density cut-off value cannot possibly be anything other than arbitrary anyway. The phrase "Best balance between sensitivity and specificity" is meaningless here. What other retroviral ELISAs also employ this dubious strategy over a similar dilution range?

Even if the proteins used were unique to HIV (which they are not) and had been proven HIV-specific (which they have not) non-specific antibody binding would remain problematic. The rationale for the high dilution (1 in 400) was to minimise non-specific antibody binding. Using a 1:2 dilution will exacerbate this non-specific effect despite the use of recombinant derived proteins and approriate adjustment of antigen quantity. If non-specific antibody binding were not a problem there would be no need whatsoever for dilution factors or indeed for optical density cut-offs.

You say that unless the exact dilution factor specified for a particualr test is adhered to, the test will give incorrect results. Therefore when the specified dilution factor IS used there is no margin of error in these tests for somone who may have a higher level of non-specific antibodies for one reason or another. They will test positive.

That ELISA tests are used for the detection of other viruses etc. does not validate their use for HIV. The most basic flaw, which applies to all these tests, is that antibody detection is not equivalent to detection of the infectious agent. For example, persistent false positive ELISAs have been reported even for the Foot-and-Mouth virus, a virus that (unlike HIV) has not only been isolated as a virus but has even been crystallised and had its crystal structure determined to 2.9 angstroms resolution!

You state:

"The primers used in HIV PCR are quite specific. If HIV was endogenous then everyone would have a detectable HIV virus load. They don't. This should be the end of the story."

Dogmatic statement.

The requisite controlled studies have not been done to establish the extent of PCR positivity in HIV negative people. We should have a study showing ABSOLUTE ZERO "viral load" without exception in a large number of healthy HIV negatives and in a large number of HIV negatives with otherwise AIDS defining conditions, the contamination excuse is no excuse. We should also see non-zero "viral load" in all HIV positives without exception, This would still not be sufficient to prove an exogenous origin because the "viral load" test may be picking up genetic sequences that are produced and transcribed only under the particular intracellular conditions indicated by a positive ELISA. Most of the "HIV" primers originate from leukaemic cell lines that have shown evidence of endogenous retroviruses induced by the methods used to "isolate" HIV. The "viral load" test detects only small stretches of DNA so zero "viral load" cannot prove the absense of other "HIV DNA" sequences thought to comprise the HIV genome.

You imply that HIV is an ordinary retrovirus by referencing mutation rates in other retroviruses:

I wonder why the author of this paper did not investigate mutation in HIV.

Grandiose claims are made for HIV on the basis of its mutative abilities and you provide a reference stating that the mutation rate of retroviruses is an order of magnitude less than polio. Why does the mainstream persist in making extraordinary claims on behalf of an ordinary retrovirus?

Consider the case of an anti-retroviral na´ve person who, as a result of the combos, attains an undetectable "viral load" and, in the continued presence of anti-retrovirals, the "viral load" remains as such for a protracted period. The virus is supposedly being specifically targeted by 3 different drugs, 2 of which target the virus in completely different ways and you also state that the virus has highly conserved regions for essential genes. It is untenable, if what you say about HIV is true, that there be sufficient viral replication going on to provide the mutations which would lead to competent mutated virus and cause the 'viral load' to become detectable and continue to rise, yet we are told this is what happens.

It has been admitted that even if "viral load" is in fact the actual number of HIV virions present then what it detects is almost entirely incompetent, non-infectious HIV, which is what would be expected for a virus with a mutation rate much higher than you claim with essential genes that are NOT highly conserved. Consider this extract from page 203 of Ho, NEJM, Vol. 332, p201-208, 1995:

"plasma cultures were uniformly negative for infectious virus in tests of nine subjects involving up to 1 ml of sample. However, particle-associated HIV-1 RNA was detectable in four subjects by an ultrasensitive branched-DNA assay, the values ranged from 839 to 11549 copies of RNA per milliliter of plasma"

So, even when the 'viral load' is 10,000 there is no detectable competent HIV, even in the wild-type. "HIV protease" genes have been found to be "extremely variable" i.e. over 40%(3).

You say:

"You can also take these cultures and purify the virus and look at it under an electron microscope. You can see the little knobs and the characteristic inner core."

Such electron micrographs of 'HIV'are of cultures grown sometimes for weeks in the total absence of an immune system. The process involves the use of cancerous cell lines stimulated with mitogens and other oxidative chemical activators.

