96 Rokeby Road

Red Hook, NY  12571

 

November 4, 2009

 

The Honorable Kathleen Sebelius                     Dr. Thomas R. Frieden, Director

U.S. Dept. of Health & Human Services           Centers for Disease Control and Prevention

200 Independence Avenue, S.W.                     Atlanta, GA 30333

Washington, D.C. 20201

 

Dear Secretary Sebelius and Dr. Frieden:

 

Subject:            AIDS policy

 

Reference:        1.         My letter, same subject, June 26, 2009, to Secretary Sebelius **

                        2.         Dr. Frieden’s letter responding to Reference 1, October 14, 2009

 

Thank you for the response to my June 26^th letter.  The original letter raised concerns regarding AIDS policy and some of its foundations, in many cases dealing with HIV testing.  The questions summarized concerns described in more detail in the presentation* accompanying Reference 1, and perhaps brevity in the letter masked some of the detail behind the concerns.

 

One objective of the letter was to discover the status of the various concerns: (A) valid, but open, with the current status; (B) valid, but resolved, with the resolution; (C) invalid, with explanation.

 

It does appear that only one of the ten concerns in Reference 1 was resolved by Dr. Frieden’s letter.

 

My response to Dr. Frieden’s letter follows, under each of the original numbered questions.  The CDC response to each question is also shown, indented, in italics. 

 

The three concerns at the end of Reference 1 regarding predictions of the HIV/AIDS theory that appear to have been wrong, though not numbered in the original, were also meant to be answered, and I have added them as items 8, 9, and 10 to the numbered list in this letter.

 

1.                   Why do criteria for a positive HIV test, unlike any other test, vary widely by geography?

 

The CDC response below distinguishes between “criteria for classifying a HIV test result as positive” (which CDC claims do not vary by geography) and “interpretive criteria for the results of one test, the Western Blot”, which do vary by geography.   

 

As the presentation made clear, the question was in regard to the Western Blot test.

 

Further, use of the Western Blot test is recommended in the U. S. to confirm HIV infection.

 

CDC contends that the differing Western Blot criteria overlap.  The question is not whether one or more “bands” may be common across geographies.  The question is:

 

a.       Whether someone said to be HIV-positive by the criteria in a given geography would be not positive by getting on a plane, going to another place, and getting tested there?

b.      Whether someone testing positive in Africa under criteria that would render that person not positive in the U. S. under CDC criteria might reasonably feel that they have gotten a bad deal compared to a similar case in the U. S.?

c.       Since our government is spending large sums for medical treatments in Africa based on HIV tests there, and the consequences of testing positive are severe, it seems logical to insure that those tests produce an accurate and consistent diagnosis.

d.      From a chart[1] in a letter to the International Journal of STD and AIDS, also found on the presentation page titled” A CLOSER LOOK AT HIV ANTIBODY TEST CONCERNS”, Item 3, “Varying criteria”, clearly someone said to be positive in Africa (AFR) [no GAG/POL band] could not be positive under the CDC 2 column, the same criteria cited in the CDC response below to this question 1.

e.        Similarly, someone with just p24 in the GAG/POL group, and p41, positive by CDC 2, would not be positive by Australian criteria.

 

Clearly, this concern seems valid, and unresolved, status A.

 

                        Oct. 14, 2009 response by CDC to original question 1:

 

The criteria for classifying a HIV test result as positive do not vary geographically.  Several different interpretive criteria for one test, the Western Blot, have been issued by different organizations and agencies.  However, these criteria, while slightly different, overlap.  In addition, all these criteria classify patients in the same way, as infected with HIV.

 

CDC’s criteria were issued in the Morbidity and Mortality Weekly Report in 1989 and can be accessed on the Internet by visiting http://www.cdc.gov/mmWR/preview/mmwrhtml/00001431.htm

 

2.                   Why is the PCR test approved for children, but not for adults?

 

Thank you for making me aware of the approval of the Aptima PCR test.  Question 2 has been a puzzle for many years, and the approval of the Aptima test would resolve that question with status B, if there are no other PCR tests which are approved only for use in children.

