Anti-Retrovirals Can Cause AIDS

This article was written in June 2000
and posted during the Internet Discussion
of the South African Presidential AIDS Advisory Panel


1. All anti-retroviral drugs are highly toxic to humans.

The following scientific facts support the assertion that "all anti-retroviral drugs are highly toxic to humans":

1.1. After more than a decade of treating and trying to prevent AIDS with antiretroviral therapies, neither individual nor public health benefits have been achieved (1,2).

2.2. Zidovudine (AZT), the most popular of the AIDS medications, was originally developed for chemotherapy in cancer, but due to its toxicity it was never approved for human use (3). AZT is now licensed by the Food and Drug Administration – FDA – As an anti-HIV medication (1,4,5).

AZT is a potent cytotoxic DNA chain-terminator (1,6,7)

The toxicity of AZT, the drug now prescribed indefinitely to both healthy "HIV-positive" individuals and to AIDS patients, has been solidly documented (1,8-13).

AZT is highly toxic to human cells, including T4 lymphocytes, at the "antiretroviral" dosage recommended by the manufacturer (12).

The immunotoxicity of AZT, as well as its myelotoxicity, are very well recognized (14). Granulocytopenia is one of the most common effects seen in persons treated with AZT (15,16)

There are also very well documented investigations showing that AZT has carcinogenic properties with respect to fast growing human and animal immune and other cells (12). In humans, AZT magnifies the risk of lymphomas by 50 (17). AZT has also been confirmed to be carcinogenic in mice (18-20). Nevertheless, AZT is sold in the United States, where it is illegal to sell drugs that are carcinogenic (19,21).

AZT can also cause anemia, lymphocytopenia, hepatitis, pancreatitis, myositis, muscle atrophy, wasting disease, dementia, lactic acidosis, severe hepatomegalia with steatosis, vasculitis, and it prevents mitochondrial DNA synthesis (22-26).

The toxicity of AZT is so well documented that the pharmaceutical company that makes and commercializes it typically writes, "Retrovir (Zidovudine) may be associated with severe hematologic toxicity including granulocytopenia and severe anemia particularly in patients with advanced HIV disease" and they add that, "Myopathy and myositis with pathologic changes similar to that produced by HIV disease, have been associated with prolonged use of Retrovir" (5).

The use of AZT for pregnant women can induce abortion, congenital malformation such as cavities in the chest, abnormal indentations at the base of the spine, misplaced ears, triangular faces, heart defects, extra digits and albinism (27). This toxicity for embryos has also been documented in animals (28).

The American National Institute of Child Health and Human Development has warned about the toxicity of AZT for children (29). It is recognized that AZT impedes normal child growth and development (29).

AZT can also destroy non-growing cells, such as neurons and muscle cells (26), thus causing muscle atrophy (22,30-34), and dementia (11,25).

It is well known that many illegal acts were committed in pursuit of the 1987 FDA marketing approval of AZT (35).

1.3. The toxicity of AZT can be potentialized by other DNA chain terminators such as gancyclovir and acyclovir, drugs that are frequently prescribed together with AZT in the treatment and prevention of opportunistic viral infections (36,37).

1.4. Currently, the HIV-AIDS supporters are prescribing hydroxyurea, an inexpensive drug used for chemotherapy of leukemia (38). This too is an inhibitor of DNA synthesis.

1.5. The toxicity of the new protease inhibitors, prescribed as part of the so-called AIDS treatment "cocktails", is also well documented (39).

The "cocktails" contain a protease inhibitor in conjunction with two DNA chain-terminators (39).

Researchers have been documenting that persons on protease inhibitors are developing abnormal fat accumulations, termed "buffalo humps" and "crixbelly" (40-42).

The hepatotoxicity of protease inhibitors has also been documented (43). Dogs and rats treated with protease inhibitors develop hepatic cell necrosis 30 minutes after administration of the drug (44).

As time passes, more and more metabolic and endocrine disturbances are described in individuals placed on protease inhibitors. Recent studies report hypertrophy of the breasts; increase of blood sugar, cholesterol, and triglycerides; abnormal subcutaneous and visceral fat accumulation; peripheral fat wasting and lipomatosis; pancreatitis and angina (40,41,45-47). Hypertriglyceridemia is being described in 79% of the individuals taking protease inhibitors (48).

It has even been documented that protease inhibitors can induce the development of AIDS-defining diseases such as mycobacterial infections (49).

All these protease inhibitor "side effects" are having a chilling effect on "cocktail euphoria" (50).

Thus, scientific evidence shows that antiretroviral drugs are highly toxic to both humans and animals.