Refer us to the electron micrograph showing only uniform purified HIV retroviral particles such as Etienne De Harven was able to easily produce in two days for other retroviruses. Continuum Vol 5 No. 5 page 57 compares the uniform image of purified retrovirus particles obtained by De Harven with the junk produced by HIV junk science (7). De Harven's image consists almost entirely of uniform viral particles. The Gluschankof et al image consists almost entirely of cellular junk. Whereas De Harven has to use three arrows to identify impurities Gluschankof et al, by total contrast, have to use three arrows to identify three "viral" dots which may or may not be HIV, or even retroviruses, in their culture-derived rubbish tip. This is a graphic illustration of the shoddy scientific standards applied in the world of HIV/AIDS.

Until the early 1980s, for the isolation of animal retroviruses, retrovirologists meant purification when they used the word isolation. Even the finding of particles with the appearances of retroviruses is not proof that such particles are retroviruses and even less is it proof that a particle is a particular retrovirus. Particles bearing the morphological characteristics of retroviruses are ubiquitous. Such particles have been frequently observed in human leukemia tissues, cultures of embryonic tisues and the majority of human placentas. To prove that retrovirus-like particles are a virus they should be isolated, their proteins and RNA characterised and it should be shown that infection of cell culture with these particles produces the same particles, proteins and RNA. This is so fundamentally obvious it should not need to be stated.

To quote the Perth group:

"When hard pressed all the HIV experts will ultimately accept the non-specificity of retroviral-like particles, reverse transcription and antibody/antigen reactions. However, to date no retrovirologists, not even Peter Duesberg, will agree with us that novel RNA may appear in cells without prior exposure to infectious agents. For all such scientists the presence of novel RNAs in AIDS patients is unambiguous proof of HIV infection although no 2 identical HIV RNAs have been reported so far."

"From the beginning of the HIV era it became obvious that no two HIV genomes are identical, not even from the same individual. While the genomes of the most variable RNA viruses do not differ by more than 1% (9) and the difference between the human and chimpanzee genomes is no more than 2%, there is up to 40% variation between the "HIV" genomes."

We know that under certain conditions such as cell shock, genomic reorganisations can occur. We also know that RNA editing can occur whereby the nucleotide sequence of an RNA molecule can change markedly from the sequence corresponding to the DNA template from which it is transcribed. This was discovered in the 1980s.

Gallo and Montagnier accepted that it is not possible to generate 'HIV', and the effects attributed to it, unless the cells are stimulated. It has also been observed that 'infected' cultures contain 'fragments' of the 'HIV genome' but after PHA stimulation there is an increase in the 'full-length genome'.

You state:

"You can download the sequences for HIV at pubmed.
Search nucleotides for "HIV complete sequence"
You can then use the BLAST progam to search the database for matches in the human genome and
in the fruit fly genome.
The closest matches for the human genome is only 30 or so base pairs."


we read:

"While the draft sequence of the human genome was officially launched early in 2001, data are produced on a continuous basis. This allows the reference human genome sequence to be further refined and completed as an ongoing process. At NCBI, NEW VERSIONS OF THE ASSEMBLED GENOMIC SEQUENCE ARE RELEASED EVERY FEW WEEKS."

Under the heading "Preparing Input Data" (for the human genome) at
we read:

"The sequence data are first screened for contaminating sequences and blasted against the genomes of other completely sequenced organisms. ANY CLONE CONTAINING SEQUENCE FROM ANOTHER ORGANISM IS ENTIRELY REMOVED FROM THE INPUT DATA SET."

Sounds like any "HIV proviral" sequences would be automatically removed from the human genome by definition. You say that your rock solid certainties about the exogenous nature of HIV are shared by your colleagues, if this is true then your colleagues would definitely ensure the removal of any such sequences from the genome.

Searching the database under "HIV-1 complete genome" reveals 265 complete "HIV-1 genomes". Equivalent searches for all other retroviruses reveal at most only 29 complete genomes. So you are telling us that you have tested all 256 'complete HIV genomes' using BLAST and get at most a 30 base pair "HIV" sequence that matches exactly with human DNA? The 265 "HIV-1 genomes" would all be the same length if they really represented complete HIV genomes. I checked the first 30 genomes listed. The mean length is 9037 bp and the range is 1162 bp! We should, as you say, have a very high degree of homology among the sequences coding for the essential retroviral proteins for all those 265 genomes, can you show this is the case? There are a large number of differing "complete HIV genomes" in even a single HIV positive individual. Piecing together bits of DNA with "overlapping" regions to produce a complete HIV genome does not reflect the genetic diversity of HIV and doing this construction is meaningless anyway if you have not proved that these bits belong to an exogenous retrovirus. As you say, all viruses need host cells to replicate, if HIV replicated to any significant degree in the cells of the human host then there would be no need to resort to in vitro cell culture to generate 'viral particles' of HIV. How many of those 265 genomes were both directly recovered from fresh patient sera without cell culture and also found in their entirety rather than having to be constructed? In 1990 the HIV genome was said to consist of 10 genes, Montagnier said in 1996 that it has eight genes and Bare-Sinoussi said in the same year that it has nine genes! If the HIV genome had been derived from purified viral paricles there would have been no equivocation regarding its genetic composition. HIV has been defined by man, not by nature.