 

The work submitted by the manufacturer as validation of the test raises, however, other questions:

 

a.       The package insert[2] for the Aptima HIV-1 RNA Qualitative Assay indicates, in the Table, “Summary of Interpretation of Specimen Results”, on Page 9, that the combination of reactive Aptima and repeatedly reactive HIV-1 antibody result should be regarded as “Confirmed HIV-1 infection*”.  The asterisk, however, says “The individual should be referred for medical follow-up and additional testing”.  Does this mean that an additional test is required to confirm infection?

 

(1)               Under “Limitations of the Procedure” on Page 16 of the same insert, describing results of tests run on a seroconversion panel, 27 specimens were both repeatedly reactive on the EIA (presumably an HIV-1 antibody test), and on the Aptima.  However, 8 of the 27 were negative on the Western Blot test, which seems to suggest the need for additional testing to confirm infection, even if the sample is repeatedly reactive on HIV-1 antibody and reactive on Aptima.

 

b.      Table 3 under “Performance Characteristics” of the same insert also seems to suggest the need for further testing of specimens that are both repeatedly reactive HIV-1 antibody and reactive on Aptima.  On the row labeled “Unknown N = 239”, at least one specimen satisfied those conditions, but had a negative p24 Ag and indeterminate Western Blot.

 

                        Oct. 14, 2009 response by CDC to original question 2:

 

The Aptima HIV-1 Qualitative RNA assay, which is a Polymerase Chain Reaction (PCR) test, is approved for both the diagnosis of acute HIV infection (e.g., the period immediately after a person is infected, during which time HIV viral loads are typically extremely high, the immune system has not yet produced detectable antibodies to the virus) and the confirmation of reactive antibody tests in adults.

 

3.                   Why do roughly 60% of nine-month old babies who test HIV-positive wind up negative at 18 - 24 months?

 

a.       As the presentation explained (“OTHER CONCERNS WITH THE HIV TESTS”, Item 15), it has long been known that babies lose all maternal antibodies by nine months.  All antibodies include any antibodies to HIV.

b.      That maternal HIV antibodies also disappear from the baby by nine months was shown by Bharat S. Parekh, of the CDC’s National Center for Infectious Disease, Division of HIV/AIDS, and co-workers, in a paper[3] published in AIDS Research and Human Retroviruses.

c.       So a baby who tests positive at or after nine months, and later loses its positive status, is losing its own positive status, not the mother’s.

d.      The only explanations are that the babies are curing themselves of HIV, or that the test is detecting something other than HIV.

e.       Two pages from a presentation on the subject explain the points above.  See Attachment 1.

 

Status A (open, not resolved). 

 

                        Oct. 14, 2009 response by CDC to original question 3:

 

Uninfected infants often test positive for maternal HIV antibodies that were transferred during pregnancy.  The observation that these antibodies disappear with time is well established.

 

For information on diagnosis of HIV infection in infants visit http://aidsinfo.nih.gov/contentfiles/pediatricguidelines.pdf

 

 

4.                   Why, given vast AIDS expenditures, has the 1985 validation of the HIV tests, clearly far from advertised accuracy, not been superseded by a more authoritative and accurate validation?

 

Again, brevity (and the assumption that the background in the presentation would be used) may account for a possible misunderstanding.

 

a.       The FDA stated in a correspondence that the original validation of the HIV tests, cited as three 1984-1985 scientific papers [4], had not been superseded. 

b.      The Weiss, et al paper assesses sensitivity and specificity of the tests; all three papers rely on a fourth paper [5], by Gallo, et al, as the basis for the “Detection Isolation” of the disease agent whose presence the tests seek to show.

c.       The Weiss paper found a positive result in only 82% of AIDS patients tested.

d.      The key Gallo “Detection and Isolation” paper isolated HIV from only 36% (26 out of 72) of AIDS patients.

e.       Further, there have been changes in the definition of AIDS since 1984-5, and one of the original signature illnesses, Kaposi’s sarcoma, seems to have causes other than HIV.  It seems reasonable to include a wide range of AIDS illnesses in a new, authoritative validation effort.

