Item #44: Antibodies Mean Immunity…Except for HIV?

most AIDS patients have no active HIV in their systems, because the virus has been neutralized by antibodies. (With all other viral diseases, by the way, the presence of antibodies signals immunity from the disease. Why this is not the case with HIV has never been demonstrated.)

Farber states "With all other viral diseases, by the way, the presence of antibodies signals immunity from the disease. Why this is not the case with HIV has never been demonstrated".

The presence of antibodies all too often does not signify immunity from disease (e.g. herpes zoster, herpes simplex, hepatitis C, hepatitis B, dengue -all of these viruses can cause disease in the presence of virus-specific antibodies). HIV is a retrovirus and as such it integrates upon infection. Antibodies specific to a retrovirus almost always means the patient is infected and the levels of antibody usually correlate to some extent with the level of virus replication. We present more detail in [endnote 70].

Note 70: The reason why HIV antibodies do not confer immunity from disease has been demonstrated. Farber may be confusing binding and neutralizing antibodies. Many antibodies to viral proteins lack antiviral activity; they are raised against viral proteins, they often bind efficiently to dissociated viral proteins or fragments of these proteins (which is why they register in diagnostic assays), but they are unable to bind to intact virus particles and inhibit their replication. Virus-neutralizing antibodies, on the other hand, do possess antiviral activity, with the caveats noted in the text. Among the very many publications on these basic immunology topics are: Hangartner L et al. (2006) Antiviral antibody responses: the two extremes of a wide spectrum. Nat Rev Immunol 2006, 6, 231-243 Burton DR. (2002) Antibodies, viruses and vaccines. Nat Rev Immunol 2002, 2, 706-713 Parren PWHI. (2001) The antiviral activity of antibodies in vitro and in vivo. Adv Immunol 2001, 77, 195-262.

The belief that HIV antibodies are not protective is critical to the HIV/AIDS theory. Questioning this theory is out of the question for people with vested interests in the maintenance of this theory for a number of reasons:

1. If antibodies to HIV were considered to be protective, the prognostic value of the HIV test would disappear.
2. If other health risk factors were considered, such as drug abuse or exposure to blood products, the prognostic value of HIV tests would be reduced, if not eliminated.
3. If the accuracy of HIV tests are questioned, such as the possibility that HIV antibody tests might react to other conditions (e.g. infections, auto-immune conditions, vaccinations or even pregnancy) was considered, there would be no way to brand people as HIV-positive.

1. The existence of LTNPs (Long Term Non-Progressors), people who are HIV-positive, are not using AIDS drugs, and are healthy after one or two decades, must be trivialized. If their experience was taken seriously HIV would no longer be seen as a guarantee of future illness, and the use of toxic drugs prior to very serious illness would decline.
2. The existence of people with AIDS-defining illnesses, such as Tuberculosis and Kaposi's Sarcoma, without a positive HIV test could be seen as proof that HIV was not necessary for ‘AIDS’. Consequently HIV must be given priority over all other possible explanations. An HIV-positive IV drug abuser must then be considered to be protected from all other causes of Tuberculosis (such as drug use, malnutrition and lack of shelter) because the only possible cause of the disease that can be accepted is HIV. If it was possible that AIDS diseases could have other explanations in the presence of HIV was accepted, then AIDS drugs could never be prescribed until other explanations were considered and eliminated.

The Gallo document, and many other writings on HIV/AIDS, have created a tautological system that is protected from scientific testing because all possible combinations of conditions are given explanations. The consequence of this, however, is that HIV/AIDS is not a scientific theory. Belief in it requires faith because of the inability of anyone to test it.

The Gallo document claims that “the levels of antibody usually correlate to some extent with the level of virus replication”. First note the subtle backpedaling, the use of the words “usually correlate” and “to some extent”, which render the sentence meaningless because if an example is given where levels of antibody do not correlate with levels of virus replication they can simply point out that they only claimed that correlation was “usual” not universal or that they were only promising a weak correlation because of the words “to some extent” .

There are a number of papers that illustrate discordance between antibody test results and viral load. This can only be explained by imagineering data, claiming that a person was in the “window period” of early infection or in later infection with a destroyed immune system. But these claims are usually speculation. The possibility should be considered that these discordances are real:

