109 Questions for Robert Gallo and other HIV/AIDS "experts":


1. If "HIV" testing is so accurate, then why did JAMA (Journal of the American Medical Association) publish an article a month ago that claimed that:


“Viral load is only able to predict progression to disease in 4% to 6% of HIV-positives studied, challenging much of the basis for current AIDS science and treatment policy?”

(Rodriquez B, Sethi AK, Cheruvu VK, et al. Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection. JAMA 296 (12):1498-506, 2006; Cohen J. Study says HIV blood levels don't predict immune decline. Science 313(5795):1868, 2006). What implications does this JAMA report have for the defendant?


"A nationwide team of orthodox AIDS researchers led by doctors Benigno Rodriguez and Michael Lederman of Case Western Reserve University in Cleveland are disputing the value of viral load tests-a standard used since 1996 to assess health, predict progression to disease, and grant approval to new AIDS drugs after their study of 2,800 HIV positives concluded viral load measures failed in more than 90% of cases to predict or explain immune status…”“Viral load is only able to predict progression to disease in 4% to 6% of HIV-positives studied, challenging much of the basis for current AIDS science and treatment policy”


2. If "HIV" is isolatable as an exogenous unique retrovirus, why would a hepatitis B vaccine (Lee, D, Eby W, Molinaro, G. HIV false positivity after Hepatitis B vaccination. Lancet 339: 1060, 1992), or flu vaccine (Simonsen L, Buffington J, Shapiro CN, et al. Multiple false reactions in viral antibody screening assays after influenza vaccination. Am J Epidemiol 141:1089-1096,1995; Christian, P. Erickson, Todd McNiff, Jeffrey D. Klausner. Influenza Vaccination and False Positive HIV Results New England Journal of Medicine,Number 13 , Volume 354:1422-1423, March 30, 2006)

cause about 2% false positives? Do you know if the defendant had any vaccines before he was "HIV" tested, and could prior vaccines account for his being "HIV-positive?


A related question is, if the Center For Biologics Evaluation and Research Advisory Committee on Vaccines and Related Biological Products claimed in November, 1998, in a chapter regarding the Update On Reverse Transcriptase Activity In Chicken Cell Derived Vaccines, by Dr. Arifa Khan (pages 13-15), that:


"Initially Boni et al. (1996) published that low level reverse transcriptase activity was detected in ALL chicken cell derived vaccines using a highly sensitive PCR-based reverse transcriptase assay called PERT, which can detect one to ten virions which was reported to the WHO, and then additional studies were done by several laboratories in Europe, as well as the U.S., including the NIBSC, the CDC, as well as labs in the FDA to confirm this initial finding. However, after further work, it was discovered that this reverse transcriptase activity could be eliminated by treatment of extracts with DNAase, and that using Alu-based EAV sequence integration studies, that no integration of anything derived from the chicken cell supernatants was detected in Human PBMC cells."


Were/are "HIV" culture extracts also treated with DNAase to test if reverse transcriptase activity is eliminated by DNAase treatment? A related question is, if reverse transcriptase activity is present in all chicken cell-derived vaccines, as the report from Khan and others (and confirmed in several European and CDC laboratories indicate are present in all chicken cell-derived vaccines), then is it possible that anyone injected with measles or other vaccines derived from chicken cell-derived vaccine preparation procedures, might also test positive for reverse transcriptase activity due to reason that have yet to be elucidated? Was the defendant ever a recipient of a chicken cell-derived vaccine or related product? If reverse transcriptase activity was used to detect "HIV" in "HIV" cultures during the early 1980's, and if reverse transcriptase is specific for "HIV," then why do market magazines concerning biotechnology stocks claim that reverse transcriptase can be found in a plethora of normal (non-"HIV"-associated) contexts (Pachez M. No need to be phased. Shares, 28-32, 2001. Papadopulos-Eleopulos E, Turner VF, Papadimitriou J, Page B, Causer D, Alfonso H, Mhlongo S, Miller T, Maniotis A, Fiala C. A critique of the Montagnier evidence for the HIV/AIDS hypothesis. Med Hypotheses 63(4):597-601, 2004)?


3. Why did the Red Cross report that even after repeated testing using different test kits, that low-risk populations, such as blood donors (or military recruits) will typically yield 12 (PCR) positive or 2 (ELISA) positive results out of 37,000,000 samples, leaving potentially 10 out of 12 false positives, depending on which test kit you believe (Stramer et al. “Detection of HIV-1 and HCV Infections among Antibody-Negative Blood Donors by Nucleic Acid–Amplification Testing. New England Journal of Medicine, Volume 351:760-768, August 19, Number 8, 2004)?  Is it possible that the defendant is among these 10 out of 12 false positives, as is the woman to whom he supposedly transmitted "HIV?"


4. If the components of "HIV" have been isolated and are unique to "HIV," why did Barre-Sinoussi (one of Luc Montagnier’s original group from whom Dr. Gallo hijacked LAV, later to be called “HIV”) come out of the closet, and say at the Toronto International AIDS festival last August that:


 “It is not clear if therapeutic vaccines might be useful, since 15 trials to date have not demonstrated definitive evidence of improved outcomes.”


5. Phase III trials are supposed to test the efficacy of a medical intervention against the best current treatment in place. If the components of "HIV" have been isolated and are immunogenic in humans,  as components of an exogenous virus would be expected to be, then why did you (Robert Gallo) say in 2004 after the failure of the AIDSVAX "HIV" trial that "a sound rationale is needed for Phase III HIV vaccine trials?" Weren't the Phase I and II trials based on a sound rationale? Do "HIV/AIDS" experts advocate progressing to phase III trials even when Phase II trials are an unmitigated failure as was the case of AIDSVAX? (Gallo and Others. A sound Rationale needed for Phase III HIV vaccine trials. Science, Vol 303 16 January, 2004).


6. If the “HIV" is an exogenous virus with a unique identity, why did a group of AIDS researchers in The Department of Microbiology, University of Minnesota publish in The Journal of Virology, that “HIV” gene sequences can be detected in non-infected humans, chimps, and monkeys?


“HIV-like sequences exist in normal in human, chimpanzee, and rhesus monkey DNAs: "Endogenous retrovirus-related sequences exist within the normal genomic DNA of all eukaryotes…Herein we describe the first report of the presence of nucleotide sequences related to HIV-1 in human, chimpanzee, and rhesus monkey DNAs from normal uninfected individuals." (Horwitz MS, Boyce-Jacino MT, Faras AJ. Novel human endogenous sequences related to human immunodeficiency virus type 1. (J Virol. Apr;66

(4):2170-9, 1992).


7. If "HIV" is a new virus, and if the "HIV" tests are specific, then why did the Journal of Clinical and Diagnostic Laboratory immunology publish an article that showed that goats and cows test positive for "HIV" but do not develop AIDS? (Willman et al., Heterophile Antibodies to Bovine and Caprine Proteins Causing False-Positive Human Immunodeficiency Virus Type 1 and Other. Enzyme-Linked Immunosorbent Assay Results. Clinical and Diagnostic Laboratory Immunology, p. 615-616, Vol. 6, No. 4, July 1999).


8. What disease(s) do the following symptoms specify?


"Then the adjacent lymph glands become swollen and rubbery, a condition known as regional lymphadenopathy.”


“Thereafter, the disease “matures” for up to six months" and can become characterized by a “macular” (spotty) roseola-like rash and other skin symptoms. The regional lymphadenopathy becomes generalized and affects the body’s whole lymphatic system; it is a “valuable diagnostic finding” and one of the most characteristic aspects of the early disease; the lymph nodes are “painless,” “enlarged,” “rubbery,” “non-tender,” and “freely moveable.”


“The patient will complain of rashes, fever, itching, sore throat, headache, malaise, vertigo, sweating, insomnia, nausea, prostration, weight loss, loss of hair, or aching in the bones and joints. Some have hypertension, kidney disease, swollen liver, or swollen spleen; others have a subacute meningitis with cranial nerve involvement. The thymus-dependent parts of the lymphatic system deteriorate, and there is consequent decrease in the numbers of T-lymphocytes. The T-helper cells are particularly affected by this: there is a decline in their number and the ratio with the T-suppressor cells is reversed."


"At this stage, such conditions as infectious mononucleosis, iritis, neruoretinitis, lichen planus, cancer, nephritis, dementia, lymphomas, psoriasis and other skin eruptions, and even drug reaction… are confused with this stage."


"Consequently, a long-term effect of syphilis is loss of, or decline in, the system of immunity, and lowering of the individuals capacity to defend himself against other infectious conditions For this reason secondary syphilis is called the great imitator” (AIDS and Syphilis-The Hidden Link, by Harris L. Coulter, North Atlantic Books, 1987).


9.  Have other medical reasons for the defendant testing positive been excluded, including prior receipt of hemodialysis, transfusions, gamma globulin, or immune globulin (as prophylaxis against infections), TB or cryptic forms of that great imitator, syphilis, malnourishment, herpes simplex I and II, arthritis, systemic lupus erythematosus, scleroderma, connective tissue disease, dermatomyostitis, malaria, hemophilia, hepatitis, alcoholic hepatitis, primary billiary cirrhosis, hyperbilirubinemia, hypergammaglobulinemia, leprocy, lipemic serum, malaria, malignant neoplasms, mycobacteriaum avium, Q-fever with associated hepatitis, primary sclerosing cholangitis, visceral leishmaniasis, renal failure, Stevens-Johnson syndrome, high levels of circulating immune complexes and ERS rates (erythrocyte sedimentation rates or “sticky blood” known to be high among Africans and other populations), free ribonucleoproteins, T-cell leukocyte antibodies, HLA antibodies (to Class I and II leukocyte antigens), p18, p24, p55, p12, p32, p51, p66, or gp160, gp41, gp120 antigens that may be present in fluids obtained from patients who have warts?


10. Patient 1, according to Montagnier, from whom he acquired the "HIV" (LAV) isolate (that Gallo was later accused by The French, The Dingell Commission, and The Office of Scientific Integrity at the NIH of stealing from the Pasteur group), was said to have had herpes, 2 cases of gonorrhea, 1 case of syphilis, cytomegalovirus, and Epstein-Barr virus. Do you think this patient 1 was a good source of your "HIV" isolate? Was the first Abbott Labs patented test kit designed around this isolate? Why did Gallo obtain the "LAV" isolate from the Montagnier group, and claim that he had discovered it?


(From John Crewdson: Gallo Case, Truth Termed A Casualty Report: Science Subverted in AIDS Dispute; Chicago Tribune (CT) - SUNDAY, January 1, 1992 from the Dingell Report):


“The violence to principles of responsible, ethical science was just as profound. At a crucial point early in the (Gallo laboratory's) HIV research, international politics and the technocrats committed to those politics virtually took over that research, claiming the laboratory's putative accomplishments as accomplishments of the United States administration and by extension, the United States itself.”


“Once done, the (Gallo laboratory's) interests became the government's interests; defending the (Gallo laboratory) scientists' reputations and claimed accomplishments became necessary for defending the honor of the United States. The defense thus became a consuming effort for significant portions of the U.S. government.”


“The result was a costly, prolonged defense of the indefensible in which the (Gallo laboratory's) “science” became an integral element of the U.S. government's public relations/advocacy efforts. The consequences for HIV research were severely damaging, leading, in part, to a corpus of scientific papers polluted with systematic exaggerations and outright falsehoods of unprecedented proportions.”


11. In 1956 Dr. Etienne de Harven was the first to show electron microscope images of the Friend virus in murine (mouse) leukemia, and in 1960, to coin the word "budding" to describe steps of virus assembly on cell surfaces. He also delivered a speech at the 12th World AIDS Conference in Geneva (June 28-July 3) at the session entitled, "HIV-testing: Open Questions about Specificity."


Why did Dr. Etienne de Harven, who is now an emeritus Professor of Pathology, University of Toronto and who worked out the ultrastructure of retroviruses throughout his professional career of 25 years at the Sloan Kettering Institute in New York and 13 years at the University of Toronto, vociferously object to the standards used to claim that "HIV" viral particles had been convincingly isolated?"


"First the antibody. ELISA, then Western Blot tests were hastily developed (at sizable financial profit eagerly split between the Pasteur Institute and the US). "Seropositivity" became synonymous with the disease itself, plunging an entire generation into behavioral panic, and exposing hundreds of thousands of people to 'preventive' antiviral AZT therapy which actually hastened the appearance of severe or lethal immunodeficiency syndrome. Appropriate controls were apparently never carried out or were never published. Still, back in 1993 it became clear that the so-called HIV antibody tests badly lacked specificity, (Papadopulos-Eleopulos E, Turner VF and Papadimitnou JM, 1993. Is a positive Western Blot proof of HIV infection? Bio/Technology 11:696-707) cross-reactivity being observed with patients suffering from a long list of pathological conditions including malaria, leprosy, auto-immune diseases and many more."