2. Anti-retroviral drugs can by themselves cause AIDS.

The following scientific facts support the assertion that the "antiretroviral drugs can by themselves cause AIDS":

2.1. Many healthy "HIV-positive" individuals along with AIDS patients, are being placed on lifetime prescriptions of nucleoside analogues that act as DNA chain-terminators, such as AZT, the analogue of the nucleoside thymidine (51,52).

Currently, protease inhibitors are being prescribed as anti-HIV medications for the lifetime of the individual (53,54).

All the drugs that are currently used as antiretroviral medications are drugs that act specifically on cells that are either metabolically active or in constant division (55). By definition, the immunocompetent cells, as well as the bone marrow cells, are cells that are dividing constantly. A very unique characteristic of the cells of the immune system is that they have to divide during the immune response (56). This makes the cells of the immune system much more vulnerable to the actions of these chemicals.

All the antiretroviral medications are known to be very toxic chemicals (1,52).

The toxic effects of AZT on people’s immune systems have been documented (57). AZT was given to 14 healthy health care professionals who were exposed to AIDS blood through needle sticks and similar accidents. Fully half of the 14 health professionals had to quit the drug because of severe toxic effects. Neutropenia developed in 36% of the 11 people who completed at least 4 weeks of AZT treatment. 5 of the 14 individuals could not even make it to four weeks due to "severe subjective symptoms". One professional had to be stopped prematurely because his neutropenia was so severe that he developed a respiratory infection. These toxic effects developed in only weeks, while persons with an HIV-positive diagnosis often take AZT for years (57).

2.2. There is a great deal of scientific evidence showing that the antiretroviral drugs can induce the development of AIDS-defining diseases. The possibility that AZT may actually contribute to the pathogenesis of AIDS is real (1,9,10,12,13,58).

The British-French Concorde trial found that AZT was unable to prevent AIDS, and instead increased mortality by 25%, compared to the untreated controls (59).

Another British study found that AZT prophylaxis decreased survival and induced wasting syndrome, cryptosporidiosis, and cytomegalovirus infection (60).

The American MAC study shows that AZT increases the risk of pneumonia, one of the AIDS defining diseases (61).

Studies often show that individuals given AZT have a worse prognosis (6,7), but the mainstream researchers prefer to blame HIV (62).

The lymphocyte counts decreased significantly in humans treated with AZT, but not in the non-treated controls (22,63). Interestingly, these are the experiments that the Food and Drug Administration Office evaluated before the licensing of AZT (1,6,7,9).

Another study similarly found that AZT users experienced more rapid CD4+ cell depletion (64).

Prophylactic AZT has also been shown to increase significantly the risk of AIDS in hemophiliacs when compared with the untreated controls (65).

Since AZT use has begun, the mortality of British "HIV-positive" hemophiliacs has increased 10-fold (66).

A similar finding has occurred with American hemophiliacs (67). However, most of the AIDS researchers insist on blaming HIV (66-68).

2.3. The immunological alterations secondary to antiretroviral therapy and described in section 1 can be reversed after individuals stop taking these medications. 10 out of 11 individuals recovered their cellular immunity after stopping AZT (69).

Even patients suffering from severe pancytopenia and bone marrow aplasia recover after discontinuing AZT (8).

Clinical manifestations of mycobacterial infection started 1-3 weeks after starting the protease inhibitor Indinavir. Symptoms disappeared after the patients stopped the medication (49).

Two babies born to mothers treated with AZT for 6 months and then treated themselves for an additional month and a half, developed Pneumocystis carinii pneumonia, one of the clinical manifestations of AIDS. Since the babies were "HIV-negative", AZT was suspended and they completely recovered, remaining healthy beyond the one-year period of observation (70,71).

2.4. Merck itself, the pharmaceutical company that produces and commercializes the protease inhibitor Crixivan warns, "It is not yet known whether taking Crixivan will extend your life or reduce your chances of getting other illnesses associated with HIV" (72).

2.5. In animals, there are several examples of immunotoxicity due to antiretroviral medications:

Rats and mice treated with AZT for 7 weeks developed anemia, neutropenia, lymphopenia, thrombocytopenia, bone marrow depletion and weight loss (73).

In a similar experiment, mice were also treated with AZT for 7 weeks and developed anemia, leukopenia, thrombocytopenia and myelodysplasia (74).

Hamsters treated with AZT for one or two weeks developed T-cell depletion and atrophy of the thymus (75).

Mice treated with the drug for 2 weeks developed anemia, nephrotoxicity, and lymphotoxicity (76).

AZT is also toxic to the liver (77).