f.        Dr. Weiss’s work used correlation of positive tests to illness in patients, but correlation only indicates the possibility of a relationship; it does not prove that there is a relationship.  For proof, the disease agent should be isolated and purified from the patient testing positive, and shown to be infectious.

g.       To try to exclude the possibility of an accidental relationship, of cross-reactions, Dr. Weiss tried the test on a small set of patients with other conditions.  But there are thousands that would have to be tried.  Proving a negative is the hard way to do things.  And, as it turned out later, there are indeed many cross reactions that occur, documented extensively in the scientific literature.  Those cross reactions are not surprising, since AIDS patients often have a variety of infections.  Further, antibody – antigen reactions are not unique – a given antibody may react with a number of different proteins (antigens).

h.       For ill patients, Dr. Weiss uses only a single ELISA test, and did not attempt to check positive results for ill patients with a different test, such as the Western Blot.

i.         CDC’s response mentions validation work done for new tests seeking approval by the FDA.  That work, however, is done by the companies who have an interest in gaining approval for the tests, and should rest on validation work by disinterested parties who have no stake in the outcome.

j.        New HIV test approval generally validates the tests based on samples from patients who have tested positive on prior tests; that chain of prior tests, however, ultimately leads back to the original 1984-1985 validation and detection and isolation work.

k.      While Gallo, et al claimed to isolate HIV from patients, their procedure is quite different from classical purification and isolation performed on serum directly from the patients.  The related query in Item 7 refers to a prior, seemingly unsuccessful, attempt to perform classical purification and isolation.  A future official validation effort should include classical purification and isolation, as well as confirmation that the isolated material is subsequently infectious, to insure confidence in the result.

l.         Both Gallo and Montagnier used detection of reverse transcriptase (RT) as evidence of retroviral activity.  Both of them, however, and many other scientists, have stated that reverse transcriptase is not unique to retroviruses.  A renewed validation effort should not rely on RT to deduce the presence of a causative agent.

m.     The taxonomy of HIV has changed since the original validation work.  HIV was thought to be an oncovirus originally, and later had been regarded as a lentivirus.  Recent work has gone back to the oncovirus view.  A renewed validation should resolve the classification issue.

n.       Several of the proteins tested for may be cellular in origin.  Montagnier regarded the p41 protein as actin, a common cell constituent.  There is evidence that others of the claimed HIV proteins also may be cellular in origin.  A monograph[6] explains the evidence in some detail, with references – see page 185, ‘Origin of the “HIV” Proteins’.

o.      The procedure Gallo utilized, culturing patient serum, and then using chemicals to break apart material in the serum to allow components of HIV to be detected by analysis of their density, has potential problems:

 

(1)               Dormant viruses, suppressed by the immune system, can exist in cells.  Those pro-viruses can become active in the absence of immune system anti-viral substances, as would be the case with a cell culture.

(2)               The components of cells, many of which can appear similar to viruses, and which are made up of the proteins and nucleic material also found in viruses, can be released by the procedures used in treating the cultures.

(3)               A small part of every human DNA is made up of endogenous retroviral sequences, which can give rise to endogenous retroviruses, as opposed to externally acquired retroviruses such as HIV.

 

Since the tests are in such widespread use, and the consequences can be so serious, and very large sums have been made available for research, it seems quite reasonable to revalidate the tests, confirming that positive results in patients correspond to actual diagnosed illness in the patient, confirmed by isolation of the disease agent from the patient and by determination that the isolated agent is subsequently infectious.

 

Otherwise, the possibility remains that the chain of tests built upon prior tests may be repeating flaws in the original validation work.

 

Many of the concerns above are described in more detail, with references, in the monograph cited in item n. above.

 

                        Oct. 14, 2009 response by CDC to original question 4:

 

Numerous HIV antibody and nucleic acid tests have been introduced since 1985, each of which has been extensively validated before approval by the Food and Drug Administration (FDA).

 

For a list of these tests and links to the Summary Basis of Approval, please visit the FDA website at http://www.fda.gov/BiologicsBloodVaccines/BloodBloodProducts/ApprovedProducts/LicensedProductsBLAs/BloodDonorScreening/InfectiousDisease/UCM080466

 

5.                   Why are HIV positive tests in various populations almost invariably ordered by race, regardless of risk group?