"Secondly, 'viral proteins'. Several proteins have been identified as 'HIV markers', most frequently because they were identified in a variety of 1.16 bands. The case of the p24 "viral" antigen is a significant example and its lack of viral specificity has been well documented. (Todak C, Klein E, Lange M et al., 1991. A clinical appraisal of the p24 antigen test. International Conference on AIDS, vol 1, Florence, Italy)."


"Third, reverse transcription. If reverse transcriptase activity were a unique feature of retroviruses, it could have been an interesting molecular marker. Unfortunately, it has been shown that reverse transcriptase is found in the uninfected cells of yeasts, insects and mammals (Varmus H, 1987. Reverse transcription Sci. Am. 257:48-54) and "has nothing to do with retroviruses as such." Moreover, K. Mullis himself does not support the use - to amplify and quantify the "HIV genome" - which is being made of the PCR methodology he developed, which is the current method of "measuring the viral load" in AIDS patients."


"More disturbing is the fact that some 'markers' are searched for in the 1.16 gradient sedimenting material which is the density where intact virions are expected to be found, but not their molecular fragments. If lysed retrovirus particles released molecular markers, the 1.16 samples should at least initially allow investigators to demonstrate virus particles by EM. They don't. However after 15 years of most intensive HIV research, two independent groups finally decided to explore by electron microscopy the ultrastructural features of the material sedimenting at the 1.16 density. Working on "HIV-1 infected T-cell" cultures supernatants, both groups found that it contains primarily cellular debris and cell membrane vesicles which could definitely not be identified with HIV particles and rare "virus-like" particles (Gluschankof P. Mondor I, Gelderblom HR, and Sattentau QJ, 1997. Cell Membrane vesicles are a major contaminant of gradient-ennched human immunodeficiency virus type-l preparations. Virology 230:125-133; Bess JW Jr., Gorelick WJ, Bosche WJ, Henderson LE, and Arthur LO, 1997. Microvesicles are a source of contaminating cellular proteins found in purified HIV-I preparations. Virology 230:134-144)."


"Still, this is the type of sample in which "viral markers" are currently identified and used to measure the effects of anti-viral drugs in current clinical trials."


"In conclusion, and after extensive reviewing of the current AIDS research literature, the following statement appears inescapable: neither electron microscopy nor molecular markers have so far permitted a scientifically sound demonstration of retrovirus isolation directly from AIDS patients."


12. A few years ago, a 3 1⁄2 year-old girl named Eliza Jane Scovill died 36 hours after being prescribed amoxicillin for the first time in her life. Commenting on the tragic death, a prominent AIDS researcher named Dr. John Moore of Cornell Medical College who spoke at last summer's Toronto International AIDS conference at the AIDS and Responsible Journalism session, strongly advocated that a Salem Witch Trial for Ms. Christine Maggiore, and her partner Robin Scovill be intensively pursued by The State and the press, because Ms. Maggiore inconsistently tested "HIV" positive 6 times (inconclusive, positive, inconclusive, positive, negative, and positive-with no 2 tests in a row indicating she was positive). For this reason, and perhaps to avoid stigmatization of her children, Ms. Maggiore did not want her daughter or son tested for "HIV." From hospital records, it was learned that the little girl had 10,800 lymphocytes/microliter at the time of her hospital admission, which is far more than the average number of lymphocytes in a normal blood sample. The WHO defines AIDS as a condition in which a person exhibits 1000 or fewer lymphocytes/microliter, and the absolute number of lymphocytes was obtained at the hospital upon admission, and according to "AIDS experts," they are just as predictive of AIDS-related death in children, if not more so than CD4/CD8 ratios. In a recent study of 3917 children, it was reported that:


“For children older than 2 years, the 12-month risk of death and AIDS increased sharply at values less than 1500-2000 cells per microliter, with little trend at higher values.” (Eliza Jane's count was 10,800 cells/microliter).


“Mortality risk was substantially higher at thresholds of total lymphocyte count recommended by WHO than at corresponding thresholds of CD4-cell percentage. When the markers were compared at the threshold values at which mortality risks were about equal, total lymphocyte count was as effective as CD4-cell percentage for identifying children before death…” (HIV Paediatric Prognostic Markers Collaborative Study. Use of total lymphocyte count for informing when to start antiretroviral therapy in HIV-infected children: a meta-analysis of longitudinal data. (Lancet. Nov 26;366 (9500):1868-74, 2005).


Why has Dr. Moore, and many members of the AIDS establishment since the death of Eliza Jane claimed that this little girl died of AIDS when her lymphocyte count was 10,800 cells/microliter? Is Dr. Moore correct in his assertion that AIDS is a disease of too many lymphocytes rather than too few lymphocytes?


13. Have you (Gallo or "HIV" expert) or anyone you work with ever written a letter of apology to the kin of the dentist, Dr. David Acer, for his committing suicide on the basis of mistaken charges that he spread “HIV” to his patients, which the CDC later exonerated him of doing (after he committed suicide), because the CDC could "find no evidence the dentist's HIV-positive patients contracted their infections from him because their virus' DNA did not match his, and also concluded the dentist's patients did not contract the virus from one another -- in effect, that unclean dental implements did not act as conduits." Ted Anthony. STUDY: HIV not contracted from dentist. Associated Press, Thursday, December 1, 1994. ww2.aegis.org/news/ap/1994/AP941233.html


14. Why have so many studies which begun even at the beginning of the AIDS era, and that have followed exposure of health care workers to "HIV" through sharps, or other injuries, found no transmission of AIDS (Hirsch MS, Wormser GP, Schooley RT, Ho DD, Felsenstein D, Hopkins CC, Joline C, Duncanson F, Sarngadharan MG, Saxinger C et al. Risk of nosocomial infection with human T-cell lymphotropic virus III (HTLV-III).N Engl J Med. Jan 3;312(1):1-4, 1985)?


15. If you are a cancer researcher, and you don't believe, for example, that the deregulation of the p53 oncogene completely, or even partially explains cancer, you are not considered a Holocaust denier, or worse perhaps, a flat-earther, irresponsible, or criminal.  Instead, other hypothesis are permitted, tolerated, and even funded. Why is it that alternate hypotheses of AIDS pathogenicity, such as the redox hypothesis of the Perth Group, the Multiple Antigen Mediated Autoimmunity hypothesis advanced by Robert Root-Bernstein, the illicit and pharmaceutical-drugs-AIDS hypothesis advanced by government researcher Harry Haverkos and NAS member Peter Duesberg, not been pursued or funded in 25 years? As a related question, why have the following letters and articles from just one group of researchers (The Perth Group) been repeatedly rejected from scientific journals? Are they poorly written? Are they filled with what you would consider to be dangerous ideas?


Gallo's experiments and a plea for clarification  

Perth Group reponse to Nature and its Durban Declaration       

gp120 and HIV infection           8K

Commentary on the Ho and Wei Nature papers           

Concerning TB in Africa          

Commentary on AZT   

Anti-HIV antibodies, ARVs and informed consent

HIV transmission from chimpanzees     

A critical analysis of HIV serology does not affirm a retroviral infection

A critical appraisal of the evidence for the existence of HIV      

Commentary on the Gallo/Montagnier HIV as the cause of AIDS paper           

Response to Declan Butler       

Letter to Lancet in response to the WHO         

Letter to NEJM July 2004       

Letter to BMJ  

Letter to Nature Medicine        

Letter to Lancet           

Letter to Structure


16. How are the chimps who were injected with AIDS-patient sera more than 20 years ago and who never developed any AIDS-indicator diseases doing in their retirement community? (The New York Times, January 7, 2003 "For Retired Chimps, a Life of Leisure," by Sheryl Gay Stolberg).


17. Why does the CDC still maintain that the average course of "HIV/AIDS" is from 5-10 years, while Dr. Bruce R. Schackman, chief of health policy at Weill Cornell Medical College in New York and lead author of a paper appearing in Medical Care in 2006, a journal published by the American Public Health Association claim that "...patients can live average 24 years, if they pay $385,000," while David Ho, Daniel Douck, Ronald Desrosiers, have claimed that "HIV" destroys the gut lymphoid tissue of "recently infected people," and essentially  “wipes clean" the lymphoid tissue lining the gut shortly after infection?


18. When the FDA recalls defective "HIV" tests or statistics package software, how long does it take the medical community to respond to the typical recall?  For instance, are testing labs immediately provided with the lot numbers of defective testing merchandise in a timely manner, and are patients who received these tests quickly notified about the recall of the test they were subjected to? A few recent cases may here be illustrative:


Recall of HIV p24 Antigen Test Kit

Globus Media REcall HIV test

ORTHO Antibody to HBsAg ELISA Test FDA recall Ortho HBsAG System

Recall of Antibody to Human Immunodeficiency Virus Type 1 p24 Antigen Test Kits

Recall lancets for HIV kit

FDA Recall of NucliSens HIV test kit

FDA Recall of HCV EIA 2.0 Test Kit

Market Withdrawal of HIV-1 - HCV Assay, FDA recall Procleix

FDA Recall HIV-1 - HIV-2 Plus O EIA Testing Software

Recall of HIV Types 1 &2 (Synthetic Peptide)

FDA Recall of Amplicor HIV test kit


19. Why did Dr. Alfred Hässig, Emeritus Professor in Immunology at the University of Bern, former Director Swiss Red Cross blood banks: Director of the Swiss Red Cross Transfusion Service, and President of the Board of Trustees of the International Society of Blood Transfusion (who, with colleagues, formed the Study Group for Nutrition and Immunity), claim the following:


“The sentence of death accompanying the medical diagnosis of AIDS should be abolished.” (Sunday Times (London) 3 April 1994).


“In the virological research, so much money is invested, and the research people want to stay in that area because if you deviate to research in other directions probably other people come in and must be funded.” (Meditel 1992).


“Virologist have nothing new to offer. They keep coming up with excuses, they find constant growth and change in the virus structure, it evades, attacks, strange things, but none of them has the courage to explain properly how these things could possibly be so.” (Continuum Jan/Feb 1996)


“AZT (anti-viral AIDS medicine) has, in countless cases, brought about the inevitable and slow asphyxiation of the patient's body cells. The doctors wrongly diagnose the fatal consequences of AZT medication as AIDS following a prior HIV infection. Treatment with AZT and allied toxic substances may be equivalent to joining a suicide squad with a time fuse.”


    “It is the duty of every doctor to preserve life at any cost -- and not death-curse people based on any test so they are so frightened they kill themselves. I am sad to say that these voodoo methods were practiced despite there never being any proof that the detected antibodies are an indication of mortality in all diagnosed people. I consider it medical malpractice to push patients into dying by prophesying an early death. We are medical scientists, not prophets!”


Did Dr. Hassig mean here when he said, “The sentence of death accompanying the medical diagnosis of AIDS should be abolished,” that, with increased testing of all pregnant women and more aggressive treatment regimens with AZT and other antiretrovirals, that AIDS might some day be abolished?  Or is he saying that the AIDS establishment has mistakenly confused the side effects of AZT and other antiretroviral treatments with the destruction imagined to be brought on by “HIV,” before they appreciated that failed anticancer chemotherapy drugs like AZT could “do all those bad things” to the human body?


20. Why did Dr. Heinrich Kremer, MD, Medical Director of the Federal Clinics for Juvenile and Young Adult Drug Offenders for five German counties, including Berlin, Bremen, and Hamburg, and author of the book, 'The Silent Revolution of the AIDS- and Cancer-Medicine.' From AIDS: DEATH BY PRESCRIPTION, Continuum, July/Aug. 1996 claim that:


“The advertising drums are beaten hard all over the world today. The same doctors are calling for obedient candidates for their experiments and holding out the same promise of a cure who have poisoned countless AIDS patients by administering the DNA blocker AZT for the past ten years in an attempt to hunt down the phantom HIV virus.


“The same doctors are now trying to conjure up a substance from the test tube under the magic name of 'protease inhibitor' and to market it as having a limitless cure potential, although nobody in fact knows what long-term reactions this molecule, which has never been tested on man, may cause in the living organism.”


“The victims and perpetrators have only recently come to realise that AZT (also known as Zidovudine or Retrovir) has, in countless cases, brought about the inevitable and slow asphyxiation of the patient's body cells, which are in particular need of oxygen and hence the equally inevitable death by poisoning of those persons who are stigmatized as HIV-positive or diagnosed as suffering from “AIDS” and who trust their doctors. Despite that realization, new test candidates are already being sought who will be voluntarily prepared, through fear of death suggested by the medical profession, not only to swallow AZT in combination with allied toxic substances, but in addition to take an inhibitor which has an incalculable impact on cell metabolism.”


