Response to CNOB: Part 2

Message first posted on on 30/03/03

This is my response to:

not posted on that thread out of respect for the rules.

Dr Noble

With regard to:

"The only confusion is that deliberately created by the Perth group. If you actually read the references given by the Perth group you find that there is no inconsistency. HIV-1 and HIV-2 each have exactly NINE genes. Of these EIGHT are common to both. This means that there are a total of TEN different HIV genes." your statement "If you actually read the references given by the Perth group you find that there is no inconsistency" is a LIE.

Figure 3 on page 272 of Lazo and Tsichlis (Seminars in Oncology, Vol.17, No.3 1990 pages 269-272) shows HIV-1 and HIV-2 as both having TEN genes with HIV-1 and HIV-2 having NINE genes in common. In Montagnier et al 1996 (MJA Vol.164 p161-173) we read on page 161 "The structure of HIV-1 is shown in box 3.1.2 (HIV-2 is very similar)" In box 3.1.2 on page 162 entitled "Structure of the human immunodeficiency virus" there are only EIGHT genes. In the article by Barre-Sinoussi published in the same year (Lancet Vol. 348, 1996, pages 31-35) figure 3 on page 33 shows HIV-1 and HIV-2 as both having NINE genes with EIGHT genes in common.

You say:

"Nor is there the uncerntainty in the number of nucleotides as they would have you believe. The HIV genome has two regions of Long Terminal Repeats that flank either side. The complete HIV genome sequences in the database differ in the amount of these LTRs. The genes themselves are in the same place."

An HIV genome with incomplete or missing LTRs is not a "complete HIV genome". Also the variability in the length of these "HIV genomes" is not solely due to incomplete or missing LTRs. Even according to Brian Foley "They (sic) HIV-1 genome is roughly 9,700 bases long (some a bit shorter, some a bit longer due to insertions and deletions, primarily in the env gene)." The "HIV genome" lacks the coherence needed to apply a basic mathematical analysis to its constitiuents. HIV is a construct.

You say:

"This is a ridiculous argument. There is roughly an inverse relationship between the variability of a genome and its size. The genomes of mammals are very constant. In comparison other viruses such as influenza and human papilloma virus show differences of more than 60% between different strains. HIV is not an exception. Comparing mammals and viruses is blatanty stupid and dishonest."

Of course the analogy comparing animals with viruses is an artifice but it serves to highlight a point. You mention two strains of flu with a greater than 60% genetic variation, reference please. Have two flu virus sequences that differ by over 60% both been shown have their essential genes conserved and therefore produce pathogenic virus? How much time was there between the appearance of these strains? Please justify with references. You are referred anyway to one of your old Virusmyth postings:

Re: I capitulate! KEY = 995000035 By Chris Noble 13 Jul '01 - 04:53 h

">A total of 105 VP1 genes of poliovirus were sequenced, and in the 95,688 nucleotides analyzed, no mutations were observed. We then calculated mutation rates of 1.5 X 10(-5) and less than 2.1 X 10(-6) mutations per nucleotide per infectious cycle for influenza virus and poliovirus, respectively."

You mentioned dishonesty, your statement proclaiming over 60% variation between different strains of human papilloma virus is YET ANOTHER LIE! Even looking at the variation of ALL papilloma viruses (not just human papilloma viruses amongst themselves) it is at most 50% (see below). Papilloma viruses comprise viruses that infect a large number of animals including horses, cows, pigs, birds, reptiles, ...etc.

To quote from J Clin Virol 2000 Oct;19(1-2):43-56: Comparison of papillomavirus and immunodeficiency virus evolutionary patterns in the context of a papillomavirus vaccine. [interjected comments are in square brackets]:

"Consideration of the major features of the phylogenetic trees of the simian immunodeficiency virus (SIV)/HIV `family' and of the papillomaviruses (Fig. 1 and Fig. 2) [all papilloma viruses, not just human] reveals certain similarities. First, THE MOST DIVERGENT ISOLATES DIFFER FROM ONE ANOTHER BY AS MUCH AS 50% on the nucleotide level, even in the most conserved regions of the genome."

