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The graph shows the percent of infants who are antibody positive on the vertical axis and age in months along the bottom horizontal axis. From 100% positive at birth, the infants gradually lose their positive test, until all but 15% have become HIV-negative by 24 months.



From 9 months on (the age at which maternal antibodies have been lost), 60% of the infants become negative by age 24 months.

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Slide 20 of 24

This means, as this graph shows, that at birth, 100% of babies are HIV positive because the test is reacting to the mother's antibodies.

And as this graph also shows, at nine months of age approximately 25% of the children have lost their positive test. And by 21-22 months all but 15% have done likewise.

Why does this happen? It happens because, over a period of time, the mother's antibodies are metabolised by her baby and disappear. And in fact the longer babies are followed the more antibody tests revert to negative.

What does all this mean? To the HIV experts it means that as the curve flattens out around 18 months about 15% of babies are infected by their mothers. They say this because by 18 months or so the test must be reacting to the child's antibodies because by this time the mother's have all gone.

The critical issue in all this is the time that the mother's antibodies disappear. To say they may persist till 18 months is pure conjecture. This is because before the AIDS era it was known that mother's antibodies disappear by nine months at the very most. Significantly, there is no evidence that maternal HIV IgG declines more slowly than total IgG. To the contrary, researchers from the CDC have "calculated that the half-life of the maternal anti-HIV-1 IgG antibodies is 28-30 days" and that it decays "to background levels by 6 months", [1] that is, at the same rate as total IgG.

So children who are positive at 6-9 months and then sometime afterwards become negative cannot be doing so because they have lost their mother's antibodies. They've already gone. And this applies to a sizeable proportion of the babies. At least 60% in fact.

The only reason the HIV experts say HIV antibodies last longer than all others is because they believe it to be so. If the experts admitted what scientists already know and have proven they would have to abandon the HIV theory of AIDS.

The reason is very simple. Let me repeat the premise to this argument. Any baby reverting from HIV positive to negative after nine months of age cannot be doing so because it has lost its mother's antibodies. These have already disappeared. And if these babies aren't losing mother's antibodies after 6-9 months they must be losing their own. This leads to one of two conclusions. Either these are HIV antibodies which the child makes and then loses. Meaning somehow babies are curing themselves of HIV infection and without any treatment including antiretroviral drugs. The other possibility is that the baby is not making HIV antibodies but whatever antibodies it is making are being picked up by this antibody test. Which means the test is responding to non-HIV antibodies. And if that can happen in 60% of the babies it can happen to all the babies. And since they're exactly the same tests used in adults, the same applies to their parents. That is, to everyone.

In the scientific literature the only justification one can find for the prolonged persistence of maternal, IgG HIV antibodies over all others is that published by the Centers for Disease Control. In 1987 the Centers for Disease Control convened a panel of consultants representing the American Academy of Pediatrics and eight other disciplines to develop a classification system for HIV infection in children [2]. The CDC reported "Most of the consultants believed that passively transferred maternal HIV antibody could sometimes persist for up to 15 months" whilst citing no evidence allowing identification and critical examination of the reasons underlying this belief. In 1991 the CDC convened another group of consultants and three years later reported that maternal HIV antibody "occasionally remains detectable until 18 months of age. Therefore, standard anti-HIV IgG antibody tests cannot be used to indicate reliably a child's infection status before 18 months of age" [3]. In 1995 infants were reported seroreverting by ELISA at 20.5 months. Furthermore, 16% of infants "seroreverting by WB testing did so after 18 months of age, with some remaining seroindeterminate as late as 128 weeks (29.5 months)...the range of WB seroreversions might eventually extend beyond 30 months", that is, at double the age applicable eight years earlier [4].

From this slide we see that 60%, over half the children, serorevert between 9 months and 21-22 months. This cannot be explained by the loss of maternal HIV antibodies unless "belief" by a panel of consultants is accepted as scientific proof. That is, there is no evidence that the metabolism of maternal HIV IgG takes over twice as long as all other antibodies of this class. Neither can the persistence of a positive antibody test be explained by maternal HIV IgA antibody adsorbed by breastfed babies. In the European Collaborative Study only "5% [of infants] were breastfed for periods from 1 to 30 weeks (median 2.5))".

In our view this argument alone is sufficient to call into question the whole HIV theory of AIDS.



REFERENCES

1. Parekh BS, Shaffer N, Coughlin R, et al. Dynamics of maternal IgG antibody decay and HIV-specific antibody synthesis in infants born to seropositive mothers. The NYC Perinatal HIV Transmission Study Group. AIDS Res Hum Retroviruses 1993;9:907-12.

2. CDC. Current Trends Classification System for Human Immunodeficiency Virus (HIV) Infection in Children Under 13 Years of Age. Morb Mortal Wkly Rep 1987;36:225-30, 235-6.

3. CDC. 1994 Revised Classification System for Human Immunodeficiency Virus Infection in Children Less Than 13 Years of Age. Morb Mortal Wkly Rep 1994;43 (RR-12):1-10.

4. Chantry CJ, Cooper ER, Pelton SI, Zorilla C, Hillyer GV, Diaz C. Seroreversion in human immunodeficiency virus-exposed but uninfected infants. Pediatr Infect Dis J 1995;14:382-7.