“A guarantee of success is secured in advance, as with AZT, because any fatal 'secondary effects' of the mixture are described as an outcome of the phantom HIV infection. These are the selfsame laboratory doctors and clinical practitioners who for years abused the confidence of anxious AIDS patients with the assertion that AZT would reliably, and with total certainty, prevent the proliferation of their 'phantom' HIV.”


Is Dr. Kramer is saying here that “beating of the advertising drums” for the use of AZT and HAART, must be non-ceasing, and unabashedly banged yet ever louder for the use of AZT and now other antiretrovirals?


21. Why did Dr. Michael Lange, MD, Head of AIDS Programme, St. Lukes Hospital, New York, claim that:


“We do not know the pathogenesis of this disease. And we were very early forced into a very dogmatic view: namely, that somehow HIV kills the T-cells.” (Spin April 1991).


“I was very upset…The cause of AIDS was discovered by government fiat...I had been working with the Pasteur Institute for six months, but then that [Gallo] announcement was made at the press conference. As far as I’m concerned, from that point on AIDS research turned into seedy, criminal politics, and it remained that way.” (Spin, June, 1992).


“I was far from convinced by the data they had then and I’m still not convinced. We were all forced into a very dogmatic and simplistic view of what caused AIDS. Today, I think even the greatest proponents of HIV no longer believe that it does all that damage to the immune system by itself. There have to be other factors involved. And because of the HIV hypothesis, there’s been little or no research done on what those other factors may be.” (Spin June 1992).


“I personally do not prescribe AZT unless a patient insists. I have continued to find that patients survive longer without it.” (Spin, April 1991).


A related issue is why is Dr. Michael Lange, MD, Head of AIDS Programme, St. Lukes Hospital, New York, being quoted in Spin Magazine, Continuum, Synapse or other popular magazines, rather than in The New England Journal of Medicine, Science, Nature, JAMA, or other high profile science or medical journals? Same question regarding Dr. Hassig, Dr. Kramer, and other high profile directors involved directly on the front lines of AIDS?


22. Why did Dr. Donald Abrams, Professor of Medicine, San Francisco General Hospital, and one of the first AIDS physicians, claim that (Synapse Vol 4, pages 1 and 5 (1996):


 "In contrast with many of my colleagues, I am not necessarily a cheerleader for anti-retroviral therapy. I have been one of the people who's questioned, from the beginning, whether or not we're really making an impact with HIV drugs and, if we are making an impact, if it's going in the right direction."I have a large population of people who have chosen not to take any antiretrovirals. They've watched all of their friends go on the antiviral bandwagon and die, so they've chose to remain naive [to therapy]. More and more, however, are now succumbing to pressure that protease inhibitors are 'it.'  We are in the middle of the honeymoon period, and whether or not this is going to be an enduring marriage is unclear to me at this time."


23. Why are antiretrovirals called "life-saving" or "life extending" when a report in The New England Journal of Medicine by The Veterans Affairs Cooperative Study Group reported that:


"AZT disproportionately harmed Blacks and Hispanics, and provided no benefit to the quelling of advancing immune suppression in Caucasians" (JD Hamilton et. al. and the Veterans Affairs Cooperative Study Group. A controlled trial of early versus late treatment with zidovudine in symptomatic human immunodifficiency virus infection" New England Journal of Medicine, 326: 437-434, 1992)?


24. Although there were many problems with record keeping, and the Boston Arm of the trail was supposed to be thrown out, the 1987 Fischl AZT trial won AZT FDA approval after 4 months when the trial was terminated for "compassionate reasons." Why are antiretrovirals still called "life-saving" or "life extending" when there was little, if any difference between the outcome of either AZT treated versus AZT-untreated groups after 1 year, and, and despite the fact that The Concorde study (that was much larger, longer, and better designed trial than The Fischl trial) concluded:


"The results of Concorde do not encourage the early use of zidovudine in symptom-free HIV-infected adults. They also call into question the uncritical use of CD4 cell counts as a surrogate endpoint for assessment of benefit from long-term antiretroviral therapy" (Seligmann et al., Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee. Lancet, Apr 9;343(8902):871-81, 1994)?


25. Why are antiretrovirals called "life-saving" and "life extending" when it has been more than 7 years since it was published in The Journal, AIDS, that children born to ZDV-treated mothers:


"are more likely to have a rapid course of HIV-1 infection compared with children born to untreated mothers, as disease progression and immunological deterioration are significantly more rapid and the risk of death is actually increased during the first 3 years of life" (de Martino et al., Rapid disease progression in HIV-1 perinatally infected children born to mothers receiving zidovudine monotherapy during pregnancy. (AIDS. 13 (8): 927-933, May 28, 1999. The Italian Register for HIV Infection in Children. AIDS, 13:927-933, 1999)?


“Results: Comparison of HIV-1-infected children whose mothers were treated with ZDV with children whose mothers were not treated showed that the former group (AZT group) had a higher probability of developing severe disease [57.3% (95% CI 40.9-74.3) versus 37.2% (95% CI 30.0-45.4); log-rank test 7.83, P=0.005; adjusted hazard ratio 1.8 (95% CI 1.1-3.1)] or severe immune suppression [53.9% (95% CI 36.3-73.5) versus 37.5% (95% CI 30.0-46.2); log-rank test 5.58, P=0.018; adjusted hazard ratio 2.4, (95% CI: 1.3-4.3)] and a lower survival [72.2% (95% CI 50.4-85.7) versus 81.0% (95% CI 73.7-86.5); log-rank test 4.23, P=0.039; adjusted hazard ratio of death 1.9 (95% CI 1.1-3.6)]..“


Why did these authors conclude that:


"Findings may suggest a need to hasten HIV-1 diagnosis in infants of ZDV-treated mothers and undertake an aggressive antiretroviral therapy in those found to be infected."


Were these claims plagued with typographical errors? Shouldn't the report have read:


"Children born to ZDV-treated mothers are more likely to have a slow course of HIV-1 infection compared with children born to untreated mothers, as disease progression and immunological deterioration are significantly more reduced and the risk of death is actually decreased during the first 3 years of life,”


and not:


Children born to ZDV-treated mothers “are more likely to have a rapid course of HIV-1 infection compared with children born to untreated mothers, as disease progression and immunological deterioration are significantly more rapid and the risk of death is actually increased during the first 3 years of life?”



26.Why are antiretrovirals called "life-saving" and "life extending" when it has come to National attention that research directors such as Edmond Tramont, who was/is still the government's chief of AIDS research, rewrite safety reports on a U.S.-funded drug studies of nevirapine (the controversial HIVNET 012 clinical trial) to change its conclusions and delete negative information, and later order that research resumed over the objections of his staff and trial safety officer, Jonathan Fishbein, who was fired because he blew the whistle on this dangerous study, and even after the company withdrew its trial in the U.S. because of reports of excessive toxicity? How often do AIDS researcher change scientific data to conform to political or financial pressures?


27. Why are antiretrovirals called life-saving when Lockman et al. with Max Essex just reported last month (1/2007) in the New England Journal of Medicine that nevirapine increased drug resistant "HIV" progression to AIDS over controls by 41.7 % in women (euphemistically called virological failure or drug resistant "HIV"), and that a single dose of nevirapine (one each to mother and infant) as compared with placebo, was associated with significantly higher rates of virologic failure and smaller CD4+percentage increases in response to subsequent nevirapine-based antiretroviral treatment?"


“Nevirapine remains central to the prevention of mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1) and to combination antiretroviral treatment throughout much of the developing world. Nevirapine administered as one dose to the mother and one to the newborn reduces mother-to-child transmission of HIV-1 by 41 to 47%, and well over 875,000 women and infants have received a single dose of nevirapine. A single dose of nevirapine is the cornerstone of the regimen recommended by the World Health Organization (WHO) to prevent mother-to-child transmission among women without access to antiretroviral treatment and among those not meeting treatment criteria. However, nevirapine resistance is detected (with the use of standard genotyping techniques) in 20 to 69% of women and 33 to 87% of infants after exposure to a single, peripartum dose of nevirapine.  Among 60 women starting antiretroviral treatment within 6 months after receiving placebo or a single dose of nevirapine, no women in the placebo group and 41.7% in the nevirapine group had virologic failure (P<0.001). Women who had received a single dose of nevirapine had significantly higher rates of virologic failure on subsequent nevirapine-based antiretroviral treatment than did women who had received placebo. This apparently deleterious effect of a single dose of nevirapine was concentrated in women who initiated antiretroviral treatment within 6 months after receiving a single dose of nevirapine…Among the 30 HIV-infected infants, a single dose of nevirapine (one each to mother and infant) as compared with placebo was associated with significantly higher rates of virologic failure and smaller CD4+percentage increases in response to subsequent nevirapine-based antiretroviral treatment” (Lockman  S. et al., Response to Antiretroviral Therapy after a Single, Peripartum Dose of Nevirapine. The New England Journal of Medicine 356  january 11, 2007).


A related question is, if "HIV" has 10 genes that are essential for its pathogenicity, and if it is constantly mutating any nucleotide comprising any of these 10 genes, how does "HIV" maintain its biological identity or its pathogenicity?


28. Why are antiretrovirals called "life-saving" or "life extending" when it was published in The Journal of Virology that severe toxicity of saquinovir and other protease inhibitors are frequently observed in patients receiving this class of drugs (Estaquier et al., Effects of Antiretroviral Drugs on Human Immunodeficiency Virus Type 1-Induced CD4+ T-Cell Death Journal of Virology, June, p. 5966-5973, Vol. 76, No. 12, 2002)?


29. Why are antiretrovirals called "life-saving" or "life extending" when Mark Harrington, a member of The Treatment Action Group (TAG-a radical group in favor of drugging everybody with antiretrovirals) summoned "the power of prayer" over "HIV" mutability, and discussed "The Chinese Menu Approach" in a description of a meeting he attended on developments regarding anti-retrovirals that included AIDS leaders such as Marc Wainberg, Director, McGill AIDS Centre, and this summer's Chair of The Toronto International AIDS Conference-who possesses several "HIV" drug patents such as lamivudine (3TC), and grants from GlaxoSmithKlein, Bristol-Myers Squibb and Boehringer-Ingelheim. Also present at the meeting was Emilio Emini, Tufts University's John Coffin, Roche's Noel Roberts, the CDC's Harold Jaffe, Chiron's David Chernoff, the ACTG's Robert ("Chip") Schooley and John Mellors (developer and champion of the viral load tests now known to be invalid), as well as treatment activist Dawn Averitt-Doherty of Atlanta-based Woman's Information Service and Exchange (WISE)?


"During the coffee break, I (Harrington) joined three activists outside to share nicotine and despair. What was the point of quitting smoking if we were still all passengers on the speeding train heading for the cliff? The Birmingham resistance data were wrenching. Our fears of multiple cross-resistance, from November 1995's 3TC and saquinavir FDA approval hearings, reared their ugly heads. Several months of post-Vancouver euphoria crumbled in a moment as it became clear that many of those who developed resistance to ritonavir and indirovine-as thousands clearly would-might have no protease inhibiting options ahead of them. Today's resistance news made for a toxic cocktail. As I left the auditorium I bumped into Emilio Emini."


"Harrington: So what do you do if you fail Crixivan?"


"Emini: [sighs] We don't know what to do."


"Harrington: Take two new nucleosides and nevirapine?"


"Emini: Yeah. And pray."


"No one had yet assessed the healing effects of prayer on viral load. This was what we'd come to. I rushed into the lobby of the Interior Department and ran into a colleague, who was wild with fear and disappointment."


"Sometimes the gap between how the researchers felt and how we felt became an abyss. They were excited about the endless possibilities opened up by the research advances of 1996; we were terrified about the limited treatment options facing people who had exhausted most of the current arsenal of antiretroviral therapy. What to do with those whose viral load refused to go undetectable? What to do with those who added a protease inhibitor to a failing two-drug regimen and appeared doomed to develop resistance, most of it-especially with ritonavir and indinovir-cross-resistant to all other protease inhibitors? What to do with those who jumped aboard last year's bandwagon, AZT+3TC, and now appeared likely to have developed 3TC resistance and, with it, cross-resistance to ddI, ddC and possibly 1592? The Chinese menu approach to antiretroviral treatment suddenly looked much less appetizing, and much less nourishing" (TAGline/Volume 4 Issue 2 February 1997).


30. Why are antiretrovirals called "life-saving" or "life extending" when a registry has been established to monitor adverse fetal outcomes born to women exposed to the AIDS drug, efavirenz" (FDAMedWatch 6/10/2005)?