"There are also salient differences. The rates of mutation and/or substitution are remarkably different. This is reflected by differences in temporal and geographic heterogeneity of sequences. There is considerable variation among geographic regions in the prevalence of HIV subtypes (differing from one another by up to 35% on the nucleotide level; reviewed by Jaffe and Schochetman, 1998). In CONTRAST HPV types (differing from one another by more than 10% in L1 [Note: JUST L1] and commonly by 30% or more) are more uniformly distributed. Only at the level of the variant (differences between isolates in CODING REGIONS generally <3%) is variation in HPV geographic distribution THE NORM. Likewise, whereas evolution of HIV sequences can readily be observed within a patient and the overall diversity of HIV-1 sequences has increased during the course of the pandemic, HPV isolates have arguably been STABLE during the period for which we have sequence data. ISOLATES THAT ARE IDENTICAL OVER MORE THAN 3500 NUCLEOTIDES HAVE BEEN OBTAINED IN DIFFERENT YEARS AND DIFFERENT GEOGRAPHIC LOCATIONS. Variants of HPV16 sequenced by Yamada et al. (1995) are identical to the corrected sequence of the HPV16 prototype (Seedorf and Myers) over such lengths. Intra-patient variation within a given HPV type is thought to be rare [Note the word RARE...while intra-patient variation is ALWAYS found for HIV for EVERY SINGLE genomic sequence.] ( Xi et al., 1995). When detected, it is arguably due to co-infection with pre-existing genotypes rather than to acquisition of mutations, since the distinct variants within an individual can generally be found in other hosts ( Ho; Ho and Xi)."

[Note: coding regions means those regions that code for protein]

"These differences between the two virus families have left their marks on the observable diversity within the HPV type/HIV subtype, as illustrated in Fig. 3 and Fig. 4. ESSENTIALLY, ANY DEGREE OF DIVERGENCE MAY BE OBSERVED BETWEEN HIV ISOLATES [What a virus--can do super-natural things!] although it is necessary to compare epidemiologically linked isolates to see highly similar viruses. There are arbitrarily many HIV isolates that would constitute new `types' by the criteria applied to papillomaviruses (>10% dissimilarity); indeed, any new HIV isolate that is not known to be epidemiologically linked to previous isolates has a good chance of satisfying these criteria. IT IS THE NORM FOR TWO CLONES FROM A SINGLE HIV ISOLATE TO SHOW AT LEAST SOME VARIATION [WHY is that-- and why only HIV]. In contrast [Note CONTRAST], within the HPVs, most types show relatively small ranges of divergence around the consensus pattern. [Note the word SMALL] Furthermore, it is not generally possible to find large numbers of new types within an extensively studied group (for example, Chan et al., 1997b), although introduction of improved detection systems within a less-well studied part of the tree may result in the identification of many new types ( Bernard; Berkhout; Shamanin and Chan, and many others). Repeated sampling from an individual reveals stability of the genome ( Xi et al., 1995)."

Here is another snipit from the boards:

Dan 23 Jul '01 - 14:43 h:

"I have posed 10 variable points related to HIV which Mr Noble has refused to answer. Virus has brilliantly searched the literature and presented the following answer were it is clear that HIV variability relative to HPV is unique and not comparable. Now that the fleeting illusion of genetic sequence has been ruthlessly destroyed by Virus were will Chris Noble go from here? What is the cut off Chris?"

For yet more evidence that genetic variation in "HIV" is exceptional consider the following quotes from Nature Medicine Vol. 2(7), 1996 p 753-759 Extensive polymorphisms observed in HIV-1 clade B protease gene sequence using high-density oligonucleotide arrays.

Page 753:

"In this report we describe the sequence analysis of the pr gene in 167 HIV-1 viral stocks from 102 protease inhibitor na´ve patients collected from different geographic regions of the United States."