The carcinogenic properties of AZT have been documented in animal experiments (75). AZT can stimulate leukemias (74).

2.6. In addition to the antiretroviral drugs, healthy people who are "HIV-positive" are taking many prescribed antibiotics, anti-mycobacterials, antifungals, antivirals, antidepresants, as well as many over-the counter medications (78,79). All are potentially immunotoxic stressor agents (80), and all help in generating AIDS (81).

The HIV-AIDS supporters will always have the excuse that HIV is mutating and developing resistance to the current medications. However, there is no scientific substantiation for the assertion that "HIV is mutating" (82).

2.7. AIDS patients are also taking a polypharmacy of immunotoxic medications (6,7) that, rather than improving, very often debilitate the patient’s immune and other systems, and therefore contribute to the eventual death of the individual. Medications such as metronydazol, pyrimethamine, daraprim, amphotericin B, clotrimaxole, dapsone, interferon, pentamidine, vincristine, fluocytosine, adriamycin, vinblastine, to mention some of the more frequently used, are potent immunotoxic, myelotoxic, lymphotoxic, nephrotoxic, hepatotoxic drugs (37,80).

2.8. It is unethical, to say the least, to treat or prevent AIDS with medications known to be highly toxic to the cells of the immune system, of the bone marrow, and to the cells of other tissues and systems. It is the equivalent of mainstream AIDS researchers attempting to stop fire with gasoline.

3. Pregnant women, infants, and children are much more vulnerable to the toxic effects of anti-retroviral drugs.

The following scientific facts support the assertion that "pregnant women and children are much more vulnerable to the toxic effects of antiretroviral drugs":

3.1. For decades, medical science has known that growing cells are much more vulnerable to the toxic effects of many different agents (83,84). This has been the very basis for the effort to avoid exposing, as much as possible, pregnant women and their fetuses to any potential toxic agent (85,86).

It is also important to keep in mind that the immune system of a child attains its own maturity only after the age of ten (56).

3.2. However, in the era of AIDS, mainstream AIDS researchers are changing all the rules. Currently, toxic medications are recommended and prescribed worldwide to pregnant women and children (87,88). As of 1993, even "HIV-free" babies are taking AZT; this is because "HIV-positive" pregnant women are prescribed AZT for the last two trimesters in the hope of preventing HIV transmission from mothers to babies (70).

Babies who test "HIV-negative" but who are born to HIV-positive mothers are nevertheless prescribed AZT for six weeks after birth (70,87,89).

3.3. Many "HIV-positive" healthy newborns, infants, and young children are placed on combinations of potentially immunotoxic medications such as antiretrovirals, antifungals, antivirals, and antibiotics. All are currently prescribed indefinitely as prophylactic drugs (90,91).

It is as if they have forgotten the vulnerability of newborns and young children to toxic substances (92).

3.4. The toxicity of antiretroviral drugs for embryos and fetuses has been documented in humans and animals, as well as In Vitro:

AZT is a potent cytotoxic DNA chain-terminator (1,6,7) and "it has been well known for many years that the compounds which can alter DNA metabolism often exhibit pronounced prenatal toxicity" (55).

The use of AZT for pregnant women can induce abortion, congenital malformation such as cavities in the chest, abnormal indentations at the base of the spine, misplaced ears, triangular faces, heart defects, extra digits and albinism (27). In some instances intrauterine growth retardation has been documented (93). The hemoglobin at birth in infants exposed to AZT was found to be significantly lower than in a placebo group (70,94,95).

The American National Institute of Child Health and Human Development is well aware of the toxicity of AZT (29). AZT has been shown to impede normal child growth and development (29).

The toxicity of AZT in animal embryos has been recognized. If used before the implantation of the embryos, the effects seem to be even worse (28).

When administered to pregnant mice, AZT reduced the number of fetuses by 60%, altered the livers of newborns, and caused a significant reduction of hematocrit in the pregnant animals (96). A similar experiment with pregnant mice also showed a significant reduction in the number of fetuses (97). These effects are worse if mice embryos are preimplanted (98).

There are also In Vitro data documenting the toxicity of AZT: it induces reduction in the number of thymocytes in cultured thymic lobes from rat fetuses (99). It inhibited the erytroid colony formation of liver cells from mouse fetuses (77). Also, exposure of two-cell mice embryos to zidovudine was consistently associated with significant inhibition of blastocyst formation (100).

3.5. A recent comprehensive review of this issue concluded: "Sufficient data regarding the safety of zidovudine in human pregnancy are not available" (55).