31. Why are antiretrovirals called "life-saving" and "life extending" when Olivero OA et al., in “3'-azido-3'-deoxythymidine (AZT) transplacental perfusion kinetics and DNA incorporation in normal human placentas perfused with AZT” (Mutat Res Fundam Mol Mech Mutagen. Jul 16;428(1-2):41-7, 1999), reported that:


“Incorporation of ZDV into DNA was detected in most of the samples from ZDV-exposed adults and infants. Therefore, the biologic significance of ZDV-DNA damage and potential subsequent events, such as mutagenicity, should be further investigated in large cohorts of HIV-positive individuals?”


32. Why are antiretrovirals called "life-saving" and "life extending" when Lallemant et al., in an article entitled, "A trial of shortened zidovudine regimens to prevent mother-to- child transmission of human immunodeficiency virus type 1" (NEJM. 2000 Oct 5;343(14):982-91) reported that:


“[Table 3 shows that congenital abnormalities occurred in 7% of infants when both mother and child had the long course of AZT (long-long), and only 1% when both had the short course (short-short). Neutropenia and leukopenia occurred in 7% of infants on the long-long course and 2% on short-short. Infections or other HIV-related events occurred in 43% on long-long and 33% on short-short. Neonatal or other obstetrical events occurred in 22% on long-long and only 14% on short-short. Number of deaths, severe anemia were similar (although severe anemia occurred significantly less (0%/1%) in the long-short and short-long treatment arms). Mothers who received the long AZT treatment had a higher rate of stillbirth (8% vs. 4%), severe anemia (7% vs 4%), infection or other HIV events (20% vs 17%), events related to pregnancy or delivery (24% vs 17%) than mothers who received the short course, although fewer died" (3% vs 8%)?



33. Why are antiretrovirals called "life-saving" and "life extending" when Kuhn L et al. in "Disease Progression and Early Viral Dynamics in Human Immunodeficiency Virus Infected Children Exposed to Zidovudine during Prenatal and Perinatal Periods" (Journal of Infectious Diseases, 2000 July;182:104-11) reported that:


“In a multicenter observational cohort study of 325 HIV-infected children born during 1986-1997, clinical progression was compared among infected children exposed or unexposed to Zdv [AZT] during prenatal and perinatal periods. Zdv exposure was associated with 1.8-fold (95% confidence interval, 1.02-3.11) increased risk of progressing to AIDS or death after adjusting for year of birth, maternal CD4 cell count, maternal AIDS diagnosis, and subsequent antiretroviral therapy of the child. Mean log10 viral copies at 712 weeks were higher among Zdv-exposed children" (P = .004)?


34. Why are antiretrovirals called "life-saving" and "life extending" when Newschaffer et al. in “Prenatal Zidovudine Use and Congenital Anomalies in a Medicaid Population. JAIDS. 2000 Jul 1;24(3):249-256) reported that:


“Children of study women who were prescribed ZDV [AZT] had increased adjusted odds of any anomaly (adjusted odds ratio [OR], 1.55; 95% CI, 1.01-2.29) [i.e. more than one-and-one-half times the risk of a birth anomaly than the HIV+ population being studied in general"]?


35. Why are antiretrovirals called "life-saving" and "life extending" when de Souza RS et al., in an article entitled, "Effect of prenatal zidovudine on disease progression in perinatally HIV-1-infected infants" ( JAIDS. 2000 Jun 1;24(2):154-161) reported that:


 “After adjusting for prematurity and maternal clinical characteristics, RPD [rapid disease progression] was three times more likely to occur in infants born to [mothers] treated [with AZT] compared with findings in untreated mothers" (RR=2.8; p = .021)?


36. Why are antiretrovirals called "life-saving" and "life extending" when Kumar et al., in “Zidovudine Use in Pregnancy: A Report on 104 Cases and the Occurrence of Birth Defects  (JAIDS.;7:1034-9, 1994) reported that:


“In reviewing the frequency of birth defects in this population [of HIV+ women taking AZT during pregnancy] we noted eight birth defects (10%) out of 80 live births?”


These included:


1. Two male infants with the "minor abnormalities" of "low-set ears, retrognathia [a mis-aligned jaw], prominent epicanthal folds [i.e., unexpected skin flaps above the eye, which can be a sign of mental retardation], hirsutism [abnormal hairiness], triangular facies with blue sclera [a triangular-shaped face with abnormally blue eyes], hyperpigmented skin macules, and prominent sacral dimple [a pronounced indentation at the bottom of the spinal cord]."


2. A female infant was born with extra fingers on both hands (the report doesn't say how many "extra digits" grew on each hand). "There was no similar family history," Kumar and co-workers noted.


3. One child was diagnosed as having "fetal alcohol syndrome," although there was no evidence that the mother consumed alcohol.


4. A male infant was born with a serious congenital heart defect ("asymptomatic atrial septal defect") and "pectus excavaatum," a depression or actual hole in the chest. This child died at the age of five months.


5. A male infant was born with an abnormally small brain (microencephaly) and chorioretinitis (a condition that rapidly results in blindness, due to lesions on the retina).


6. Another male infant was born with the same type of hole in his chest as the previously described child ("pectus excavatum").


7. A female was born with albinism (no pigmentation) and congenital ptosis, a condition in which the upper eyelid droops uncontrollably (which interferes with eyesight) because of nerve damage.


37. Why are antiretrovirals called "life-saving" and "life extending" when Panther et al. published a paper entitled, "Genital tract human immunodeficiency virus type 1 (HIV-1) shedding and inflammation and HIV-1 env diversity in perinatal HIV-1 transmission"

( Journal of Infectious Diseases 2000 Feb;181:555-63)  claiming that:


 “All women [in this study] received oral zidovudine [AZT] prior to delivery and/or intravenous zidovudine at delivery...Of 42 subjects...24 had a CVL [cervicovaginal lavage] taken...Of these 24 women, 7 transmitted HIV-1 to their infants and 17 did not...In the CVL samples, 41% yielded culturable HIV-1, 67% were PCR positive for proviral HIV-1 DNA, 30% were positive for cell-free HIV-1 RNA and 45% were positive for cell-associated HIV-1 RNA. Peripheral CD4 cell counts did not correlate with levels of HIV-1 in the CVL by DNA or RNA PCR or by amount of genital tract inflammation...Although all subjects in our study received zidovudine therapy in the third trimester, the high rate (29%) of HIV-1 perinatal transmission in this data set does not agree with the largest prospective, randomized study addressing this question, ACTG 076 [in fact, this rate is higher than the transmission rate in the placebo arm of ACTG 076]?”


38. Why are antiretrovirals called "life-saving" and "life extending" when Smith et al. in, "Timing of perinatal human immunodeficiency virus type 1 infection and rate of neurodevelopment" (Pediatr Infect Dis J. 2000;19:862-71) reported that:


“Infants with early positive HIV-1 cultures demonstrated a notable decrement in neurodevelopmental functioning within the first 30 months of life. They achieved motor developmental scores that were increasingly and significantly discrepant [worse] both from the average and from scores achieved by late HIV-1-positive children over the course of the study period. Those children with early HIV-1-positive cultures also demonstrated a trend toward a similar decline in mental functioning over time...The mothers of infants with early [HIV] positive cultures were more likely to receive ZDV [AZT] treatment during pregnancy, and their infants were more likely to receive ZDV treatment prophylactically during the first 6 weeks of life...Because antiretroviral therapy has been shown to improve neurodevelopmental function in children whose CNS has been affected by the HIV-1 virus...Infants with early HIV-1 culture positivity should be treated with multiple drugs with well-established CNS penetration to reduce the likelihood that resistance will develop in the CNS compartment?"


Why did the authors of this study, for some reason, ignore the fact that early positive HIV-1 cultures equate with infants who have been on AZT the longest, and advance the idea that hitting the infants aggressively with multiple drugs will block "HIV's" destruction of brain tissue. Why do they conclude this?


39. Why are antiretrovirals called "life-saving" and "life extending" when Blanche et al. in "Persistent mitochondrial dysfunction and perinatal exposure to antiretroviral nucleoside analogues," (Lancet, 1999 Sep 25) conclude that:


 “We analysed observations of a trial of tolerance of combined zidovudine [AZT] and lamivudine and preliminary results of a continuing retrospective analysis of clinical and biological symptoms of mitochondrial dysfunction in children born to HIV-1-infected women in France....Findings: Eight children had mitochondrial dysfunction. Five, of whom two died, presented with delayed neurological symptoms and three were symptom-free but had severe biological or neurological abnormalities. Four of these children had been exposed to combined zidovudine and lamivudine, and four to zidovudine alone. No child was infected with HIV-1..."

" Our findings support the hypothesis of a link between mitochondrial dysfunction and the perinatal administration of prophylactic nucleoside analogues. Current recommendations for zidovudine monotherapy should however be maintained[!]. Further assessment of the toxic effects of these drugs is required!”


40. Why are antiretrovirals called "life-saving" and "life extending" when Neenyah Ostrom (07/12/2000) reviewed the Blanche study in the following way:


"The French study, led by Stephane Blanche at the Necker Hospital in Paris, was published in The Lancet. Of 1,754 mother-child pairs exposed to AZT during the mother's pregnancy (or just after birth, for the child), Blanche and colleagues discovered eight children whose mitochondria didn't function properly. The mitochondria are our cells' energy producing organelles; if they malfunction, neurological development is delayed, and the result can be fatal. Four of the children with mitochondrial dysfunction had been exposed to a combination of AZT and another anti-HIV drug, lamivudine; the other four had been exposed to AZT alone. "No child was infected with HIV-1," Blanche and co-workers pointed out."


"Five of the eight children developed "delayed" neurological symptoms (meaning they weren't present at birth, but became obvious later); two of these children died. The other three children "were symptom-free but had severe biological or neurological abnormalities," according to the French scientists."


"One of the two children with neurological symptoms who died, Patient A, was partially blind. When Patient A was 4 months old, an MRI showed that the child had demyelinating lesions in the brainstem (a primitive part of the brain that controls basic life functions). Over time, these lesions -- which were really just areas of dead brain tissue -- spread throughout the child's brain. Patient A's growth was "abnormal," according to the doctors, and the child vomited frequently. At 13 months of age, Patient A died from heart and lung disorders."


"Patient B died at the age of 11 months. At 4 months old, Patient B developed epilepsy as well as suffering severe deterioration of cognitive and motor abilities. This child, too, was found to have "diffuse demyelinating lesions associated with massive cortical necrosis," that is, widespread brain tissue death."


"The other children who developed symptoms of mitochondrial dysfunction had seizures, heart dysfunction, brain lesions (one child with, and one without, brain tissue death), blindness associated with a too-small head ("microencephaly" a problem identified earlier in babies treated in utero with AZT), and numerous biochemical abnormalities (including abnormal liver and pancreatic enzyme levels, among others).


"In their discussion of how AZT probably contributed to the illness and deaths of these children, Blanche and colleagues noted that researchers at the US National Cancer Institute have demonstrated that AZT crosses the placenta from mother to fetus. In monkey fetuses, AZT is incorporated into the mitochondrial DNA. Fetal monkeys dosed with AZT for periods of time and with doses similar to those used for pregnant women developed mitochondrial dysfunction after birth, Blanche and co-workers pointed out. They added, 'The experimental [monkey] model does not show whether the toxic effects are reversible after birth. Also, it gives no insight into the possible clinical impact of this type of dysfunction throughout a tissue, especially a long time after the drug is stopped…. As with other drug-induced toxic effects in mitochondria, these lasting abnormalities may be associated with a symptomless constitutional dysfunction.' In other words: Many more children exposed to AZT in utero may have mutations in their mitochondria that we don't detect because they don't immediately produce identifiable symptoms. The type of mitochondrial illness observed in these eight children (out of 1,754 French children treated with AZT) was found in only 21 children out of 12 million studied in the United Kingdom."


"We are aware that the suggestion that antiretroviral drugs are toxic raises delicate issues," the French scientists wrote, concluding that "the current recommendations for zidovudine [AZT] monotherapy prophylaxis should be maintained." They added, however, "Pregnant women should be informed of the potential effects associated with these treatments during pregnancy."


41. Why are antiretrovirals called "life-saving" and "life extending" when The UK's Committee on Safety of Medicines in Perinatal AZT: New warning on potential risk to infants. www.aidsmap.com. 1999 Jul 21, http://www.aidsmap.com/namsearch.htm/news/07jul99/story6.htm issued a warning to doctors about the risk of mitochondrial dysfunction in infants born to HIV infected mothers treated with zidovudine (AZT) to prevent vertical transmission."


The warning came in advance of the publication of data from a French study in which it was discovered that 8 out of approximately 200 infants developed mitochondrial dysfunction following exposure to zidovudine, with or without 3TC treatment, for the prevention of vertical transmission of HIV infection.


