The video below from the Perth Group is 12 and a half minutes long and it is worth every second. It is a simple explanation, given the information publicly available in the medical literature, of why HIV antibodies cannot be specific to HIV, given information on the inheritance of maternal antibodies to HIV in babies born to HIV-antibody-positive mothers. I encourage everyone to watch this video; for those who would like a little explanation, I have summarized their points and conclusion below, followed by a short discussion.
Perth group on maternal antibodies
Babies born to HIV-positive mothers test HIV-antibody-positive at a high rate—close to 100%—however, the vast majority lose their maternal antibodies eventually. (This is not unusual, as babies inherit many antibodies from their mother, most of which eventually disappear .) Where this picture gets interesting is that inherited maternal antibodies to pathogens other than HIV—measles, for example—are universally acknowledged to disappear by 5 months, and usually sooner. However, the CDC stated in 1987 that passive (from the mother and not created in response to an active infection of any sort in the infant) antibodies to HIV may persist for up to 15 months. Like the “latent period” from HIV-positivity to AIDS, this figure has only increased. By 1991, the CDC was saying that these antibodies may persist for 18 months; in 1995, they revised this estimate upward to “perhaps >30 months.”
This is in contrast to the CDC’s own statement that the observation has been of “rapid decay of maternal antibodies by 6 months [half-life of 28-30 days].”
In this video, the Perth Group examines two studies of mother to child transmission of HIV-positivity. The European Collaborative Study from 1988 enrolled mostly intravenous drug users. 271 babies were born, virtually all of whom were HIV-antibody-positive at birth. By 9 months, 75% persisted in testing antibody positive. Intriguingly, however, between 9 and 24 months (at which point testing stopped), only 15% of babies continued to test positive. Similarly, the Ariel study from 1999 showed that among 209 babies, fully 42% lost their antibodies between 12 and 18 months.
Since the entirety of the mainstream literature indicates that, in general, with maternal antibodies to any agent, these antibodies disappear by 6-9 months at the most, what is happening with HIV antibodies beyond 9 months, the point at which, per the studies mentioned above, all maternal antibodies are cleared? Are the babies magically clearing a genuine infection on their own, which we have been told is nigh unto impossible, or is something else going on?
Are these results false positives? Given the studies in which most antibodies are lost after 9 months, we can safely infer that in 40-60% of the cases (the ones which the maternal antibodies are lost “too late”; after 9 months of age), the tests likely register false positives. This could be due to the tests being too sensitive at the expense of specificity (i.e. few false negatives result but many false positives do), or we could perhaps go further and ask if the specificity is in fact zero, and that the antibody tests are not measuring anything to do with HIV at all.
The problem is further confounded with the use of the viral load test to “eliminate false positives,” as indicated by the CDC. This includes testing of infants and children. Readers with some familiarity with this subject will recall that until very recently, viral load was neither approved nor recommended for diagnosis; the inventor of the technology has himself famously stated that PCR (the technology on which the viral load test was based) is entirely inappropriate for diagnosis and even less appropriate for quantification. Now, however, PCR is authorized for use in determining “active/acute HIV infection” in mostly antibody-negative individuals. The viral load test has, for almost thirty years, been universally acknowledged to be less accurate than the antibody tests; not least due to the enormous numbers of false positives these tests register. The so-called viral load test has not improved, so why is it suddenly okay to use in diagnosis (albeit in a limited number of cases)? (Wishful thinking perhaps? There is no shortage of that in HIV “science.”)
The problems are manifold, but the main problem is the following. During so-called “acute HIV infection,” before antibody production has begun to neutralize any pathogens, it should be easy to find copious amounts of HIV in the patient, as its replication is not hindered by the presence of antibodies. However, this is never the case. We know that PCR magnifies genetic material like an exponential photocopier—and furthermore, only magnifies tiny segments of “HIV”—but in the case of a fulminant initial infection, why do we even need it to see the pathogen?
Given the issues with disappearing antibodies, as well as the faults in the viral load test, which are legion, it may be appropriate to ask about the cost/benefit analysis of administering antiretroviral therapy to pregnant mothers. The debilitating side effects are well known, including potential heart defects. If the tests given to mothers and babies are as nonspecific as the literature inevitably leads one to conclude, it is time to seriously reevaluate the use of the HIV antibody test during pregnancy (indeed, pregnancy itself is a known cause of false positives), and to even more seriously reevaluate the use of the totally nonspecific “anti-HIV drugs” for the purposes of preventing the transmission of antibodies that are both nonspecific, and in most cases will be eliminated without intervention.
For more information on mother to child transmission, I urge the interested reader to refer to the Perth Group’s monograph on mother to child transmission.
The Real AIDS Epidemic available here.
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In a 2020 BMJ editorial, Professor Allyson Pollock wrote:
"It’s also unclear to what extent people with no symptoms transmit SARS-CoV-2. The only test for live virus is viral culture. PCR and lateral flow tests do not distinguish live virus. No test of infection or infectiousness is currently available for routine use. As things stand, a person who tests positive with any kind of test may or may not have an active infection with live virus, and may or may not be infectious.
The relations between viral load, viral shedding, infection, infectiousness, and duration of infectiousness are not well understood. In a recent systematic review, no study was able to culture live virus from symptomatic participants after the ninth day of illness, despite persistently high viral loads in quantitative PCR diagnostic tests. However, cycle threshold (Ct) values from PCR tests are not direct measures of viral load and are subject to error."
While viral load seems to be similar in people with and without symptoms, the presence of RNA does not necessarily represent transmissible live virus. The duration of viral RNA shedding (interval between first and last positive PCR result for any sample) is shorter in people who remain asymptomatic, so they are probably less infectious than people who develop symptoms"
"PCR and lateral flow tests do not distinguish live virus. No test of infection or infectiousness is currently available for routine use"
https://www.bmj.com/content/371/bmj.m4851