"Given the enzymes relatively small size and the constraints in its structure imposed by function, it was reasonable to conclude that sequence variability in HIV-1 would be limited."

Page 754:

"A cross-sectional analysis of gene sequences from 167 isolates revealed the pr gene to be HIGHLY polymorphic. A TOTAL OF 41% OF THE NUCLEOTIDES AND 49.5% OF THE AMINO ACIDS WERE VARIABLE"

Page 753:

"These studies have helped foster an appreciation of the virus's EXTRAORDINARY GENETIC VARIABILITY"

Note that this is a 41% variation in an ESSENTIAL gene. This is unheard of in other viruses.

It is my understanding that Eigen invented the term quasispecies to describe self replicating RNA in the absence of a "template", however, the "HIV RNA", is said not to be a self replicating RNA, but replicates through a DNA intermediate. HIV therefore does not meet the definition of a quasispecies and this definition has been appropriated by AIDS Inc. to mask the extrordinary genetic variability of "HIV". 1% sequence differences refer to self replicating RNA in the presence of a template and as such do not meet the quasispecies definition either. It is notable that the genetic variability attributed to SELF REPLICATING RNA IN THE ABSENCE OF A TEMPLATE is about 40%! Does that figure ring any bells in relation to HIV?

Finally, here is another quote from Brian Foley:

"Almost all regions of the HIV-1 or HIV-2 or SIV genome are "novel" or unique to the individual viral isolate from which they are obtained. The pol gene evolves more slowly than the env gene over time, but all regions of the genome evolve at some rate. ONLY VERY SHORT REGIONS, SUCH AS THE LYS-TRNA PRIMER-BINDING SITE, AND THE POLYPURINE TRACT, ARE HIGHLY CONSERVED IN ALL SIVs AND HIVs. THESE SHORT REGIONS ARE LESS THAN 50 BP IN LENGTH."

In which "HIV" genes do these short "identifying" sequences occur? Because they don't vary ,it must be the sequences from these short regions to which the PCR primers are complementary, isn't that right? And what gene products are used in the antibody tests for identifying HIV? Could it be products from the gag, pol and env genes that also happen to be expressed in all endogenous retroviruses which can generate immune responses in humans? (1, 2) No, of course not.

You say:

"John Kirkham also hides there because that and a few other Denialist websites are the places where he can put his pseudoscientific drivel without any challenge."

This comment says more about you than it does about me. You have no grounds for saying that I hide. I have "debated" with you several times in the past and it was not me that banned you from the Alternative Views forum, indeed I prepared a very long response (Response to CNOB) to all of the claims you made while you were still posting there. As Mark knows from my discussion with him on the Alternative Views forum I don't think it is right to pound this forum with dissident postings and you should respect that. If anyone wants a comprehensive presenation of the dissident case they can search through the great many postings on the Alternative Views forum where your posts remain undeleted by the way.

To someone who appreciates the value of controls and the application of rigorous scientific standards, HIV/AIDS is pseudoscientific, it cannot be otherwise. I am now at the stage where I have said almost everything I have to say on HIV/AIDS. For me the AIDS debate comes down to the following: Should fear, self-interest and deference to authority be allowed to short-circuit critical thought and extinguish the freedom of expression of those who are still willing and able to execise their critical faculties on HIV/AIDS? A recent example that HIV/AIDS is driven by dogmatic declarations from a small group of "experts" is the UN insistence upon the correctness of the official position on the sexual transmission of "HIV" in Africa.

In HIV/AIDS, insistence substitutes for scientific method.

John Kirkham

1.Lower et al (1996) Proc. Natl. Acad. Sci. USA, The viruses in all of us: Characteristics and biological significance of human endogenous retrovirus sequences. Vol. 93:5177-5184.

2.Nakagawa and Harrison (1996) Immunological Reviews, The potential roles of endogenous retroviruses in autoimmunity. No.152, p192-236.