42. Why are antiretrovirals called "life-saving" and "life extending" when Olivero et al. in an article entitled, "3'-azido-3'-deoxythymidine (AZT) transplacental perfusion kinetics and DNA incorporation in normal human placentas perfused with AZT" ( Mutat Res Fundam Mol Mech Mutagen. 1999 Jul 16;428(1-2):41-7) reported that:


“The data show that AZT crosses the human placenta and becomes rapidly incorporated into DNA of placental tissue in a dose-dependent fashion, suggesting that even short exposures to this drug might induce fetal genotoxicity and might also inhibit maternal-fetal viral transmission?”


43. Why are antiretrovirals called "life-saving" and "life extending" when Olivero OA et al., in a presentation entitled, "3'-azido-3'-deoxythymidine (AZT) transplacental perfusion kinetics and DNA incorporation in normal human placentas perfused with AZT” (Third Conference on Environmental Mutagens in Human Populations. 1999 Feb 18) claimed that:


transplacental exposure studies demonstrated that AZT is a moderate to strong transplacental carcinogen in mice...Since AZT-DNA incorporation in human placenta occurs rapidly by 2 hr of AZT perfusion, infants exposed to AZT even for short periods of time during gestation may sustain genotoxic damage. In previous studies AZT has been shown to produce both, large scale DNA damage and point mutations...the consequences of any fetal exposure to a nucleoside analog, in utero, remain unknown”


44. Why are antiretrovirals called "life-saving" and "life extending" when an article in Reuters. (1999 Feb 2) stated that HIV drugs may show adverse effects in babies:


“…these two [HIV+ babies taking AZT+3TC] died of an extremely rare disease caused by genetic damage to the mitochondrial DNA - which is found in the cell body rather than in the nucleus with the genes. One died at 11 months and one died at 13 months, both from severe brain damage. Blanche [of the French medical research institute INSERM] told the meeting that there was no proof the drugs caused the damage. But he said there was also no evidence the babies had inherited abnormalities, and HIV drugs are known to cause mitochondrial damage.”


45. Why are antiretrovirals called "life-saving" and "life extending" when Bennett and Foster concluded in an article entitled, "Mandatory testing of pregnant women and newborns: a necessary evil? Realistic alternatives to breastfeeding in the HIV/AIDS era. (AIDS Information Exchange. 1998) reported that:


“At present, data regarding the effects of ZDV use on vertical transmission rates are inconclusive and incomplete. In addition, the long-term effects of ZDV use during pregnancy and after birth on the woman and any resulting child are yet to be discovered…the possibility has not yet been ruled out that this ‘risk-reducing’ measure may not be effective and may prove detrimental to the health of both mother and child.”


46. Why are antiretrovirals called "life-saving" and "life extending" when Lorenzi et al. wrote an article entitled, "Antiretroviral therapies in pregnancy: maternal fetal and neonatal effects"  (AIDS. 1998;12:F241-247) which concluded that:


"In HIV-infected pregnant women treated with two RTI [nucleoside analogs, of which AZT was the most common] with or without protease inhibitors, one or more adverse events occurred in 29 out of 37 women and in 14 out of 30 babies.”


47. Why are antiretrovirals called "life-saving" and "life extending" when Patterson et al. in an article entitled,  "Transplacental pharmacokinetics and fetal distribution of azidothymidine, its glucoronide, and phosphorylated metabolites in late-term rhesus macaques after maternal infusion"  (Drug Metab Dispos. 1997;25(4):453-459) reported that:


“The authors selected six patients who were HIV positive and who had requested termination of pregnancy to study the passage of zidovudine through the placenta...1 gram of zidovudine [AZT] was given in five doses of 200 mg each orally...At a mean age of 17.5 weeks [into the pregnancy], samples were taken from the mothers’ blood, from the amniotic fluid and from the fetal blood...The concentrations of [AZT] in the [amniotic fluid] and in the fetal blood were higher or equaled those found in the maternal blood...The drug remains contra-indicated in pregnancy.”


48. Why are antiretrovirals called "life-saving" and "life extending" when McKinney et al., in an article entitled,  "A multicenter trial of oral zidovudine in children with advanced human immunodeficiency virus disease" (NEJM. 1991 Apr 11;324(15):1018-25) reported that:


 “Children treated with zidovudine continued to have bacterial and opportunistic infections. The effect of the drug on the frequency of these events could not be assessed because of the lack of control groups...One or more episodes of hematologic toxicity occurred in 54 children (61 percent)anemia (hemoglobin level, <75g per liter) in 23 children (26 percent) and neutropenia (neutrophil count, <0.75X10^9 per liter) in 42 (48 percent).


49. Why are antiretrovirals called "life-saving" and "life extending" when Gerschenson et al., in an article entitled,  "Fetal mitochondrial heart and skeletal muscle damage in Erythrocebus patas monkeys exposed in utero to 3'-azido-3'-deoxythymidine" (AIDS Res Hum Retroviruses. 2000 May 1;16(7):645-44) reported that:


“3'-azido-3'-deoxythymidine (AZT) is given to pregnant women positive for the human immunodeficiency virus type 1 (HIV-1) to reduce maternal-fetal viral transmission. To explore fetal mitochondrial consequences of this exposure, pregnant Erythrocebus patas monkeys were given daily doses of 1.5 mg (21% of the human daily dose) and 6.0 mg (86% of the human daily dose) of AZT/kg body weight (bw), for the second half of gestation. At term, electron microscopy of fetal cardiac and skeletal muscle showed abnormal and disrupted sarcomeres with myofibrillar loss. Some abnormally shaped mitochondria with disrupted cristae were observed in skeletal muscle myocytes. Oxidative phosphorylation (OXPHOS) enzyme assays showed dose-dependent alterations. At the human-equivalent dose of AZT (6 mg of AZT/kg bw), there was an approximately 85% decrease in the specific activity of NADH dehydrogenase (complex I) and three- to sixfold increases in specific activities of succinate dehydrogenase (complex II) and cytochrome-c oxidase (complex IV). Furthermore, a dose-dependent depletion of mitochondrial DNA levels was observed in both tissues. The data demonstrate that transplacental AZT exposure causes cardiac and skeletal muscle mitochondrial myopathy in the patas monkey fetus.”


50. Why are antiretrovirals called "life-saving" and "life extending" when Ha et al., in an article entitled,  "Fetal, infant, and maternal toxicity of zidovudine (azidothymidine) administered throughout pregnancy in Macaca nemestrina," (JAIDS, 1998 May 1;18(1):27-38) reported a study showing that:


“The AZT animals [Macaques given AZT during pregnancy] developed an asymptomatic macrocytic anemia, but hematologic parameters returned to normal when AZT was discontinued. Total leukocyte count decreased during pregnancy and was further affected by AZT administration. AZT-exposed infants were mildly anemic at birth. AZT caused deficits in growth, rooting and snouting reflexes, and the ability to fixate and follow near stimuli visually?


51. Why are antiretrovirals called "life-saving" and "life extending" when Diwan et al., in "Transplacental carcinogenicity of 3'-azido-3'-deoxythmidine (AZT) in mice” (Proc Am Assoc Cancer Res. 1998;39:21) reported that:


“CD-1 mice exposed prenatally to 12.5 and 25.0 mg of AZT...had statistically significant increases in numbers of liver, lung and female reproductive tract tumors. These observations have been extended to offspring at 2 years of age...there was a 2- to 3-fold increase in the incidence (from 20% in controls to 55-60% in AZT groups) and multiplicities of lung tumors in AZT-exposed mice. The incidence of hepatocellular adenomas in the female mice exposed to prenatal AZT increase from 0 in the control group to 20% in the high dose AZT group, and hepatocellular carcinomas mestastasizing to lungs were observed only in AZT-treated mice. Prenatal administration of AZT also increased the incidence of neoplasms of reproductive tract, female mammary gland epithelium and squamous cell epithelium of forestomach. AZT...significantly reduced the incidence of hematopoietic tumors?”


52. Why are antiretrovirals called "life-saving" and "life extending" when Olivero OA et al., in  "Transplacental effects of 3'-azido-2',3'-dideoxythymidine (AZT): tumorigenicity in mice and genotoxicity in mice and monkeys" (J Natl Cancer Inst. 1997 Nov 5;89(21):1602-8) reported that:


“At 1 year of age, the offspring of AZT-treated mice exhibited statistically significant, dose-dependent increases in tumor incidence and tumor multiplicity in the lungs, liver, and female reproductive organs...AZT is genotoxic in fetal mice and monkeys and is a moderately strong transplacental carcinogen in mice examined at 1 year of age?”


53. Why are antiretrovirals called "life-saving" and "life extending" when Olivero OA et al., in "AZT is a Genotoxic Transplacental Carcinogen in Animal Models" (JAIDS. 1997 Apr 1;14(4):A29) reported that:.


“…in adult mice, lifetime AZT administration induces vaginal tumors at a 10-20% incidence...In newborn monkeys and mice, AZT was incorporated into DNA of many fetal tissues...AZT appears to be a moderately-strong transplacental carcinogen [i.e. it crosses the placenta and may cause cancer in the fetus]?”


54. Why are antiretrovirals called "life-saving" and "life extending" when Ha et al., in "Fetal toxicity of zidovudine (azidothymidine) in Macaca nemestrina: preliminary observations" (JAIDS. 1994;7(2):154-7) reported that:


“Hemoglobin dropped significantly in the AZT-treated animals [Macaques] after treatment began and remained low until the end of the study...Postnatal weight increase was significantly lower in AZT-exposed infants...Infant hematocrits taken at time of birth were lower in the AZT-exposed group...AZT-exposed infants took three times as many sessions as controls to meet criterion on Black-White Learning, a simple discrimination task...It took significantly more matings to achieve the six AZT pregnancies than the six control pregnancies?”


55. Why are antiretrovirals called "life-saving" and "life extending" when Olivero OA et al., in "Vaginal epithelial DNA damage and expression of preneoplastic markers in mice during chronic dosing with tumorigenic levels of 3'-azido-2',3'-dideoxythymidine (AZT)" (Cancer Res. 1994;54:6235-42) reported that:


we have found positive correlations between the dose of AZT administered to female CD-1 mice, the incorporation of AZT into vaginal DNA, the hyperproliferation of the vaginal epithelial basal layer, and the aberrant expression of alpha-6 integrin toward the epithelial suprabasal strata of the vagina, a target organ for carcinogenesis in mice. These results suggest that there is an ordered progression of abnormal events leading to tumorigenesis in vaginal epithelial tissues?”


56. Why are antiretrovirals called "life-saving" and "life extending" when Toltzis et al., in "Zidovudine-associated embryonic toxicity in mice" (Journal of Infectious Diseases, 1991;163:1212-8) reported that:.


“Mice receiving AZT during gestation yielded fewer fetuses…and greater numbers of resorptions…Exposure to AZT was highly correlated with failure to develop to the blastocyst stage…These data indicate that AZT has a direct toxic effect on the developing mouse embryo?”


57. Why are antiretrovirals called "life-saving" and "life extending" when Mansuri et al., in "Comparison of In Vitro Biological Properties and Mouse Toxicities of Three Thymidine Analogs Active against Human Immunodeficiency Virus" (Antimicrobial Agents and Chemotherapy. 1990;34(4):637-641) reported:


“[in mice] AZT had a profound effect on the number of erythrocytes [mature red blood cells] and a small effect on the number of leukocytes [white blood cells]…anemia was seen in all the mice tested at 1,000 mg/kg per day?”


58. Why are antiretrovirals called "life-saving" and "life extending" when Zietz et al., in "An unusual cluster of cases of Castleman's disease during highly active antiretroviral therapy for AIDS"  (NEJM. 1999 Jun 17;340:1923-4) reported:


"Recently, we observed an unusual cluster of cases of rapidly progressing multicentric Castleman's disease. Fever, weakness, generalized enlargement of lymph nodes, and marked polyclonal gammopathy developed in three patients with AIDS...Two of these patients died within one week after the diagnosis, with generalized involvement of the lymphatic system, liver, and bone marrow at autopsy. A fourth patient with AIDS who died equally rapidly after the diagnosis of multicentric Castleman's disease had been seen in our hospital 14 months earlier... symptoms of multicentric Castleman’s disease started after the initiation of highly active antiretroviral therapy in these three patients?”