 

Perhaps “sequenced by race” would have been a better rendering of the question, and yes, the question does pertain to CDC surveillance data.

 

The answer below did not address the basic question, explained more fully in the presentation (“HIV TEST CONCERNS”, Item 5), and in great detail by the work of Professor Henry H. Bauer (please see “The Origin, Persistence and Failings of the HIV/AIDS Theory”, ISBN 978-0-7864-3048-2).  Briefly, he discovered that surveillance data, regardless of risk group, generally showed that Blacks had the highest incidence of positive tests, followed by Hispanics, Whites, and Asians, in that order.  His work also identified other statistics from the data that were inconsistent with a sexually transmitted disease.

 

The results on race raise the possibility that some innate characteristic of race (Vitamin D stress from various levels of pigmentation is one idea) is responsible for heightened antibody levels.  If so, the interpretation of the test, and the diagnosis, would need to be changed.

 

Professor Bauer’s analysis has been available for some years, in book form and on the Internet, and it is surprising CDC’s response seemed unaware of the matter.  If his analysis is correct, and factors other than HIV account for the disproportionate number of positive tests among black people, a more hopeful and curable diagnosis than AIDS may be possible for many.

 

                        Oct. 14, 2009 response by CDC to original question 5:

 

It is not accurate that HIV tests are ordered by race and ethnicity.  HIV test are ordered for individuals regardless of race, ethnicity, or perceived risk behavior.  CDC’s 2006 recommendations for HIV testing in healthcare settings for adults, adolescents, and pregnant women, recommend routine HIV screening for all patients ages 13 to 64 in all healthcare settings.  The recommendations emphasize the importance of voluntary testing by the individual.

 

Your question may relate to how CDC presents surveillance data.  CDC presents data according to a number of demographic and risk characteristics in order to paint a complete picture of the distribution of HIV and AIDS cases in the United States.  This allows a clear picture of populations and risk groups most affected by the epidemic.  It also, in turn, provides valuable information for targeting resources and prevention programs in the most effective way.

 

6.                   Why, despite widespread drug treatments, has the median age of death from AIDS remained under 45 years?

 

As Professor Henry Bauer explains in the web link (http://hivskeptic.wordpress.com/2009/02/18/deaths-from-“hiv-diseaseâ€�-why-has-the-median-age-drifted-upwards/), the gradual drift upward in the median age of death from AIDS can be explained by a similar upward drift in the median age of people living with AIDS (PWA) and in the median age when people test positive.  People living with AIDS have increasingly been those who (1) became AIDS statistics through the 1993 redefinition that included healthy people with low CD4 counts, thus increasing the proportion of healthy patients; (2) were black, and who tended to both die more often, and die at older ages, than other people with AIDS.

 

The objective, surely, is to have treatments or diagnoses that move the age of death for AIDS patients so it approaches or equals that of the general population.  That anti-retroviral treatment is so far from that objective, and that age of death, properly analyzed, has hardly budged, suggests the possibility of a mismatch between treatment and illness, which implies either the need for different treatments for HIV, or that HIV may not be the source of many of the illnesses.

 

                        Oct. 14, 2009 response by CDC to original question 6:

 

In the United States, the median age at death due to HIV disease increased almost linearly from 36 years in 1987 to 39 years in 1995, and to 45 years in 2005.  This is a reflection of the postponement to older ages of HIV-attributable deaths that were not entirely prevented by improved treatment.

 

An example of the mortality slide set is on the Internet by visiting http://www.cdc.gov/hiv/topics/surveillance/resources/slides/mortality/slides/mortality9.pdf.

 

There are a few things likely to impact the median age of death due to HIV.  First, individuals who test late in the course of their disease may not receive the full benefits of treatment and as a result survival is not prolonged by treatment.  Second, for various reasons, individuals may not receive care after a diagnosis (early or late diagnosis).  Third, there is a cohort of HIV-infected individuals that are benefiting from antiretroviral therapy and have not yet died.  When these individuals die, they will be at a much older age and at that point, we would expect to see the death median age increase.