In spite of the scientific evidence about the toxicity of AZT for pregnant women, a review of the issue by the National Center for Toxicological Research of the Food and Drug Administration (FDA) states that: "Initial human studies suggest that maternal use of AZT during pregnancy is very well tolerated by both mother and child and provides a promising degree of protection from vertical HIV transmission to the infant." And that: "Although in vitro and in vivo laboratory animal studies suggest the potential for toxicity with preimplantation exposure, the risk for teratogenic events after postimplantational exposures appears to be low at therapeutically effective concentrations of these dideoxynucleosides" (101).

It is unethical, to say the least, to insist on prescribing AZT and other antiretrovirals to prevent AIDS in healthy "HIV-positive" pregnant women, in infants, in children, or in anybody. The potential cytotoxic, mutagenic, theratogenic, immunotoxic, and carcinogenic properties of these chemicals have been scientifically documented (6,7,88,102-104).

Before the AIDS epidemic, antimicrobials were only prescribed prophylactically for the prevention of a relapse of rheumatic fever. There were no other exceptions. Additionally, antimicrobials, especially antibiotics, were only prescribed for short periods of time, such as a few days for the treatment of an infectious disease. Why are the rules being changed now? Where is the scientific justification that researchers have for changing the rules now?

4. Conclusions.

4.1. Scientific data presented here demonstrate that it is not rational to treat or prevent AIDS with toxic antiretroviral drugs in any patient. It is contrary to common sense to treat or prevent a highly toxicological syndrome with even more toxicity.

4.2. The use of antiretroviral medications to treat or prevent AIDS in pregnant women, infants, children, and anyone else should therefore be stopped immediately.