59. Why are antiretrovirals called "life-saving" and "life extending" when Sussman et al., in a presentation entitled,  "Mutagenicity of AZT in the human lymphoblastoid cell line, TK6" (2nd National AIDS Malignancy Conference 1998) reported:


“Perinatal treatment with 3'-azido-3'-deoxythymidine (AZT) has been found to reduce the rate of maternal-infant transmission of HIV; however, AZT is clastogenic at therapeutic doses in adult patients and induces cancers in the offspring of mice treated in utero. The purpose of the present study was to investigate the mutagenicity of AZT at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus of the human lymphoblastoid cell line, TK6, following in vitro exposures. ..There was a significant increase over background in hprt Mfs [mutation frequencies] in TK6 cells exposed to 300mM AZT for 3 days (1.8-fold increase). In cells exposed for 6 days, there was a decrease in...cell survival. These preliminary results indicate that AZT treatment is mutagenic and produces large deletions in human cells?”


60. Why are antiretrovirals called "life-saving" and "life extending" when Agarwal et al., in "Genotoxicity and mitochondrial damage in human lymphocytic cells chronically exposed to 3'-azido-2',3'-dideoxythymidine" (Mutat Res. 1997 May 23;390(3):223-231) reported that:


 “AZT … induces significant toxic effects in humans exposed to therapeutic doses...Cytogenetic observations on H9-AZT cells showed an increase in chromosomal aberrations and nuclear fragmentation when compared with unexposed H9 cells...The toxicities explored here suggest that the mechanisms of AZT induced cytotoxicity in bone marrow of the patients chronically exposed to the drug in vivo may involve both chromosomal and mitochondrial DNA damage?”


61. Why are antiretrovirals called "life-saving" and "life extending" when Lewis W. Dalakas in "Mitochondrial toxicity of antiviral drugs" (Nat Med. 1995 May;1(5):417-22) claimed that:


“Clinical manifestations of ANA [Antiviral Nucleoside Analogs, such as AZT] toxicity: It is self-evident that ANAs, like all drugs, have side-effects. However, the prevalent and at times serious ANA mitochondrial toxic side-effects are particularly broad ranging with respect to their tissue target and mechanisms of toxicity: … Haematalogical toxicity [anemia, and other blood disorders] … Myopathy [muscle disorders] … Cardiotoxicity [heart disorders] … Hepatic toxicity [liver disorders] … Peripheral neuropathy [nerve damage]?”


62. Why are antiretrovirals called "life-saving" and "life extending" when an article appearing in Neurology (1994;44:1982-1900) suggested that:


“among the subjects with CD4+ [immune system] cell counts < 200/mm3, the risk of developing HIV dementia among those reporting any antiretroviral use (AZT, ddI, ddC, or d4T) was 97% higher than among those not using this antiretroviral therapy...In addition, the findings of our analysis seem to confirm previous observation of a neurotoxic effect of antiretroviral agents.”


63. Why are antiretrovirals called "life-saving" and "life extending" when Fischl MA et al. in "Prolonged zidovudine therapy in patients with AIDS and advanced AIDS-related complex"  (JAMA. 1989;262(17):2405-10) in a follow-up study to the 1987 study which ushered AZT through FDA approval concluded:


58% of all subjects with AIDS and AIDS-related complex receiving zidovudine experienced granulocytopenia of grade 3 or higher...Serious anemia occurred in 32% of all subjects receiving zidovudine...and could be typically managed by dose attenuation, temporary dose interruption of zidovudine therapy and/or red blood cell transfusions...12% of subjects...had an episode of thrombocytopenia [low platelet count] after the initiation of zidovudine therapy...Ten patients had liver enzyme levels elevated...and were managed with dose attenuations or interruptions of zidovudine therapy...One report of a grand mal seizure, two events associated with cardiac dysfunction, and five reports of myopathy were the only new serious potentially drug-related adverse events reported during extended periods of zidovudine administration?”


64. Why are antiretrovirals called "life-saving" and "life extending" when Dournon et al., in "Effects of zidovudine in 365 consecutive patients with AIDS or AIDS-related complex"  (Lancet. 1988 Dec 3;2:1297-1302) concluded that:


“AZT was started at full dose in 260 patients, 64 with ARC and 196 with AIDS. In 58 of these patients, AZT had to be stopped at least once for a minimum of 7 days. In 142 other patients, dosage was reduced by half because of leucopenia (79), leucopenia and anaemia (32), anaemia (20), rash (3), vomiting (3), headaches and insomnia (2), myalgia (2), or hepatitis (1). 3 patients reduced the dose with no medical reason. Later on, progression of toxicity led to suspension of AZT (for at least 7 days) in 85 of the 142 patients whose treatment had been reduced to half dose. Thus AZT was stopped at least once in 143 (55%) patients who began the full-dose regimen. Because of their initial haematological status 105 (28.8%) patients were treated from the start with half-dose AZT - toxicity led to cessation of treatment in 71 (67.6%) cases?”


65. Why are antiretrovirals called "life-saving" and "life extending" when Mocroft A et al., in "Anaemia is an independent predictive marker for clinical prognosis of HIV-infected patients from across Europe" (AIDS. 1999;13:943-50) reported:


“We found that 78.2% of the patients with mild or severe anaemia at baseline had received zidovudine [AZT]”


66. Why are antiretrovirals called "life-saving" and "life extending" when Hymes et al., in "The Effect of Azidothymidine on HIV-related Thrombocytopenia" (NEJM. 1998 Feb 25;318(8):516-7) reported:


"The hematocrit [red blood cell count] decreased in the same patients...with three of eight patients requiring red-cell transfusion by the fourth week of treatment?”


67. Why are antiretrovirals called "life-saving" and "life extending" when the advertisement for PROCRIT, 1997 solicited that:


“While effective drug therapy is continued in zidovudine [AZT]-treated HIV-infected patients…PROCRIT Reduces Transfusion Requirements and Helps Lift the Burden of Anemia?”


68. Why are antiretrovirals called "life-saving" and "life extending" when Fischl MA et al., in "A randomized controlled trial of a reduced daily dose of Zidovudine in patients with the Acquired Immunodeficiency Syndrome" (NEJM. 1990;323(15):1009-14) reported that:


“178 subjects (34%) had a hemoglobin concentration below 5 mmol per liter [anemia]...A greater proportion of subjects in the standard-treatment [high dose AZT] group had a first episode of severe anemia earlier in the study, as compared with the proportion in the low-dose group. 134 subjects (26%) received red-cell transfusions (65 in the standard-treatment group and 69 in the low-dose group)...230 subjects(44%) had a [low] neutrophil [infection fighting white blood cells] count...134 (51%) in the standard-treatment group and 96 (37%) in the low-dose group...22 subjects (4%) had a [low] platelet [blood clotting cells] count?”


69. Why are antiretrovirals called "life-saving" and "life extending" when Mir et al., in "Zidovudine and Bone Marrow"  (Lancet. 1988 Nov 19;1195-6) reported:


“Zidovudine is well known to produce haematological toxicity in vitro and in some patients...It is worrying that bone marrow changes in patients on zidovudine seem not to be readily reversed when the drug is withdrawn…These findings have serious implications for the use of zidovudine in HIV positive but symptom-free individuals?”


70. Why are antiretrovirals called "life-saving" and "life extending" when Dainiak et al., in "3’-Azido-3’-deoxythymidine (AZT) inhibits proliferation in vitro of human haematopoietic progenitor cells" (British Journal of Haematology, 1988;69:299-304) claimed:


nearly one half of patients treated with AZT for [HIV]-associated disease develop transfusion-dependent anaemia due to bone marrow depression”


The good news of course is that half of patients don’t experience hematotoxicity!


71. Why are antiretrovirals called "life-saving" and "life extending" when Costello., in "Haematological abnormalities in human immunodeficiency virus (HIV) disease" (J Clin Pathol. 1988;41:711-5) reported that:


“Blood transfusion is often necessary in patients with AIDS, especially in those receiving AZT, a drug which produces severe anaemia in a proportion of recipients. Forty nine (36%) of 138 patients treated with AZT … required blood transfusion at least once?”


72. Why are antiretrovirals called "life-saving" and "life extending" when Walker et al., in "Anemia and erythropoiesis in patients with the acquired immunodeficiency syndrome (AIDS) and Kaposi sarcoma treated with zidovudine" (Ann Int Med. 1988;108:372-6) reported:


“In the current study, transfusion-dependent anemia occurred in 6 of 15 patients with AIDS and Kaposi sarcoma who were receiving zidovudine therapy. All 6 affected patients required their first blood transfusion between 3 and 9 weeks after starting zidovudine therapy, and each required 4 to 14 units of packed erythrocytes to maintain a hemoglobin level above 100 g/L over a 12-week study.”


73. Why are antiretrovirals called "life-saving" and "life extending" when Gina Kolata of the New York Times health desk wrote: "Imminent marketing of AZT raises problems; marrow suppression hampers AZT use in AIDS victims." (Science. 1987 Mar 20;235:1462-3) where she argued that:


more than half of all AIDS patients may not benefit from the drug because it is more toxic for them than their AIDS infection. The most serious side effect of AZT is to suppress the bone marrow, leaving patients highly vulnerable to bacterial infections?”


74. Why are antiretrovirals called "life-saving" and "life extending" when Richman et al., in "The Toxicity of Azidothymidine (AZT) in the Treatment of Patients with AIDS and AIDS-Related Complex" (NEJM. 1987;317:192-197) reported that:


“Anemia…developed in 24% of AZT recipients and 4% of placebo recipients (P<0.001). 21% of AZT recipients and 4% of placebo recipients required multiple red-cell transfusions (P<0.001). Neutropenia (<500 cells per cubic millimeter) occurred in 16% of AZT recipients, as compared with 2% of placebo recipients (P<0.001)?”


75. Why are antiretrovirals called "life-saving" and "life extending" when Gill PS et al., in "Azidothymidine Associated with Bone Marrow Failure in the Acquired Immunodeficiency Syndrome (AIDS)" (Ann Int Med. 1987;107:502-505) reported that:


Four patients with [AIDS], and a history of Pneumocystis carinii pneumonia developed severe pancytopenia [marked decrease in all types of blood cells]…12 to 17 weeks after the initiation of azidothymidine (AZT) therapy…Partial bone marrow recovery was documented within 4 to 5 weeks in three patients, but no marrow recovery has yet occurred in one patient during the more than 6 months since AZT treatment was discontinued?”


76. Why are antiretrovirals called "life-saving" and "life extending" when P. Chariot, and R. Gherardi ., in "Partial cytochrome c oxidase deficiency and cytoplasmic bodies in patients with zidovudine myopathy” (Neuro muscul Disorders. 1991;1:357-363) reported:


“Long term therapy with [AZT] can induce a toxic myopathy associated with mitochondrial changes?”


77. Why are antiretrovirals called "life-saving" and "life extending" when Hayakawa  et al., in "Massive conversion of guanosine to 8-hydroxy-guanosine in mouse liver mitochondrial DNA by administration of azidothymidine, Biochem Biophys Res Commun. 1991;176:87-93) reported that:


“typical mitochondrial myopathy has been reported to be expressed among many patients with AIDS treated with long-term azidothymidine (AZT) therapy" and "for AIDS patients, it is urgently necessary to develop a remedy substituting this toxic substance, AZT?”


78. Why are antiretrovirals called "life-saving" and "life extending" when Coker R et al., in "Exacerbation of HIV-associated myopathy by zidovudine, AIDS, 1991;5(2):229-31) claimed that:


“A clinically significant myopathy that precedes the development of zidovudine associated mitochondrial myopathy has been a rarity in our experience?”


79. Why are antiretrovirals called "life-saving" and "life extending" when Dalakas et al., in "Mitochondrial myopathy caused by long-term zidovudine therapy. NEJM. 1990;322(16):1098-1105) wrote:


“Before 1986, when zidovudine (formerly called azidothymidine [AZT]) was introduced…the number of patients with HIV-associated myopathy was small, and myopathy [muscle disorders] was considered a rare complication of HIV infection. During the past two years [1988-1989], an increasing number of patients receiving long-term zidovudine therapy have had myopathic symptoms such as myalgia (in up to 8 percent of patients), elevated serum creatine kinase levels (in up to 15 percent), and muscle weakness. These symptoms generally improve when zidovudine is discontinued...We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection?”


80. Why are antiretrovirals called "life-saving" and "life extending" when M. Till , and K.B. MacDonnell, in "Myopathy with Human Immunodeficiency Virus type 1 (HIV-1) infection: HIV-1 or zidovudine?"  (Ann Int Med. 1990;113(7):492-4) reported that:


“In our review of our clinic patients who have received zidovudine therapy for more than 6 months, 16% (14 of 86 patients) have had persistently elevated creatine kinase values. Six percent of these patients (5 of 86) developed symptomatic myalgia and objective proximal muscle weakness. These 5 symptomatic patients had received zidovudine for an average of 45 weeks and had had creatine kinase elevations for several weeks before onset of symptoms. Of these 5 patients, 4 had creatine kinase values return to normal and symptoms resolve after zidovudine was withdrawn...Three patients were rechallenged with zidovudine: each had recurrent creatine kinase elevations at a dose of 600 mg/d. The zidovudine dose was increased to 1200 mg/d in 2 patients: after a few days, both developed recurrent muscle symptoms that again responded to dose reduction. ...Results of quadriceps muscle biopsies done on our patients who responded to zidovudine withdrawal showed severe myopathic changes without evidence of inflammatory infiltrates. Electron microscopy revealed many ultrastructural changes, including destruction of the sarcomere profile with z-band change in the form of streaming and rod bodies. Muscle mitochondria showed wide variation in size, swelling, degeneration and laminar bodies. ...There have been 40 case reports [to 1990] of patients who have developed myopathy while taking zidovudine (including our 5 symptomatic patients). Zidovudine therapy was discontinued in 34 of these patients and 26 improved?”


