'Fear of the Invisible'

Statistics

OS : Linux b
PHP : 5.2.17
MySQL : 5.5.29-log
Time : 19:14
Caching : Disabled
GZIP : Disabled
Members : 2325
Content : 83
Web Links : 3
Content View Hits : 363535
Home What the HIV test really tells us
What the HIV Test really tells us PDF Print E-mail
Written by Administrator   
Monday, 18 August 2008 22:03

WHAT the HIV Test really tells us

from Fear of the Invisible 

 

Earlier in this chapter I mentioned there were two possible explanations for why the antibodies detected with the HIV test are useless to protect us against HIV. One was that the antibodies were really against something else entirely; the other was that these antibodies could not find HIV as it hid itself inside our cells.

HIV science chose the second alternative as a focus for its research  - but this route has in over 20 years produced no remedy or vaccine. So -perhaps it is time to consider the alternative - that the antibody detected is there for another purpose than attacking HIV?

I asked myself: what do we know about the illnesses that started the AIDS epidemic, the ‘opportunistic infections'?  Was it at all possible that the antibodies detected with the HIV test are present to fight, not HIV, but these very real illnesses?  If they are, couldn't this explain a correlation between positive results and a risk of getting AIDS - without requiring the presence of HIV, without proving it the cause of AIDS?

Fungal Pneumonia (PCP), alongside severe Thrush, was long the major cause of death in AIDS cases in the West.  These fungal infestations still affect over 70% of Western AIDS patients.  So, could these antibodies be present to mark fungi for destruction?

In Africa those diagnosed with AIDS often have TB, a disease in which mycobacteria play a major role.  Was it possible that the antibodies found with the HIV test are also able to attack these mycobacteria? 

Could I go one step further? Could the ‘HIV antibodies' found with the test be produced against both mycobacteria and fungi?  This at first seemed a highly unlikely hypothesis - for it was just too obvious.  Surely this possibility would have been checked when AIDS was first investigated?    Then I came across scientific research that showed this is exactly what is happening!   

Much to my amazement I have learnt that, since at least the 1980s, it has been scientifically established that these antibodies directly attach to proteins of both  mycobacteria and fungi! For me, discovering this was like finding the final missing piece in a jigsaw.  It explained why Africans and Westerners tested positive with the same HIV test despite often suffering with very different opportunistic diseases.

The primary research on mycobacteria is in a paper produced by a scientific team that included Myron Essex of Harvard, a colleague of Gallo in the US Government's AIDS task force, and a co-winner with him of the prestigious Lasker Award.

A paper he co-authored on leprosy, a disease linked to mycobacteria, states ‘leprosy patients and their contacts show an unexpectedly high rate of false positive reactivity of HIV-1 proteins on WB (Western Blot tests) [83.6% patients; 64.1% contacts] and ELISA (the HIV Test) ... Sera from 63.6% of leprosy patients and 23% of their contacts were repeatedly positive for HIV-1 by ELISA.' 

The paper then went on to consider other widespread illnesses linked to mycobacteria, such as TB, saying ‘HIV antibodies' also attack TB mycobacteria, giving a false positive result with the HIV test.

It explained that the antibodies found with the HIV Blood tests (both the Elisa and Western Blot) target a ‘carbohydrate-containing' feature on the surface of Mycobacterium Tuberculosis and other mycobacteria. The paper concluded:  ‘ELISA and WB may not be sufficient for HIV diagnosis in AIDS-endemic areas of Central Africa where the prevalence of mycobacterial diseases is quite high'.  It warned that even the contacts of TB patients are liable to falsely test positive for HIV.

 Other scientists later confirmed and extended this finding. They reported the carbohydrate structure targeted by the ‘HIV' antibody is also on molecules from fungi, including the thrush fungus better known as yeast!  This to my mind is enormously important. It shows why the HIV test can detect a risk for AIDS without HIV being present, in both TB-infected Africa, and among fungi-infected Western AIDS victims.