As you said yourself, the human genome contains endogenous retroviuses (HERVs). At the time of Gallo and Montagnier's discovery of "HIV", HERVs were thought not to exist.

Alu retrotransposable elements represent over 5% of the mass of the human genome. They are transcribed by RNA pol III, reverse transcribed and inserted in a new place in the genome (1). This process is stimulated by cellular stresses and can produce novel genetic sequences (2). One of the proteins made by 'HIV' associated genes, the tat protein, up-regulated the expression of Alu retroelements (4). Tat activity has been found in some HERVs (5). We already know that in the HIV negative human genome there are two HIV-like sequences that are important in HIV and in endogenous retroviruses (6). Maybe this "normal human DNA" is capable of combining with HERV sequences through Alu mediated recombination to form unique genomic sequences which are simply called HIV when they are found.

All the proteins used in the HIV test are associated with Gag, Pol, and Env genes which are found in all endogenous retroviruses and HERVs can generate immune responses in humans.

You say:

"If we take these same sequences and insert them in bacteria then the bacteria start producing exactly the same proteins that make up the 'alleged' HIV."

So what? Why does this mean that HIV must be exogenous?

What it boils down to is that until you can show that these HIV associated genetic sequences are actually derived from viral particles by obtaining pure retroviral particles you will never be able to prove that HIV is exogenous. Furthermore, it should be obvious to a scientifically minded person that such pictures of densly packed, pure retroviral HIV particles must be obtained from the fresh plasma of HIV positive subjects rather than derived from cell culture. It is unscientific to call a genetic sequence an exogenous retrovirus when the possibility that it could instead result from dynamic endogenous genetic processes (about which there is much more to learn and discover anyway) has not been eliminated.

One final point:

Lee et al (J. of AIDS, Vol. 7, 1994, p381-388) found that in the absense of "antiretrovirals" there was "little or no change in the concentration of circulating HIV DNA positive cells from study entry to the 5 year follow up visit for most subjects" although all had continuous CD4 count decline. Fig. 3 on page 385 shows little change in HIV DNA copy number from the initial value at seroconversion, there are even transient and sustained decreases. Despite this there were CD4 cell count declines from 1049 to 46 and from 1063 to 276 cells/ml 5 years postseroconversion. T-cells are short-lived and AZT is supposed to prevent the spread of "HIV provirus" to other T-cells so HIV RT inhibitors should therefore eventually cause complete clearance of HIV 'provirus' from peripheral blood T-cells. In fact "proviral HIV" otherwise known as "viral burden", was found to be CONSTANT in the presence of AZT (8). The only possible explanations for this are that AZT is a useless inhibitor of HIV RT and/or HIV DNA is endogenous. To employ your own phrase "You can weasel all you want but you can't get away from this." If AZT has no effect on "viral burden" because it is a useless inhibitor of HIV RT but yet it makes "viral load" (as "HIV RNA") go down then "viral load" cannot be measuring an HIV-specific effect. Think about it.


1. Deininger, P. L. et al, 1999. Alu repeats and human disease. Mol Genet Metab. 67(3):183-93.

2. Urnovitz, H. B. et al 1999. RNAs in the Sera of Persian Gulf War Veterans Have Segments Homologous to Chromosome 22q11.2. Clin Diagn Lab Immunol. 6(3):330-335.

3. Kozal, M. J. et al 1996. Extensive polymorphisms observed in HIV-1 clade B protease gene using high-density oligonucleotide arrays. Nature Medicine 4(7):753-759

4. Jang, K. L., et al 1992. The human immunodeficiency virus tat protein increases the transcription of human Alu repeated sequences by increasing the activity of the cellular transcription factor TFIIIC. J. Acquir Immune Defic Syndr. 5:1142-7.

5.Nakagawa, K. et al, 1996. The potential roles of endogenous retroviruses in autoimmunity. Immunol Rev. 152:193-236.

6. Horwitz, M. S. et al 1992 Novel human endogenous sequences related to human immunodeficiency virus type 1. J. Virol. 66: 2170-2179

7. Gluschankof et al, 1997. Cell membrane vesicles are a major contaminant of gradient-enriched Human Immunodeficiency Virus Type-1 preparations. Virology 230:125-133.

8. Donovan, R. M. et al, 1991. HIV-1 proviral number in blood mononuclear cells from AIDS pateints on Zidovudine therapy. J. Aquir. Immune. Defic. Syndr. 4:766-9.

9. Steinhauer and Holland, 1987. Rapid evolution of RNA viruses. Ann. Rev. Microbiology 41:409-33