Before the AIDS era it was known that mothers transfer antibodies of all types to their unborn children and increasingly so as the time of birth approaches.  These antibodies are said to “protect” the newborn from infectious diseases until the baby builds up its own repertoire.


It was also known that the newborn metabolises its mother’s antibodies such that by the time the baby is nine months old all maternal antibodies have completely disappeared (dashed line labeled “Maternal IgG Contribution” and blue arrow).  Of course during this time (dashed line “Newborn IgG Contribution”) the baby gradually produces its own antibodies.  Thus, for a few months after birth, the baby’s antibodies are the sum of its declining mother’s antibodies and its own increasing antibodies.


We now consider an HIV positive mother.  She is HIV positive because she possesses antibodies which react in an HIV test.  Along with the hundreds of other maternal (non-HIV) antibodies these antibodies find their way into the baby’s circulation.  This means all newborn babies of HIV positive mothers will be HIV positive if tested at or shortly after birth because the test is reacting to the presence of the mother’s HIV antibodies.


Then, along with all the others, the maternal HIV antibodies are metabolised.  And like all the others, the HIV antibodies are expected to have vanished by the time the baby is nine months old.  This is because the biochemical mechanisms which are involved in the breakdown of antibodies cannot distinguish one antibody from another.  Thus, at least before the AIDS era, if a baby were to be tested just after the age of say ten months and was found to have an antibody which reacted say with bacterium E. coli, or the measles virus, scientists would say this particular antibody must have come from the baby, not the mother.  This is because by then antibodies the mother has manufactured will have been metabolised and be gone.


On the other hand, if the antibodies which react in the HIV test have not disappeared the only way this could occur is because this baby is one of the 25% of babies who become infected by their mothers and the antibodies belong to the baby.   Furthermore, since HIV is for life, including babies, no baby who is found HIV positive after nine months should revert and become HIV negative at a later date.


What do the data show?


(Next Slide)


The graph on this slide is taken from the European Collaborative Study of mother to child transmission  of HIV.  It is the only study we know that contains these type of data and was published in the Lancet in 1988.  As expected it shows that at birth, 100% of babies are HIV positive because the test is reacting to the mother’s antibodies.


At nine months of age approximately 25% of the children have lost their positive test.  This leaves 75% still positive at nine months.  We also see that by the age of about 18 months only 15% of babies are still HIV positive.  We also note that although the graph begins to flatten out between about 15-18 months of age infants continue to revert from HIV positive to negative up to 22 months beyond which there are no data.   At least in this study.


This graph raises a number of very important issues:


1.  Sixty per cent,  over half the children HIV positive at birth, lose their positive test between 9 and 18 months of age.  This cannot be explained by the disappearance of the mother’s antibodies.  Neither can it be explained on the basis of baby’s obtaining HIV antibodies from breastmilk.  The former is because of metabolism and the latter because in this study only 5% of infants were breastfed and then only for periods from 1 to 30 weeks (median 2.5).

2. Do experts accept the pre-AIDS data that maternal antibodies completely disappear by the time the infant is 9 months old?  No they do not.  They appear to think “HIV” is an exception.   In fact during the AIDS era the time at which maternal antibodies are said to disappear began at 15 months of age but has been extended since.  Why the original 15 months?  Because in 1987 the CDC 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 [1].  At this conference “Most of the consultants believed that passively transferred maternal HIV antibody could sometimes persist for up to 15 months” but cited no evidence permitting identification and critical examination of the reasons for what all but the minority of experts “believed” to be true.  Presumably the CDC was not concerned with the implications of the minority view.

3.  Why do HIV experts keep extending the time beyond 15 months?  Because more and more children are found to lose their positive antibody test beyond this time.   Four years after their original “belief” was published, in 1991, the time to metabolise mother’s antibodies was set at 18 months and most recently 30 months.  This is double the 1987 rate and over three times the pre-AIDS era rate.

4. How can we reconcile maternal antibodies disappearing at nine months of age, which was the case before the AIDS era, with what the HIV experts now tell us?  We cannot because to accept the former would require abandoning the HIV theory of AIDS.  On what basis may we draw this conclusion?  The reason is very simple.  Let us repeat the premise to support the argument.  A baby reverting from HIV positive to HIV negative after nine months of age cannot be doing so because it has lost its mother’s antibodies.  These have already disappeared.  If these babies aren’t losing mother’s antibodies after nine months they must be losing their own.  This leads to one of two conclusions.  First, these could be genuine HIV antibodies which the child has made because the child has become infected with HIV.  But since these are then lost we must conclude that somehow these babies are curing themselves of HIV infection without any treatment including antiretroviral drugs.  The second possibility is that the baby is not making genuine HIV antibodies but rather genuine, non-HIV antibodies which cross-react in the test.  If this true for 60% of babies it might also be true for all the babies.  And since these are exactly the same tests as used in adults, the same can be argued for the babies’ mothers.  And the same could apply to the babies’ fathers.  In other words to everyone who has ever had an antibody test.

5.  Apart from opinions or beliefs has any scientist independently established the time it takes infants to metabolise their mother’s HIV antibodies?  Yes.  And it is of great significance is that this was reported by CDC researchers in 1993.  They proved that in distinction to antibodies in general, the actual maternal HIV antibodies are metabolised by six months of age [2].   This only strengthens the argument that whatever the antibodies are that cause people to become HIV positive, they are not due to a retrovirus HIV.  But this data has not been reflected in the how the CDC or HIV experts in general interpret the reversion of positive antibody test in the infants of HIV positive mothers.


In our view these alone are sufficient to immediately reject the HIV theory of AIDS.


1. CDC. Current Trends Classification System for Human Immunodeficiency Virus (HIV) Infection in Children Under 13 Years of Age. Morbidity and Mortality Weekly Reports 1987;36:225-30, 235-6.

2. Parekh BS, Shaffer N, Coughlin R, Hung CH, Krasinski K, Abrams E, 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.



Abstract of this paper


We have used a human immunodeficiency virus type 1 (HIV-1)-specific IgG- Fc capture enzyme immunoassay (IgG-CEIA) to elucidate the dynamics of HIV-1 maternal antibody decay and de novo synthesis of HIV-1 antibodies in infants. Two hundred and thirty-nine serum specimens from 77 infants were analyzed by the IgG-CEIA and by two different conventional EIAs. With the IgG-CEIA, IgG was captured by an anti-human IgG monoclonal antibody (3C8) that reacts with all subclasses and was detected by recombinant HIV-1 envelope protein (CBre3)-peroxidase conjugate. Unlike the conventional EIAs, the IgG-CEIA showed a rapid decay of HIV-1- specific antibody in uninfected infants, with decline to background levels by 6 months (T1/2 [half-life] = 28-30 days). All 69 specimens collected from 39 uninfected infants between 6 and 15 months of age were negative by IgG-CEIA. However, HIV-1 antibodies remained high in infected infants; 20/22 infants (90.9%) with specimens between the ages of 6 to 23 months were positive by IgG-CEIA. Subtracting mean IgG-CEIA optical density values of seroreverting infants from those of HIV-1- infected infants in corresponding age groups provided a model for seroconversion in infected infants, with detectable IgG antibody synthesis starting about 3 months after birth. The IgG-CEIA may be a simple and important tool for early diagnosis of HIV-1 infection in infants at 6 months of age.


(Parekh has indicated in correspondence there is no reason to believe the decay of maternal HIV antibody should differ between “infected” and “uninfected” infants).