Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY
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Here we see an excellent example of the Perth Group taking facts out of context.
1) Is it true that once infected with "HIV", always infected.
All the evidence to date has shown that HIV is culturable from all stages of AIDS, from the initial seroconversion stage to the final AIDS stage [1-4]. I have not heard of any report of a person spontaneously regaining the CD4's in the absence of therapy (with the exception of the resolution of the acute seroconversion syndrome). Even in a study looking specifically at clearance of HIV through immune hyper-activation to remove the proviral reservoir, HIV persisted . Estimates of the proviral turnover suggest that even with complete suppression of the virus it would takes decades, and has not been demonstrated . So, yes.
2) In 59% of infant seroreversions occurred after 9 months.
In some studies, not in other cohorts [7, 8]. Even if that's so, why the dogmatic hang-up with the magical 9 month value. 
3) Infants seroreverting after 9 months cannot be doing so on the basis of loss of transplacentally transferred maternal antibodies.
Why not? I say that's the most obvious explanation. The antibodies must be coming from somewhere, the mother is the most likely source because of...(read on)
4) Hence the antibodies that are disappearing must have been generated by the infant and not the mother.
No. The antibodies disappeared: almost by definition they must be an external source. This is the "500 millions years of evolution" bit the Perth Group missed. Why would antibodies disappear if they are supposed to be induced as a means of life-long specific immunity? I freely admit that antibody titres decline to some pathogens during life, but not usually if the infection is real as opposed to a vaccination. About the only time I can recall seeing hypogammaglobinaemia is with inborne immune deficiencies or very late-stage AIDS.
5) If the antibodies are "HIV" specific they can only have been the result of "HIV" infection of the infant.
This is a rather dogmatic, entirely unsupported and unscientific statement. They are also likely to be from the mother: this is why IN INFANTS the serology is useless.
6) If yes to Q5 since the antibodies disappeared without specific antiretroviral therapy the infants themselves must have eliminated "HIV".
Can the Perth Group please point to any other infection where elimination results in the LOSS of specific immunity? A clue: specific immune responses generally appear JUST PRIOR TO or AFTER an acute infection is cleared by the innate immune system. Even if HIV were eliminated, one would expect the antibodies to persist. This question highlights a fundamental lack of understanding of what antibodies actually mean - exposure to a pathogen. Certain pathogens establish life-long infections: CMV, HSV, VZV, HCV, HBV and HIV among them. Depending on the pathogen therefore, antibody serostatus is an indicator of current infection with that pathogen. Other infections result in life-long antibody titres that indicate clearance of the infection - it all depends on the pathogen.
7) If no to Q5 then in at least 59% of infants the "HIV" antigens are reacting non-specifically with antibodies whose genesis cannot be "HIV" infection.
Why not? It is well known that in HIV infection there is a state of hypergammaglobinaemia (too many antibodies). If a higher titre of antibodies is transferred transplacentally, is it any surprise that they persist for longer?
8) "HIV" antibody tests cannot distinguish between sera obtained from infants, mothers, fathers, brothers, sisters, uncles, aunts, cousins or indeed any other person.
Of course not, that's why we label vials. I don't see the point of this question.
9) If the "HIV" antibody tests are non-specific in 59% of infants they may also be non-specific in mothers, fathers, brothers, sisters, uncles, aunts, cousins or indeed any other person.
No, because the serology problem of maternal transfer ONLY APPLIES TO INFANTS.
You may as well argue: infants cannot see further than a few feet in from of them, therefore all adults can only see a few feet.
10) The HIV theory or AIDS is predicated on the correlation between a positive antibody test and the presence or development of AIDS defining diseases.
Pretty much, yes. Other factors come into play, but the fact that the AIDS-indicator diseases are far more common in HIV+ people means the diagnostic criteria make sense. IN ADULTS.
11) If the antibodies are not “HIV” specific in 59% of infants does not this mean that the “HIV” theory of AIDS cannot be upheld.
IN INFANTS the serology is not helpful. This is why other criteria are recommended, as stated previously [10, 11]. It has no implications for the HIV "theory" of AIDS at all. I don't think you're really trying.
Nick Bennett firstname.lastname@example.org
1. Jackson et al J Clinical Mole Bio 1988 pp1418-1418 "Rapid and sensitive viral culture method for human immunodeficiency virus type 1."
2. Jackson et al J Clinical Mole Bio 1990 pp 16-19 "Human immunodeficiency virus type 1 detected in all seropositive symptomatic and asymptomatic individuals."
3. Ho et al NEJM 1989 321:pp 1621-1625 "Quantitation of human immunodeficiency virus type 1 in the blood of infected persons."
4. Schacker et al Ann Intern Med. 1996 Aug 15;125(4):257-64. "Clinical and epidemiologic features of primary HIV infection."
5. Davey et al. Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):15109- 14. "HIV-1 and T cell dynamics after interruption of highly active antiretroviral therapy (HAART) in patients with a history of sustained viral suppression."
6. Ramratnam et al. J Acquir Immune Defic Syndr. 2004 Jan 1;35(1):33- 7. "Intensification of antiretroviral therapy accelerates the decay of the HIV-1 latent reservoir and decreases, but does not eliminate, ongoing virus replication."
7. Parekh et al. AIDS Res Hum Retroviruses. 1993 Sep;9(9):907-12. "Dynamics of maternal IgG antibody decay and HIV-specific antibody synthesis in infants born to seropositive mothers. The NYC Perinatal HIV Transmission Study Group."
8. Madurai et al. J Trop Pediatr. 1996 Dec;42(6):359-61. "Use of HIV- 1 specific immunoglobulin G3 as a serological marker of vertical transmission."
9. Palasanthiran et al. J Infect Dis. 1994 Dec;170(6):1593-6. "Decay of transplacental human immunodeficiency virus type 1 antibodies in neonates and infants."
10. 4.A. Fischer et al J Clin Microbiol. 2004 January; 42 (1): 16–20 DOI: "Simple DNA Extraction Method for Dried Blood Spots and Comparison of Two PCR Assays for Diagnosis of Vertical Human Immunodeficiency Virus Type 1 Transmission in Rwanda"
11. Katrien et al. Molecular and Cellular Probes Volume 8, Issue 4 , August 1994, Pages 317-322 "Design and evaluation of new, highly sensitive and specific primers for polymerase chain reaction detection of HIV-1 infected primary lymphocytes."
Competing interests: None declared