81. Why are antiretrovirals called "life-saving" and "life extending" when Helbert et al., in "Zidovudine-associated myopathy" (Lancet, 1988 Sep 17;2:689-90) claimed that:


“A severe proximal myopathy, predominantly affecting the legs, seems to be a significant complication of long-term zidovudine therapy, even at reduced doses; it affected 18% of our patients who had received treatment for more than 200 days. Other drugs could not be implicated. The pathogenesis is obscure; the myopathy resolves on cessation of zidovudine, but not on dose-reduction, though there is then a risk of rebound encephalitis?”


82. Why are antiretrovirals called "life-saving" and "life extending" when D.V. Havlir and P.F. Barnes., in "Tuberculosis in patients with human immunodeficiency virus infection" (NEJM. 1999 Feb 4;340:367-73) reported that:


“Antiretroviral therapy may be initiated early during antituberculosis therapy in HIV-infected patients with tuberculosis. After initial clinical improvement, paradoxical worsening of disease developed in up to 36 percent of these patients, characterized by fever, worsening chest infiltrates on radiograph, and peripheral and mediastinal lymphadenopathy...In contrast, only 7 percent of patients who received antituberculosis therapy but not antiretroviral therapy had paradoxical reactions?”


83. Why are antiretrovirals called "life-saving" and "life extending" when Kelleher et al., in "Immunological effects of antiretroviral and immune therapies for HIV" (AIDS, 1997;Vol 11 (suppl A):S149-155) reported that:


“[AZT may] unmask silent opportunistic infections...Lack of strong evidence exists for sustained immune reconstitution by current therapies...If [immune reconstitution] does not occur with time, despite prolonged viral suppression, then the case for immunorestorative strategies...could be justifiably explored?”


84. Why are antiretrovirals called "life-saving" and "life extending" when The Canadian Pharmaceutical Association Compendium of Pharmaceuticals & Specialities (1997;1357-61) recommended that:


“The long-term consequences of in-utero and infant exposure to zidovudine [AZT] are unknown. The long-term effects of early or short-term use of zidovudine in pregnant women are also unknown...The incidence of adverse reactions [to AZT] appears to increase with disease progression, and patients should be monitored carefully, especially as disease progression occurs. [i.e. AZT does not prevent progression to AIDS]?”


85. Why are antiretrovirals called "life-saving" and "life extending" when The Physicians Desk Reference, (Mosby-Year Book Inc.. 1996, http://www.virusmyth.com/aids/data/pdrazt.htm) claimed:


“[in these clinical trials] it was often difficult to distinguish adverse events possibly associated with administration of Retrovir from underlying signs of HIV disease or intercurrent illnesses [i.e. AZT can cause AIDS-defining illnesses]?”


86. Why are antiretrovirals called "life-saving" and "life extending" when Sperling et al., in "Maternal viral load, zidovudine treatment and the risk of transmission of human immunodeficiency virus type 1 from mother to infant" (NEJM. 1996;335(22):1621-9) reported that:


“Overall, zidovudine treatment was associated with only a small reduction in circulating levels of plasma RNA...Explanations need to be considered for the apparent lack of association between the observed RNA levels and the effect of zidovudine treatment [i.e. lower rates of transmission from mothers on zidovudine to their children cannot be due to lower levels of virus!]?”


87. Why are antiretrovirals called "life-saving" and "life extending" when Bacellar et al., in "Incidence of clinical AIDS conditions in a cohort of homosexual men with CD4+ cell counts < 100/cubic mm" (JID. 1994;170:1284-7) reported that:


“The median CD4 lymphocyte count did not differ in the 3 groups: 54 for the group receiving neither antiretroviral nor P. carinii pneumonia prophylaxis, 53 for the group receiving only antiretroviral therapy, and 52 for the combined treatment group. There were also no major differences in the median CD8 lymphocyte count of the 3 groups...Other illnesses now have elevated incidence rates among persons receiving P. carinii pneumonia prophylaxis [and AZT or didanosine]: M. avium complex, nonretinitis cyomegalovirus disease, cytomegalovirus retinitis, candida esophagitis, and wasting syndrome?”


88. Why are antiretrovirals called "life-saving" and "life extending" when Sheppard et al., in "Viral burden and HIV disease" ( Nature. 1993 Jul 22;364(6435):291-2) reported that:


the high level of plasma virus observed by Piatak et al, was about 99.9 per cent non-culturable, suggesting that it was either neutralized or defective. Therefore, rather than supporting a cytopathic model, this observation actually may help explain the relatively slow dissemination of the infected cell burden and thus the relative ineffectiveness of therapy with nucleoside analogues which target this process?”


89. Why are antiretrovirals called "life-saving" and "life extending" when The National Institute of Allergy and Infectious Diseases State-of-the-Art Panel on Anti-Retroviral Therapy for Adult HIV-Infected Patients, in "Anti-retroviral therapy for adult HIV-infected patients. Recommendations from a state-of-the-art conference" (JAMA. 1993;270:2583-9) concluded that:


“Some HIV-infected individuals have remained healthy for more than 15 years following seroconversion. Lower numbers of CD4+ peripheral blood lymphoctyes have generally been found to indicate the advancement of HIV disease... [but] The CD4+ cell counts vary from day to day and laboratory to laboratory, and similar levels do not necessarily reflect the same disease status in all patients. For example, very low CD4+ cell counts (less than 0.05x10**9/L (50/microL)) usually indicate advanced disease; however, some patients with these levels remain asymptomatic for extended periods of time while others succumb rapidly...While knowledge of the clinical use of zidovudine has increased during the last several years, the panel was concerned overall by the drug’s limited effectiveness and durability of response?”


90. Why are antiretrovirals called "life-saving" and "life extending" when Lu et al., in "Similar replication capacities of primary human immunodeficiency virus type 1 isolates derived from a wide range of clinical sources" (J Virol. 1992 Jan;66(1):334-340) concluded that:


“Replication curves and cytopathic effect of a standard inoculum (1 ng of p24) of 66 primary HIV-1 isolates were similar regardless of the clinical stage of the patient...There was no difference between viruses derived from patients sensitive to zidovudine and those derived from patients resistant to zidovudine?”


91. Why are antiretrovirals called "life-saving" and "life extending" when Reinvang et al., in "Only temporary improvement in impaired neuropsychological function in AIDS patients treated with zidovudine" (AIDS. 1991;5(2):228-9) reported that:


“Doubts may be raised about the long-term beneficial effects of zidovudine treatment on AIDS-related cognitive impairments?”


92. Why are antiretrovirals called "life-saving" and "life extending" when In 1990, Fischl MA et al. in NEJM (1990;323(15):1009-14) reported that:


thirteen subjects of 146 tested who were negative for HIV antigen before treatment later had detectable levels of antigen during the 128 weeks of treatment"!


How does AZT make you test HIV-positive?


93. Why are antiretrovirals called "life-saving" and "life extending" when Phillips et al., in "Viral load and combination therapy for Human Immunodeficiency Virus"  (NEJM. 1997 Mar 27;336(13), www.nejm.org/content/1997/0336/0013/0958.asp) suggested that:


“Extended follow-up of patients in one [AZT] trial, the Concorde study, has shown a significantly increased risk of death among the patients treated early...where is the evidence that for a patient with a CD4 count of 450 cells per cubic millimeter and a low plasma viral level, it would not be better to wait before initiating therapy?...In 1990...a patient with a CD4 count of 450 cells per cubic millimeter would have been advised to start monotherapy with zidovudine. We now tell such a patient that, in fact, follow-up data for up to 4.5 years since that time have shown no survival benefit?”


94. Why are antiretrovirals called "life-saving" and "life extending" when White et al., in "Impact of treatment changes on the interpretation of the Concorde trial” (AIDS, 1997;11:999-1006) suggested that:


“participants of open-label ZDV [AZT] still had four to five times the incidence of ARC/AIDS/death of participants on blinded therapy [of which approximately half were on AZT and half on placebo]...The unadjusted hazard of ARC/AIDS/death was 4.6 times higher for participants [in the deferred group] who had received ZDV...after adjustment for latest CD4 this became 1.6...There was a suggestion of a benefit in terms of [slower] progression to ARC, AIDS or death [with AZT], no effect on progression to AIDS or death, and a suggestion of an increase in mortality?”


95. Why are antiretrovirals called "life-saving" and "life extending" when Chaisson et al., in  "Sex, race, drug use and progression of human immunodeficiency virus disease" (NEJM. 1995;333(12):751-6) reported that.


The mortality rate was significantly higher among [a group of 1372] patients who had received antiretroviral therapy [principally AZT] before enrollment in the clinic?”


96. Why are antiretrovirals called "life-saving" and "life extending" when Buchbinder et al., in "Long-term HIV-1 infection without immunologic progression" (AIDS, 1994; 8:1123) reported that:


“Only 38% of the HLP [Healthy long-term positives] had ever used zidovudine [AZT] or other nucleoside analogues, compared with 94% of the progressors?”


97. Why are antiretrovirals called "life-saving" and "life extending" when Pluda et al., in "Development of Non-Hodgkin Lymphoma in a Cohort of Patients with Severe Human Immunodeficiency Virus (HIV) Infection on Long-Term Antiretroviral Therapy" (Ann Int Med. 1990;113:276-282) claimed that AZT caused cancer?


after starting antiretroviral treatment...the estimated probability of developing lymphoma ...by 36 months, [was] 46.4% (CI, 19.6% to 75.5%)...a direct role of therapy itself cannot be totally discounted...Zidovudine can act as a mutagen.”


98. Why are antiretrovirals called "life-saving" and "life extending" when Costello (1988) reported in the Journal of Clinical Pathology that, “Blood transfusion is often necessary in patients with AIDS, especially in those receiving AZT, a drug which produces severe anaemia in a proportion of recipients. Forty nine (36%) of 138 patients treated with AZT required blood transfusion at least once?”


99. Why are antiretrovirals called "life-saving" and "life extending" when Harrison's Principles of Internal Medicine states: “[AZT], used for treating [HIV], often causes severe megaloblastic anemia caused by impaired DNA synthesis?"


100. Writing in the journal Palliat Med. (1997 Mar;11(2):152-8), Kelleher et al. published a paper entitled, "HIV infection: the spectrum of symptoms and disease in male and female patients attending a London hospice," in which they concluded that:


“Lack of strong evidence exists for sustained immune reconstitution by current therapies [comprising AZT and other drugs], and AZT may unmask silent opportunistic infections. Not only can AZT unmask silent opportunistic infections, it can exacerbate clinically conspicuous ones.”


101. Why are antiretrovirals called "life-saving" and "life extending" when AZT has some of the following caveats on the AZT package insert printed in bold and CAPITALIZED type?






“Persistent headaches lasting longer than 1 month, anemia, dementia, diarrhea,

muscle wasting, candidiasis, non-specific oral lesions, severe fatigue,

enlarged liver and liver failure, heart failure, diabetes, unmasking of opportunistic

infections including CMV retinitis, spontaneous bleeding in hemophiliacs, lymphoma, severe skin rashes, Stevens-Johnson syndrome, and other toxic reactions, back pain, body odor, chest pain, chills, edema of the lip, fever, flu syndrome, hyperalgesia, syncope, vasodilation, bleeding gums, constipation, dysphagia, edema of the tongue, eructation, flatulence, mouth ulcer, rectal hemorrhage, lymphadenopathy, arthralgia, muscle spasm, tremor, twitch, anxiety, confusion, depression, dizziness, emotional lability, loss of mental acuity, nervousness, paresthesia, somnolence, cough, dyspnea, epistaxis, hoarseness, pharyngitis, rhinitis, sinusitis, acne, changes in skin and nail pigmentation, pruritus, rash, sweat, urticaria, amblyopia, hearing loss,photophobia, taste perversion, dysuria, polyuria, urinary frequency, urinary hesitancy.”