1. “This report describes the field and laboratory investigation of eight patients who had clinical evidence of HIV infection, but repeatedly negative HIV-1 antibody screening results in the course of their clinical care. In all patients, HIV infection was proven [sic] by other diagnostic methods [PCR/viral load, p24 antigen and culture techniques]” [1]
2. “False-positive and false-negative results were observed in [7 French] laboratories (concordance [of viral load] with serology [ELISA/Western Blot antibody tests] varied from 40% to 100%)” [2]
3. “there is an approximately 15% probability that an HIV-negative sample will evidence nonspecific reactions to p24 on WB [Western Blot]...samples with strong reactivity to gag antigens...including p17, p24, p32, p46...and p55...can be misinterpreted as p17, p24, p31, gp41 and p55 bands, and this results in an overall positive interpretation...The 4 donors we studied all lacked HIV risk factors and were proven by HIV PCR and, in two cases, culture and p24 antigen analyses not to be infected” [3]
4. “LTNP [long-term non-progressor (to AIDS)] status was defined as asymptomatic HIV-1 infection for at least 8 years with stable CD4+ cell counts and no antiretroviral therapy...A wide range of plasma viral loads was observed among the LTNPs with HIV-1 RNA levels ranging from < 20 up to 860,000 RNA copies/ml plasma and a similar range was observed for the controls [Median: 40,000; Range: 2,200 up to 1,860,000] (Table I)...Among the 47 LTNPs with plasma viral load higher than 800 copies/ml, 30 had a viral load higher than 10,000 copies/ml and 3 had a viral load higher than 500,000 copies/ml despite fulfilling the inclusion criteria.” [4]
5. “The eight persons at risk who were positive for anti-nef protein antibodies were also positive for HIV DNA; five of the eight remained anti-nef antibody positive and HIV seronegative (by ELISA and Western blotting) and p24/25 antigen negative for eight months (one person...) and four months (four people), respectively, after the detection of HIV DNA” [5]
6. “In the CVL [cervico-vaginal lavage] samples [from HIV antibody positive women], 9 (41%) of 22 yielded culturable HIV-1, 16 (67%) of 24 were PCR positive for proviral HIV-1 DNA, 7 (30%) of 23 were positive for cell-free HIV-1 RNA, and 11 (45%) of 24 were positive for cell-associated HIV-1 RNA.” [6]
7. “Infectious virus was recovered from the serum of 20 (25.6%) of [78 randomly selected, HIV+ individuals, of whom about 30% were asymptomatic] and was generally present in low titers. Only undiluted serum (not a tenfold dilution) yielded infectious virus…In one serum sample, 25,000 infectious particles per milliliter were detected as measured by end dilution of the serum. This sample came from a clinically healthy individual with very low levels of antibody to HIV. Nine of the positive serum samples came from 39 individuals whose PMCs [peripheral blood mononuclear cells] were also tested. Virus was isolated from the PMCs of approximately 50% of these individuals and one third also yielded infectious virus in their serum. Three serum samples contained infectious HIV without any virus being recovered from the individuals’ PMCs…These studies demonstrate further that not all seropositive individuals have virus recoverable from their PMCs and that isolation from serum is not a common event” [7]
8. “A number of patients (31%) exhibited discordant responses with immunologic improvement and virologic failure [in a group of children receiving anti-viral medications]” [8]
9. “There were 140 P1 children [HIV infected without any clinical signs], 96 were seropositive...44 had become seronegative but had viral markers...4 subjects had positive viral cultures (3 repeatedly), 6 had serum p24 antigen (3 consistently), 9 had proviral DNA sequences by polymerase chain reaction [‘viral load’] (5 consistently), and 7 had expression of viral antigens in peripheral-blood mononuclear cells by direct immunofluorescence test (all confirmed); the remaining 18 subjects had two or more of these markers” [9]
10. “13 of 21 (62%) RNA samples from seropositive subjects were positive for HIV RNA” [10]
11. “In HIV carriers [those with an established HIV infection], the HIV RNA load is elevated, but infectivity is low [as measured by the success of cell cultures]. The low infectivity…could be due to neutralization by antibody in serum, resulting in immune complexes (ICs)” [11]
12. “The virological status of the 20% seropositive individuals who had negative cultures and no viral RNA detected remains unexplained.” [12]

1. Sullivan PS et al. Persistently negative HIV-1 antibody enzyme immunoassay screening results for patients with HIV-1 infection and AIDS: serologic, clinical, and virologic results. AIDS. 1999 Jan 14; 13(1): 89-96.
2. Defer C et al. Multicenter quality control of polymerase chain reaction for detection of HIV DNA. AIDS. 1992; 6: 659-63.
3. Sayre KR et al. False positive HIV-1 Western Blot tests in noninfected blood donors. Transfusion. 1996; 36: 45-52.
4. Candotti D et al. Status of long-term asymptomatic HIV-1 infection correlates with viral load but not with virus replication properties and cell tropism. J Med Virol. 1999 Jul; 58(3): 256-63.
5. Ameisen JC et al. Persistent antibody response to HIV-1-infected seronegative persons. N Engl J Med. 1989 Jan 26; 320(4): 251-2.
6. Panther LA et al. Genital tract human immunodeficiency virus type 1 (HIV-1) shedding and inflammation and HIV-1 env diversity in perinatal HIV-1 transmission. J Infect Dis. 2000 Feb; 181: 555-63.
7. Michaelis BA et al. Recovery of human immunodeficiency virus from serum (letter). JAMA. 1987 Mar 13; 257(10): 1327.
8. Nikolic-Djokic D et al. Immunoreconstitution in Children Receiving Highly Active Antiretroviral Therapy Depends on the CD4 Cell Percentage at Baseline. J Infect Dis. 2002 Jan 8; 184.
9. Tovo PA et al. Prognostic factors and survival in children with perinatal HIV-1 infection. Lancet. 1992; 339: 1249-53.
10. Hart C et al. Direct detection of HIV RNA expression in seropositive subjects. Lancet. 1988 Sep 10; 2: 596-9.
11. Dianzani F et al. Is human immunodeficiency virus RNA load composed of neutralized immune complexes? J Infect Dis. 2002 Apr 15; 185(8): 1051-4.
12. Richman D et al. Detecting Human Immunodeficiency Virus RNA in peripheral blood mononuclear cells by nucleic acid hybridization. J Infect Dis. 1987 Nov; 156(5): 823-7.