  1. DUESBERG PH. AIDS Acquired by Drug Consumption and other Non Contagious Risk Factors. Pharmac Ther 1992; 55:201-277.
  2. HAND T. Why Antiviral Drugs Cannot Resolve AIDS. Reappraising AIDS 1996; 4(9):1-4.
  3. HORWITZ JP, CHUA J & NOEL M. Nucleosides. V. The Monomesylates of 1-(2’-Deoxy-Beta-D-Lyxofuranosyl) Thymidine. J Org Chem 1964; 29:2076.
  4. KOLATA G. Imminent Marketing of AZT Raises Problems; Marrow Suppression Hampers AZT Victims. Science 1987; 235: 1462-1463.
  5. GLAXO WELLCOME. Retrovir (Zidovudine). In: Physician’s Desck Reference. Montvale, NJ: Medical Economic Co., 1998: 1167-1175.
  6. DUESBERG PH & RASNICK D. The Drug-AIDS Hypothesis. Continuum (London) 1997; 4(5): S1-S24.
  7. DUESBERG PH & RASNICK D. The AIDS Dilema. Drug Diseases Blamed on a Passenger Virus. Genetica 1998; 104: 85-132.
  8. GILL PS, RARICK M, BYRNES RK, et al. Azidothymidine Associated with Bone Marrow Failure in the Acquired Immunodeficiency Syndrome (AIDS). Ann Intern Med 1987; 107:502-505.
  9. LAURITSEN J. Poison by Prescription: The AZT Story. New York: Asklepios, 1990.
  10. LAURITSEN J. AZT: Iatrogenic Genocide. In: The AIDS War: Propaganda, Profiteering and Genocide from the Medical-Industrial Complex. New York: Asklepios, 1993: 71-86.
  11. SMOTHERS K. Acquired Immunodeficiency Syndrome: Pharmacology and Toxicology. In: GOLDFRANK LR, FLOMENBAUM NE, LEWIN NA, et al. Goldfrank’s Toxicologic Emergencies. Fith Edition. Norwalk, Connecticut: Appleton & Lange, 1994: 455-472.
  12. CHIU DT and DUESBERG PH. Toxicity of Azidothymidine (AZT) on Human and Animal Cells in Culture at Concentrations Used for Antiviral Therapy. Genetica 1995; 95:103-109.
  13. ZARETSKY MD. AZT Toxicity and AIDS Prophylaxis: Is AZT Benefitial for HIV + Asymptomatic Persons with 500 or More T4 Cell per Cubic Milimeter ? Genetica 1995; 95:91-101.
  14. ROSENTHAL GJ and KOWOLENKO M. Immunotoxicologic Manifestations of AIDS Therapeutics. In DEAN JH, LUSTER MI, MUNSON AE and KIMBER I. Immunotoxicology and Immunopharmacology. Second Edition. New York: Raven Press, 1994: 249-265.
  15. YARCHOAN R, MITSUYA H, MYERS CE, et al. Clinical Pharmacology of 3’-azido-1’, 3’-dideoxythymidine (Zidovudine) and Related Dideoxynucleosides. NEJM 1989; 321:726-739.
  16. KHOO SH & WILKINS EGL. Review: Controversies in Anti-Retroviral Therapy of Adults. J Antimicrob Chemother 1995; 35:245-262.
  17. PLUDA JM, YARCHOAN R, JAFFE ES, et al. Development of Non-Hodgkin Lymphoma in a Cohort of Patients with Severe Human Immunodeficiency Virus (HIV) Infection on Long-Term Antiretroviral Therapy. Ann Intern Med 1990; 113:276-282.
  18. COHEN SS. Antiretroviral Therapy for AIDS. NEJM 1987; 317:629.
  19. YARCHOAN R & BRODER S. Antiretroviral Therapy for AIDS. NEJM 1987; 317:630.
  20. COHEN J. The Media’s Love Affair with AIDS Research: Hope vs. Hype. Science 1997; 275:298-299.
  21. DUESBERG PH. Infectious AIDS; Have We Been Misled? Berkeley, CA: North Athantic Books, 1996: 582.
  22. RICHMAN DD, FISCHL MA, GRIECO MH, et al., and The AZT Collaborative Working Group. The Toxicity of Azidothymidine (AZT) in the Treatment of Patients with AIDS and AIDS-Related-Complex. NEJM 1987; 317:192-197.
  23. MCLEOD GX & HAMMER SM. Zidovudine: Five Years Later. Ann Intern Med 1992; 117:487-501.
  24. FREIMEN JP, HELFERT KE, HAMRELL MR, et al. Hepatomegaly with Severe Steatosis in HIV-Seropositive Patients. AIDS 1993; 7: 379-385.
  25. BACELLAR H, MUNOZ A, MILLER EN, et al. Temporal Trends in the Incidence of HIV-1-related Neurologic Diseases: Multicenter AIDS Cohort Study, 1985-1992. Neurology 1994; 44: 1892-1900.
  26. PARKER WB & CHENG YC. Mitochondrial Toxicity of antiviral Nucleoside Analogs. The J of NIH Research 1994; 6:57-61.
  27. KUMAR RM, HUGHES PF & KHURRANNA A. Zidovudine Use in Pregnancy: A Report of 104 Cases and the Occurrence of Birth Defects. J Acquire Immunodeficiency Syndromes 1994; 7:1034-1039.