 “Zidovudine was administered orally at three dosage levels to separate groups of mice and rats (60 females and 60 males in each group). Initial single daily doses were 30, 60, and 120 mg/kg/day in mice and 80, 220, and 600 mg/kg/day in rats. The doses in mice were reduced to 20, 30, and 40 mg/kg/day after day 90 because of treatment- related anemia, whereas in rats only the high dose was reduced to 450 mg/kg/day on day 91 and then to 300 mg/kg/day on day 279.”


“In mice, seven late-appearing (after 19 months) vaginal neoplasms (5 nonmetastasizing squamous cell carcinomas, one squamous cell papilloma, and one squamous polyp) occurred in animals given the highest dose. One late-appearing squamous cell papilloma occurred in the vagina of a middle dose animal. No vaginal tumors were found at the lowest dose.”


“In rats, two late-appearing (after 20 months), non-metastasizing vaginal squamous cell carcinomas occurred in animals given the highest dose. No vaginal tumors occurred at the low or middle dose in rats. No other drug-related tumors were observed in either sex of either species.”


“It is not known how predictive the results of rodent carcinogenicity studies may be for humans. At doses that produced tumors in mice and rats, the estimated drug exposure (as measured by AUC) was approximately 3 times (mouse) and 24 times (rat) the estimated human exposure at the recommended therapeutic dose of 100 mg every 4 hours.” “ In the presence of metabolic activation, the drug was weakly mutagenic at concentrations of 1000 A?g/ml and higher. In an in vitro mammalian cell transformation assay, zidovudine (AZT) was positive at concentrations of 0.5 ug/ml and higher. In an in vitro cytogenetic study performed in cultured human lymphocytes, zidovudine induced dose-related structural chromosomal abnormalities at concentrations of 3 ug/ ml and higher.”


“In two in vivo micronucleus studies (designed to measure chromosome breakage or mitotic spindle apparatus damage) in male mice, oral doses of zidovudine 100 to 1000 mg/kg/day administered once daily for approximately 4 weeks induced dose-related increases in micronucleated erythrocytes. Similar results were also seen after 4 or 7 days of dosing at 500 mg/kg/day in rats and mice.” Nothing wrong with a few micronucleated cells or mitotic spindle damage.


“In a study involving 11 AIDS patients, it was reported that the seven patients who were receiving Retrovir (1200 mg/day) as their only medication for 4 weeks to 7 months showed a chromosome breakage frequency of 8.29ug/ml2.65 breaks per 100 peripheral lymphocytes. This was significantly (P< 0.05) higher than the incidence of 0.5ug/ml 0.29 breaks per 100 calls that was observed in the four AIDS patients who had not received Retrovir.


102. Why are antiretrovirals called "life-saving" and "life extending" when Brinkman et al., reported that "Mitochondrial toxicity induced by nucleoside-analogue reverse transcriptase inhibitors is a key in the pathogenesis of antiretroviral-related lipodystrophy." (Lancet. 1999 Sep 25;354:1112-15.1999), and concluded that:


“Highly active antiretroviral therapy (HAART) can induce a characteristic lipodystrophy syndrome of peripheral fat wasting and central adiposity. HIV-1 protease inhibitors are generally believed to be the causal agents, although the syndrome has also been observed with protease-inhibitor-sparing regimens. Here, we postulate that the mitochondrial toxicity of the nucleoside-analogue reverse-transcriptase inhibitors plays an essential part in the development of this lipodystrophy, similar to the role of mitochondrial defects in the development of multiple symmetrical lipomatosis?”


103. Why are antiretrovirals called "life-saving" and "life extending" when Estaquier, et al., reported in an article entitled, "Effects of Antiretroviral Drugs on Human Immunodeficiency Virus Type 1-Induced CD4+ T-Cell Death" (Journal of Virology, Vol. 76, No. 12, p. 5966-5973, June 2002) that:


"We treated PBMC from HIV-seronegative healthy donors with increasing concentrations of IDV, SQV, or ddI for 3 days and monitored T-cell proliferation and cell death. Both IDV and SQV decreased T-cell proliferation mediated by CD3 MAb in three independent experiments performed with healthy donor cells with a mean decrease for SQV of 53% ± 15% and a mean decrease for IDV of 48% ± 12% (Fig. 4A). Moreover, in the absence of T-cell activation, we observed that 10 µM IDV and SQV induced a loss in membrane mitochondrial potential (m) as assessed by flow cytometry using DiOC6."


104. Why are antiretrovirals called "life-saving" and "life extending" when Martinez et al., in "Risk of lipodystrophy in HIV-1 infected patients treated with protease inhibitors: a prospective cohort study" (Lancet. 2001;357(9256):592-8, 2001), suggested that:


“Clinical research on lipodystrophy has usually rested on the idea that it was merely a complex adverse event related to individual antiretroviral agents or families of drugs...Our study suggests that the risk of lipodystrophy is mainly related to the total exposure to HAART and only to a lesser degree to specific antiretroviral drugs.”


105. Why are antiretrovirals called "life-saving" and "life extending" when Tsiodras et al., also described the "Effects of Protease Inhibitors on Hyperglycemia, Hyperlipidemia, and Lipodystrophy" (Arch Intern Med. 2000 Jul 10;160(13):2050-6, 2000), where they suggested that:


“Our study reports an independent association between PI [protease inhibitors] use and ... lipodystrophy, on the basis of a 5-year cohort study that encompassed the pre-PI and post-PI therapeutic eras. Although these metabolic changes were occasionally observed in patients not exposed to PIs, they were much more frequent after initiation of PI therapy.”


106. Why are antiretrovirals called "life-saving" and "life extending" when

Bica et al (2001) stated:


“In 1998-1999, 11 (50%) of 22 deaths were due to end-stage liver disease [a common side effect of AIDS drugs]... End-stage liver disease is now the leading cause of death in our hospitalized HIV-seropositive population.”


107. Why are antiretrovirals called "life-saving" and "life extending" when Lederman MM, Valdez H. (2000), published a study that claimed:


“Of recent HIV-related deaths occurring in the University Hospitals of Cleveland although OIs [Opportunistic Infections] constituted less than 25% of deaths in 1999, end-organ failures [which could well be caused by medication] constituted nearly half. Importantly, the median CD4 cell count among the patients who died in our clinic has risen, and about 20% of recent deaths have occurred among patients with plasma HIV RNA levels below the limit of detection?


108. If antiretrovirals such as AZT or combinations such as HAART are indeed "life-saving" and "life extending," then why has there been the need to make so many of them? Here is a more or less complete list of "the life saving drugs that have been improperly called or considered as "antiretrovirals" that are aggressively peddled by the pharmaceutical giants in collusion with the current Public Health Service administrations (eg. Agenerase (amprenavir), GlaxoSmithKline; Combivir, (lamivudine and zidovudine), GlaxoSmithKline; Crixivan, (indinavir, IDV, MK-639), Merck; Emtriva, (FTC, emtricitabine), Gilead Sciences; Epivir, (lamivudine, 3TC Epzicom, abacavir) GlaxoSmithKline; Fortovase, (saquinavir), Hoffmann-La Roche; Fuzeon, (enfuvirtide, T-20), Hoffmann-La Roche & Trimeris; Hivid, (zalcitabine, ddC, dideoxycytidine), Hoffmann-La Roche; Invirase, (saquinavir mesylate, SQV), Hoffmann-La Roche; Kaletra, (lopinavir and ritonavir), Abbott Laboratories; Lexiva, (Fosamprenavir Calcium), GlaxoSmithKline; Norvir, (ritonavir, ABT-538), Abbott Laboratories; Rescriptor, (delavirdine, DLV), Pfizer; Retrovir (zidovudine, AZT, azidothymidine, ZDV) GlaxoSmithKline; Reyataz, (atazanavir sulfate), Bristol-Myers Squibb; Sustiva, (efavirenz), Bristol Myers-Squibb; Truvada, (tenofovir disoproxil/emtricitabine), Gilead Sciences, Inc.; Videx EC, (enteric coated didanosine), Bristol Myers-Squibb; Videx, (didanosine, ddI, dideoxyinosine), Bristol Myers-Squibb; Viracept, (nelfinavir mesylate, NFV), Agouron Pharmaceuticals; Viramune, (nevirapine, BI-RG-587), Boehringer Ingelheim; Viread, (tenofovir disoproxil fumarate), Gilead; Zerit, (stavudine, d4T) Bristol Myers-Squibb; Ziagen (abacavir) GlaxoSmithKline.


109. Why do some AIDS researchers such as Gisselquist et al. who have studied Africa and African AIDS extensively, claim that "HIV/AIDS" is caused mostly by doctors, and are now advocating that this is how the Tripoli Six infected more than 400 children in a Libyan hospital, and who are said to be soon executed by firing squad!  The reasons in support of the Gisselquist et al. claims have been published repeatedly in the International Journal of STD’s and  AIDS (Gisselquist D, Friedman E, Potterat JJ, Minkin SF, Brody S. Four policies to reduce HIV transmission through unsterile health care. Int J STD AIDS. 2003 Nov;14(11):717-22; Gisselquist D, Potterat JJ, Brody S, Vachon F. Let it be sexual: how health care transmission of AIDS in Africa was ignored. Int J STD AIDS. 2003 Mar;14(3):148-61; Brewer DD, Brody S, Drucker E, Gisselquist D, Minkin SF, Potterat JJ, Rothenberg RB, Vachon F. Mounting anomalies in the epidemiology of HIV in Africa: cry the beloved paradigm. Int J STD AIDS. 2003 Mar;14(3):144-7; Gisselquist D, Potterat JJ, Epstein P, Vachon F, Minkin SF. AIDS in Africa. Lancet. 2002 Nov 2;360(9343):1422-3; author reply 1423-4; Gisselquist D, Rothenberg R, Potterat J, Drucker E. HIV infections in sub-Saharan Africa not explained by sexual or vertical transmission. Int J STD AIDS. 2002 Oct;13(10):657-66) include the following types of reasons for the claim that “HIV/AIDS” is caused by doctors (a synopsis can be obtained at Editorial with Gisselquist, statistics quoted from: International Journal of STD & AIDS Royal Society of Medicine, October 2002 Africa HIV/AIDS through unsafe medical care. Also available: Africa Policy E-Journal. www.africaaction.org/docs02/hiv0210t.htm):


"An expanding body of evidence challenges the conventional hypothesis that sexual transmission is responsible for more than 90% of adult HIV infections in Africa. Differences in epidemic trajectories across Africa do not correspond to differences in sexual behavior. Studies among African couples find low rates of heterosexual transmission, as in developed countries. Many studies report HIV infections in African adults with no sexual exposure to HIV and in children with HIV-negative mothers. Unexplained high rates of HIV incidence have been observed in African women during antenatal and postpartum periods. Many studies show 20%-40% of HIV infections in African adults associated with injections (though direction of causation is unknown). These and other findings that challenge the conventional hypothesis point to the possibility that HIV transmission through unsafe medical care may be an important factor in Africa's HIV epidemic. More research is warranted to clarify risks for HIV."


"The assumption that historic and continuing high rates of epidemic increasesamong African adults are almost exclusively due to sexual transmission requires much higher rates of heterosexual transmission in Africa than in the developed world. However, a recent study of HIV incidence in serodiscordant couples in Africa (only 1.2% reported consistent condom use) estimated a rate of transmission per coital act of only 0.0011,(23) comparable to rates of 0.0003-0.0015 from similar studies in the US and Europe [22].


"A study in Kinshasha in 1985 found 39% (17 of 44) of HIV-positive inpatient andoutpatient children 1-24 months old to have HIV-negative mothers; only five of 16 (with information) had been transfused... In a later report from Rwanda, 7.3% (54 of 704) of mothers of children with AIDS were HIV-negative; transfusions were identified as the risk factor for 22 of the 54 children… rates of unexplained incidence among African women are comparable to rates of maternal mortality from puerperal fever of 6% to 16% observed by Semmelweis during 1841-46 in the First Clinic at the University of Vienna's obstetric department. "


"Starting in the 1950s Africans experienced a massive increase in medical injections associated with mass injection campaigns targeted at yaws, with introduction and spread of parenteral therapies to treat other diseases, and with plummeting prices for antibiotics and injection equipment. For example, UNICEF administered 12 million injections for yaws in Central Africa alone during 1952-57. From the 1950s into the 1980s, unsafe injections may have contributed to the silent spread of HIV in Africa in much the same way that unsafe injections for schistosomiasis and other treatments in Egypt established hepatitis C as a major blood-borne pathogen, infecting about 15% to 20% of the general population at the end of the 1990s."


"Our observations raise the serious possibility that an important portion of HIV transmission in Africa may occur through unsafe injections and other unsterile medical procedures."




The author wishes to thank Dr. Andrew Maniotis, College of Medicine, University of Illinois at Chicago for his work in developing these questions and his permission to use them on this website.

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