Also, as countless millions of otherwise healthy people are infected by yeast and minor fungal infections are everywhere, I wondered if this could explain why so many more people test positive than get AIDS; in the UK over twenty times more.  A positive HIV result thus might indicate no more than a need for an antifungal medicine.

As for mycobacteria, they are everywhere, even in tap water, but they are normally harmless, even if sometimes they can test as if HIV. Gallo in the 1980s detected ‘HIV' in Haiti at a time when mycobacteria-linked TB was prevalent there, as it is a disease strongly associated with poverty and poor living conditions. TB was also at that time treated with large doses of antibiotics, which are very immune suppressant.  The same reasons may explain why ‘HIV' is now detected among Blacks living in poor conditions within the USA.

At a recent AIDS conference, Professor Papadopoulos-Eliopoulos of Western Australia presented a transparency contrasting the results of tests for 'HIV antibodies' on leprosy, TB and AIDS patients. The results were indistinguishable from one another. All the samples tested as if positive for 'HIV.'

When I looked at how HIV-positive patients are medically treated today, I found anti-fungal and anti-mycobacterial medicines are commonly prescribed alongside antiretrovirals, and even given priority over antiretrovirals on the basis that the antiretrovirals interfere with the former's effectiveness. Could this explain beneficial effects from this treatment, despite the absence of a retroviral infection?

When I dug deeper, I found the antibodies detected with the ‘HIV test' are now known to target even more molecules. Today the test manufactures warn that ‘false-positive' results may occur after a recent flu or tetanus vaccination as well as during malaria, kidney failure, rheumatoid arthritis, herpes, hepatitis and even pregnancy! 

This is not a problem that is now fixed.  These reports are current. The Indian Government lists online the following as falsely producing a positive HIV test.

‘- Multiple pregnancies

- Multiple transfusions

- Antibody to gammaglobulinemia (HLA-DR4) (a common arthritis risk )

- Hypergammaglobulinemia (low antibody numbers)

- Antipolystyrene antibodies  (sensitivity to polystyrene)

- Chronic alcoholism

- Hepatitis

- Hepatitis immunisation

- Technical error etc.'

Also, a medical work published in 2005, co-authored by Professor Elizabeth Dax, whom we came across as an ‘Expert' in the 2007 Australian trial, reports: ‘Among the medical conditions that are suspected or occasionally known to produce false-positive screening test results are as follows:

  •               Malaria
  •               Syphilis
  •               Pregnancy
  •               Hypergammaglobulinemia, renal failure, liver disease
  •               Some parasitic diseases and viral diseases (e.g., influenza)
  •               Auto-antibodies (autoimmune diseases)
  •               HIV vaccination (becoming a major cause)
  •               Transfusions (usually multiple)'


Kashala O, Marlink R, Ilunga M, et al. Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. J Infect Dis 1994;169:296-304.

Kashala O, et al.  J Infec Dis.  1994;169:296-304

    Muller WEG, Schroder HC, Reuter P, Maidhof A, Uhlenbruck G, Winkler I. (1990). Polyclonal antibodies to mannan from yeast also recognize the carbohydrate structure of gp120 of the AIDS virus: an approach to raise neutralizing antibodies to HIV-1 infection in vitro. AIDS 4:159-162.

O'Riordan DM, Standing JE, Limper AH. Pneumocystis carinni glycoprotein A binds macrophage mannose receptors. Infect-Immun 1995;63:779-784.

Matthews R, Smith D, Midgley J,. Candida and AIDS: Evidence for protective antibody. Lancet 1988;263-266.

 The Coming Plague. Pp. 515-6.

‘transfusions, transplantation, or pregnancy, autoimmune disorders, malignancies, alcoholic liver disease, or for reasons that are unclear...' (Archives of Family Medicine. Sept/Oct.2000). ‘liver diseases, parenteral substance abuse, hemodialysis, or vaccinations for hepatitis B, rabies, or influenza...' (Archives of Internal Medicine, August 2000).

http://www.bmj.com/cgi/content/full/311/7021/1665 - this risk is found more prevalent among senior academics!

Constantine, Saville and Dax Retroviral Testing and Quality Assurance, Essentials for Laboratory Diagnosis