  28. BOX JL, FEARON ER, HAMILTON SR, et al.Prevalance of Ras Gene Mutations in Human Colorectal Cancers. Nature (London) 1987; 327: 293-297.
  29. MOYE J, RICH KC, KALISH LA, et al. Natural History of Somatic Growth in Infants Born to Women Infected by Human Immunodeficiency Virus. J Pediatrics 1996; 128:58-67.
  30. BESSEN LJ, GREENE JB, LOUIE E, et al. Severe Polymyositis-like Syndrome Associated with Zidovudine Therapy of AIDS and ARC. NEJM 1988; 318: 708.
  31. GORARD DA & GUILODD RJ. Necrotizing Myopathy and Zidovudine. Lancet 1988; i:1050.
  32. HELBERT M, FLETCHER T, PEDDLE B, et al. Zidovudine-Associated Myopathy. Lancet 1988; ii:689-690.
  33. DALAKAS MC, ILLA I, PEZESHKPOUR GH, et al. Mitochondrial Myopathy Caused by Long-Term Zidovudine Therapy. NEJM 1990; 322:1098-1105.
  34. TILL M & MACDONNELL KB. Myopathy with Human Immunodeficiency Virus Type 1 (HIV-1) Infection: HIV-1 or Zidovudine? Ann Intern Med 1990; 113:492-494.
  35. LAURITSEN J. FDA Documents Show Fraud in AZT Trials. New York Native, March 30, 1992.
  36. JACOBSON MA, DE MIRANDA P, GORDON SM, et al. Prolongued Pancytopenia Due to Combined Ganciclovir and Zidovudine Therapy. J Inf Dis 1988; 158:489-490.
  37. FOGELMAN I, LIM L, BASSETT R, et al. Prevalence and Patterns of Use of Concomitant Medications Among Participants in Three Multicenter Human Immunodeficiency Virus Type 1 Clinical Trials. J of Acquired Immunodeficienmcy Syndr 1994; 7:1057-1063.
  38. MAUGH II TH. Researchers on Path to First Inexpensive AIDS Medication. San Francisco Chronicle, February 6, 1998: A6.
  39. STOLBERG SG. Despite New AIDS Drugs, Many Still Lose the Battle. The New York Times, August 22 1997: A1, A6.
  40. LIPSKY JJ. Abnormal Fat Accumulation in Patients with HIV-1 Infection. Lancet 1998; 351:847-848.
  41. MILLER KD, JAMES E, YANOVSKI J, et al. Visceral Abdominal-Fat Accumulation Associated with Use of Indinavir. Lancet 1998; 351:871-875.
  42. LO JC, MULLIGAN K, TAI VW, et al. "Buffalo Hump" in Men with HIV-1 Infection. Lancet 1998; 351:867-870.
  43. BRAEU N, LEAF HL, WIECZORCK RL, et al. Severe Hepatitis in Three AIDS Patients Treated with Indinavir. Lancet 1997; 349: 924-925.
  44. GROSSMAN SJ, REINFOED N, EYDELLOTH RS, et al. Hepatotoxicity of an HIV Protease Inhibitor in Dogs & Rats. Toxicol. Appl. Pharmacol. 1997;146: 40-52.
  45. HENGEL RC, WARTTS NB & LENNOX JL. Benign Symmetric Lipomatosis Associatted with Protease Inhibitors. Lancet 1997; 350:1596.
  46. HERRY I, BERNARD L, DE TRUCHIS P, et al. Hypertrophy of the Breasts in a Patient Treated With Indinavir. Clin Inf Dis 1997; 25:937-938.
  47. JAMES JS. Protease Inhibitors Metabolic Side Effects: Cholesterol, Triglycerides, Blood Sugar, and "Crixbelly". In: AIDS Treatment News 1997, Issue No. 273, August 15, 1997.
  48. DI PERVI G, DEL BRAVO P & CONCIA E. HIV - Protease Inhibitors. NEJM 1998; 339:773-774.
  49. RACE EM, ADELSON-MITTY J, KRIEGEL GR, et al. Focal Mycobacterial Lymphadenitis Following Initiation of Protease-inhibitor Therapy in Patients with Advanced HIV-1Disease. Lancet 1998; 351:252-255.
  50. ISMACH J. AIDS’98 Protease Impediments: Lipodystrophy and Drug Resistance Take the Edge Off Cocktail Euphoria. News From the Geneva 12th World AIDS Conference. Physician Weekly 1998; 15(33):1.
  51. CONNOLLY L and JENKINS M. Strategies for Antiviral Therapy Based on the Retroviral Life Cycle. In: COHEN PT, SANDE MA and VOLBERDING PA. The AIDS Knowledge BASE. Boston: Little Brown and Company, 1994: 3.5.
  52. FADEN RR, KASS NE, ACUFF KL, et al. HIV Infection and Childbearing: A Proposal for Public Policy and Clinical Practice. In: FADEN RR and KASS NE. HIV, AIDS and Childbearing. Public Policy, Private Lives. New York: Oxford University Press, 1996: 447-462.
  53. HITTI J and WATTS DH. Antiviral Therapy During Pregnancy. In: COTTON D and WATTS DH. The Medical Management of AIDS in Women. New York: John Wiley & Sons, 1997: 213-220.
  54. LEVY JA. Antiviral Therapies. In: HIV and the Pathogenesis of AIDS. Second Edition. Washington DC: ASM Press, 1998b: 339-364.
