Alexander H Russell,
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Regarding my question regarding the supposition that 'HIV' is sexually transmitted, Mr. Nicholas Bennett replied:
"The sexual nature of the infection was suggested and confirmed by several studies, some of which are even quoted as proof that HIV cannot be sexually transmitted! Low rates do not mean no rates. The fact that female sexual partners of gay men, or sexual partners of IV drug users developed HIV infection and AIDS, was one of the early key pointers away from drugs or lifestyle and towards a sexually transmitted infection."
Suggestion is not science; suggestion is not enough. We need empirical data of isolated 'HIV' from fresh semen samples and not guessing games. So-called 'HIV infection' is merely a metaphor and a marker for 'high-risk behaviour' like recreational drug use, repeated STD infections and consequent high dependence on antibiotics etc.
Mr. Bennett goes on with further unfounded and absurd assertions:
"HIV can also be detected in cervico-vaginal secretions. There is plenty of evidence to suggest and support a sexual mode of transmission!"
No: 'HIV' has not been detected in cervico-vaginal secretions using visual confirmation by electronmicroscopy. And even if this were so, how would the insertive partner be 'infected' either cervically or anally? How does 'HIV' get into the blood stream of the insertive partner? There is no evidence to suggest and support a sexual mode of transmission of 'HIV' at all. Why is it more difficult for women to 'infect' men with 'HIV'? Where are all these Western women with hypothetical 'HIV infection'?
Mr. Bennett gets confused and contradictory here:
"I agree that STD rates and, in some countries, teenage pregnancies are rising, whereas HIV rates may be static or dropping. This is no surprise if we see that the STDs are in teenage heterosexuals and the HIV rates are in gay men."
The STDs are also in the gay men - as the increase in syphilis in that group shows. Why does 'HIV' still discriminate against Western teenage heterosexual? You cannot have a pathogen that is restricted to one particular sexually orientated group ad infinitum. How did 'HIV' get to homosexuals before anyone else? Why does 'HIV' still prefer 'infecting' homosexuals in the West?
Will Mr. Bennett give me an exact description of the mechansim of the sexual transmission of 'HIV' supported by references. Any references which depend on scientifically umproven suppositions will not suffice.
Why has 'HIV' never been shown to be equally bitransitive when it comes to transmission?
Why should 'HIV' be more readily transmitted male to female but not female to male? In which case where do heterosexual males get 'HIV' from? Also, where does the active (insertive) homosexual get 'HIV' from? How does a passive (receptive) homosexual transmit 'HIV' to an active (insertive) homosexual? I want the precise mechanism please. To date Mr. Bennett refuses point blank to answer these simple questions.
Mr. Bennett makes further false claims:
"Quantitative measures of HIV in semen have been performed using DNA, RNA and Culture assays: the level of HIV depends on whether or not the patient is treated and the presence of other ongoing infections."
These so-called 'measures' all down to arbitrary, symbolic and metaphorical measures. Where is the visual evidence of 'HIV' isolated from semen confirmed by electronmicrographs? Why have they never been published in the scientific literature?
Naively Mr. Bennett stated: "HIV transmission can be demonstrated in animal models." This is absolute rubbish: what has been 'shown' is a completely artificial construct conjured up in the laboratory. Analogous animal infections, usually relying on 'SIV' in monkeys, have to use hugely inflated titres of alleged 'virus' - which have never been observed in vivo - in order to achieve systemic 'infection'. For instance, as Michael Verney-Elliott observed:
"In studies by Ruth Ruprecht et al at the Dana Farber Cancer Institute, Tulane and Tufts Universities, published in 'Science' (7.6.96) using SIV animal modelling, sought by analogy to show whether unprotected oral sex ran a risk of 'HIV' infection due to cell-free virus in semen infecting human oral mucosal cells, even in the absence of mouth lesions and gastric acid inhibitors. The paper describes a 'cell-free SIV solution' dribbled onto the tongues of SIV-free macaque monkeys, and 6 out of 7 previously uninfected monkeys were thus systemically infected.
The studies showed that the same SIV solution rectally administered by endoscope needed a concentration of virus 6000 times higher to achieve systemic infection than the orally administered virus solution. As already stated - cell-free virus has never been found in human semen without extensive culturing, so it is impossible to extrapolate any conclusions from this study concerning 'HIV' oral transmission in semen. The kind of SIV titres used by Ruprecht and her colleagues have never been seen, or even 'implied' in vivo."
Mr. Bennett concludes: "The 'lentivirus' as a clinical/structural classification is no longer appropriate, but nowadays is still used as a genetic classification."
The putative 'lentivirus' is merely a dormant passenger virus, an epiphenomenal marker and not a cause of any disease condition. It is good to see people at last catching up with Peter Duesberg who observed many years ago that there are no such things as slow viruses- only slow virologists.
"I only wish Mr Russell's case WOULD rest..."
My case will rest once Mr. Bennett has directly answered my questions: to date he has still failed to do so.
In passing, as 'HIV' has never been recovered from a fresh blood sample, what is Mr. Bennett's explanation for the supposed 'infection' of haemophiliacs via their clotting factor? Or will that flim-flam be consigned to the same oubliette as the 'lentiviral' fiction?
There are still no in vivo images of 'HIV'. Why not?
Competing interests: None declared