 

7.                   Why was standard isolation and purification of the presumed disease agent from patient blood not attempted until 1997?  Why was the disease agent that was found too large?  Why were supposed HIV proteins also detected in non-infected samples, albeit more faintly?

 

The question referred to a specific effort to isolate and purify HIV directly from AIDS patients, done by Bess, et al [7] in 1997.  Since HIV antibody tests done on patient samples rely on detecting antibodies presumed to be against HIV, there should be HIV in the samples that gave rise to the antibodies. 

 

Thus it should be possible to perform classic isolation and purification of the disease agent directly from patient blood, rather than the method used by Gallo, et al in growing and specially treating cultures of blood.

 

That classic isolation and purification procedure was what the Bess, et al study attempted to do.  Yet the result was strikingly non-pure, with many extraneous particles, and the particles regarded as HIV were significantly larger than the size claimed for HIV.  A protein gel electrophoresis procedure run on the Bess study samples detected the same proteins in both healthy and infected samples, though the healthy ones were fainter.  This suggests that what is being detected exists in both the infected and healthy subjects.

 

The three concerns the study raises (impurity of the result, size mismatch, and detection of supposed specific proteins in both healthy and sick patient samples) demand explanations.

 

                        Oct. 14, 2009 response by CDC to original question 7:

 

In 1983, scientists discovered the virus that causes AIDS.  The virus was first named HTLV-III/LAV (human T-cell lymphotropic virus-type III/lymphadenopathy-associated virus).  For many years scientists theorized as to the origins of HIV and how it appeared in the human population, most believing that HIV originated in other primates.  Then, in 1999, an international team of researchers reported that they had discovered the origins of HIV-1, the predominant strain of HIV in the developed world.  A subspecies of chimpanzee native to west equatorial Africa had been identified as the original source of the virus.  The researchers believe that HIV-1 was introduced into the human population when hunters became exposed to infected blood.

 

For more information, visit the National Institute for Allergies and Infectious Diseases at http://www3.niaid.nih.gov/news/newsreleases/1999/hivorigin.htm.

 

HIV-1 has the morphology, particle size, buoyant density, genome organization, and genome size typical of the lentivirus genus of the Retroviridae.  Highly sensitive PCR assays do not detect viral DNA or RNA in samples from uninfected individuals.  For more information of the biology of HIV visit http://www3.niaid.nih.gov/topics/HIVAIDS/Understanding/Biology/.

 

8.                  Why did expectations of a heterosexual AIDS epidemic not materialize [8], and does such an incorrect prediction, differing from usual sexually transmitted diseases, suggest the need to reconsider the cause of illness in AIDS patients?  If not, why not?

 

9.                  The study referenced in the footnote [9] found that sexual transmission could not explain most African AIDS cases.  Here again, does this finding, contrary to expectations, suggest the need to reconsider the cause of African AIDS?  If not, why not?  If most African AIDS cannot be accounted for by sexual transmission, does that suggest a reconsideration of sexual transmission as the cause of most U. S. AIDS cases?  If not, why not?

 

10.              Given concerns regarding the correlation of PCR results with patient immune system status, such as the footnoted study [10], should PCR tests currently approved for use with patients be revalidated, ideally with isolation and purification of disease agent from sick patients whose PCR test is positive for HIV?  If not, why not?

 

Underlying the PCR, like all the tests for HIV, is the Gallo, et al detection and isolation paper, with the concerns raised in Item 4, sub-items k. through o.  A revalidation of the PCR procedure with classical purification, isolation, and proof of infectivity, could resolve concerns regarding the use of the PCR procedure to detect HIV.

 

I greatly appreciate the efforts of HHS and the CDC seeking to resolve these questions, and look forward to a response to the questions and detail above.

 

Sincerely,

 

 

 

 

Frank Stoppenbach

 

Phone:              845 758-1726

E-mail:              frankst@attglobal.net

 

cc:        The Honorable Charles Schumer

            The Honorable Kirsten Gillibrand

            The Honorable Scott Murphy

 

* Also available at www.aidspetition.org/WhyReexamine.htm

** A copy of the original letter is available at www.aidspetition.org/hhsletter.htm