  55. STAHLMANN R & KLUG S. Antiviral Agents: Nucleoside and Non-Nucleoside Analogues. In KAVLOCK RJ & DASTON GP. Drug Toxicity in Embryonic Development. Advances in Understanding Mechanisms of Birth Defects: Mechanisting Understanding of Human Developmental Toxicants. Berlin: Springer, 1997: 231-264.
  56. MALE D, COOK A, WOEN M, et al. The Immune System. In: Advanced Immunology. London: Mosby, 1996: 1.1.
  57. SCHMITZ SH, SCHEDING S, VOLIOTIS D, et al. Side Effects of AZT Prophylaxis After Occupational Exposure to HIV-Infected Blood. Ann Hematol 1994; 69:135-138.
  58. GIRALDO RA, et al. Is It Rational To Treat or Prevent AIDS With Toxic Antiretroviral Drugs in Pregnant Women, Infants, Childre, and Anybody Else? The Answer is Negative. Continuum (London) 1999; 5(6): 38-52.
  59. SELIGMAN M, WARRELL DA, ABOULKER JP, et al. Concorde: MRC/ANRS Randomized Double-Blind Controlled Trial of Immediate and Deferred Zidovudine in Symptom-free HIV Infection. Lancet 1994; 343:872-881.
  60. POZNANSKY MC, COKER R, SKINNER C, et al. HIV Positive Patients First Presenting with an AIDS-Defining Illness: Characteristics and Survival. Br. Med J 1995; 311:156-158.
  61. SAAH AJ, HOOVER DR, PENG Y, et al., and the Multicenter AIDS Cohort Study. Predictors For Failure of Pneumocystis carinii Pneumonia Prophylaxis. JAMA 1995; 273:1197-1202.
  62. SABIN CA, PHILLIPS AN & LEE CA. Response: Arguments Contradict the "Foreign Protein-Zidovudine" Hypothesis. Br Med J 1996; 312:211-212.
  63. FISCHL MA, RICHMAN DD, GRIECO MH, et al. The Efficacy of Azidothymidine (AZT) in The Treatment of Patients with AIDS & AIDS-Related Complex. NEJM 1987; 317: 185-191.
  64. ALCABES P, SCHOENBAUM EE & KLEIN RS. Correlates of the Rate of Decline of CD4+ Lymphocytes Among Infection Drug Users Infected with the Human Immunodeficiency Virus. Amm J Epidemiol 1993; 137:989-1000.
  65. GOEDERT JJ, COHEN AR, KESSLER CM, et al. Risks of Immunodeficiency, AIDS, & Death Related to Purity of Factor VIII Concentrate. Lancet 1994; 344: 791-792.
  66. DARBY SC, EWART DW, GIANGRANDE LF, et al. Mortality Before & After HIV Infection in Complete UK Population of Haemophiliacs (letter). Nature (London) 1995; 377:79-82.
  67. CHORBA TL, HOLMAN RC, STRINE TW, et al. Changes in Longevity & Causes of Death Among Persons with Hemophilia A. Am. J. Hematol 1994; 45: 112-121.
  68. MADDOX J. More Conviction on HIV and AIDS. Nature 1995; 377:1.
  69. SCOLARO M, DURHAM R & PIECZENIK G. Potential Molecular Competitor for HIV. Lancet 1991; 337:731-732.
  70. CONNOR EM, SPERLING RS, GELBER R, et al. Reduction of Maternal-Infant Transmission of Human Immunodeficiency Virus Type 1 With Zidovudine Tretment. NEJM 1994; 331: 1173-1180.
  71. HERESI GP, CACERES E, ATKINSJT, et al. Pneumocystis carinii Pneumonia in Infants Who Were Exposed to Human Immunodeficiency Virus But Were not Infected: An Exception to the AIDS Sirveillance Case Definition. Clin Infect Dis 1997; 25:739-740.
  72. MERCK and Company. Crixivan (Indinavir Sulfate): Patient Information About Crixivan. SPIN June, 1997: 111-114.
  73. MATSUOKA A, OZAKI M, TAKESHITA K, et al. Aneuploid Induction by Benzo[a]Pyrene and Polyploid Induction by 7,12-Dimetylbenz[a]Antracene in Chinese Hamster Cells V79-MZ and V79. Mutagenesis 1997; 12:365-372.
  74. LEWIS R. Genetic Imprecision. BioScience 1991; 41:288-293.
  75. BENEDICT WF. Early Changes in Number and Structure After Treatment of Fetal Hamster Cultures with Transforming Doses of Polycyclic Hydrocarbons. J Natl Cancer Inst 1972; 49: 585-590.
  76. SANDLER L & HECHT F. Genetics Effects of Aneuploidy. Amer J Hum Genet 1973; 25:332-339.
  77. GOGU SR, BECKMAN BS & AGRAWAL KC. Anti HIV-Drugs: Comparative Toxicities in Murine Fetal Liver and Bone Marrow Erythroid Progenitor Cells. Life Sci 1989; 45: iii-vii.
  78. GREENBLAT RM, HOLLANDER H, Mc MASTER JR, et al. Polypharmacy Among Patients Attending an AIDS Clinic: Utilization of Prescribed, unorthodox, & Investigational Treatments. Journal of Acquried Immune Deficiency Syndromes 1991; 4: 136-143.
  79. HAYES T, ALTMAN R, AKILI-OBIKA A, et al. HIV-Releted Deaths from Selected Infectious Disease Among Persons Without AIDS in New Jersey. Journal of Acquired Immune Deficiency Syndromes 1994; 7: 1074-1078.
  80. GIRALDO RA. AIDS and Stressors II: A Proposal for the Pathogenesis of AIDS. In: AIDS and Stressors. Medellín: Impresos Begón, 1997: 57-96.
  81. GIRALDO RA. AIDS and Stressors III: A Proposal for the Natural History of AIDS. In: AIDS and Stressors. Medellín: Impresos Begón, 1997: 97-131.
  82. MARTINEZ M. The Existence of Human Immunodeficiency Virus Resistance to Nucleoside-Analog Drugs Has not Been Shown. Med Hypothesis 1997; 49:235-240.
  83. ROGERS J & KAVLOCK R. Developmental Toxicology. In: KLAASSEN CD, AMDUR MO & DOULL J. Casarett and Doull’s Toxicology. The Basic Science of Poisons. Fith Edition. New York: McGraw-Hill, 1996: 301-332.
  84. DESESSO JM & HARRIS SB. Principles Underlying Developmental Toxicology. In: FAN AM & CHANG LW. Toxicology and Risk Assessment. Principles, Methods, and Applications. New York: Marcel Dekker, 1996: 37-56.
  85. MILLER RK, KELLOG CK & SALTZMAN RA. Reproductive and Perinatal Toxicology. In: HALEY TJ & BERNDT WO. Hadbook of Toxicology. Cambridge: Hemisphere Publishing Corporation, 1987: 195-309.
  86. NEEDLEMAN HL & BELLINGER D. Prenatal Exposure to Toxicants: Developmental Consequences. Baltimore: Johns Hopkins University Press, 1994: 321.
  87. LANCET. Zidovudine for Mother, Fetus, and Child: Hope or Poison? Lancet 1994; 344:207-209.
  88. PHILPOTT P. AZT for Pregnant HIV+ Women and Their Newborns. Reappraising AIDS 1997b; 5(2):1-2.
  89. COTTON P. Trial Halted After Drug Cuts Maternal HIV Transmission Rate By Two Thirds JAMA 1994; 271: 807.
  90. GRUBMAN S, GROSS E, LERNER-WEISS N, et al. Older Childern & Adolescents with Perinatally Acquried Human Immunodeficiency Virus Infection. Pediatrics 1995; 95: 657-663.
  91. LUZURIAGA K, BRYSON Y, KROGSTAND P. et al. Combination Treatment with Zidovidine, Diadenosine, and Nevirapine in Infants with Human Immunodeficiency Virus Type 1 Infection. NEJM 1997; 336:1343-1349.
  92. KACEW S & REASOR MJ. Toxicology and the Newborn. Amsterdam: Elsevier, 1984: 291.
  93. SPERLING RS, STRATTON P, O’SULLIVAN MJ, et al. A Survey of Zidovudine Use in Pregnant Women With Human Immunodeficiency Virus Infection. NEJM 1992; 326:857-861.
  94. ROGERS M & JAFFE HW. Reducing the Risk of Maternal-Infant Transmission of HIV: A Door is Opened. NEJM 1994; 331:1222-1223.
  95. BAYER R. Ethical Challenges Posed by Zidovudine Treatment to Reduce Vertical Transmission of HIV. NEJM 1994; 331: 1223-1225.
  96. GOGU SR, BECKMAN BS & AGRAWAL KC. Amelioration of Zidovudine-Induced Fetal Toxicity in Pregnant Mice. Antimicrob Agents Chemother 1992; 36:2370-2374.
  97. TOLTZIS P, MARX CM, KLEINMAN N, et al. Ziduvudine-Associated Embryonic Toxicity in Mice. J Infect Dis 1991; 163:1212-1218.
  98. TOLTZIS P, MOURTON T & MAGNUSON T. Effect of Zidovudine on Preimplantation Murine Embryos. Antimicrob Agents Chemother 1993; 37:1610-1613.
  99. FOERSTER M, MERKER H-J, STAHLMANN R, et al. In vitro Effect of Acyclovir on Lymphopoiesis in Fetal Rat Thymus. Toxicol In Vitro 1992; 6:207-217.
  100. TOLTZIS P. MOURTON T & MAGNUSON T. Comparative Embryonic Cytotoxicity of Antiretroviral Nucleosides. J Infect Dis 1994; 169:1100-1102.
  101. SANDBERG JA & SLIKKER JR W. Developmental Pharmacology and Toxicology of Anti-HIV Therapeutic Agents: Dideoxynucleosides. FASEB J 1995; 9:1157-1163.
  102. FARBER C. AZT on Trial. The Treatment for AIDS Accused of Being Deadlier than the Disease itself. Spin July 1996.
  103. FARBER C. AZT Roulette: The Impossible Choices Facing HIV-Positive Women. Mothering 1998b Sept/Oct No. 90: 53-65.
  104. DUESBERG PH. HIV, AIDS & Zidovudine. Lancet 1992b; 339: 805-806.
Roberto A. Giraldo