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Is HIV the Precurssor to AIDS?

HIV (AIDS) viruses in blood with red blood cells and white blood cells. 3D illustration

I have written several articles on the coronavirus and on masks and healthcare issues. A series of links have been provided at the bottom of this article for your convenience. This article will, however address a different aspect of the virus or on healthcare issues in general.

I want to start this discussion about my understanding of HIV annd AIDS. I have read about the subject from the very onset oset of AIDS in the early 80s. The first article I read on the subject was on the defunct magazine Science Digest. It was a great magazine that only lasted a few years. I am not sure why they stopped publishing it, unless it was just too costly to produce. I knew from the beginnning that AIDS was going to be something very difficult to eliminate. Initially the spread was blammed on sodomy. The first article I read even blammed pigs that were engaged in sodomy. That was quickly refuted. They just never seemed to find out where it came from. Just because it was casued by HIV, doesn’t mean we know where it originated from. It is postulated that in Africa, HIV the virus that causes AIDS jumped from chimpanzees to humans sometime early in the 20th century. To date, the earliest known case of HIV-1 infection in human blood is from a sample taken in 1959 from a man who’d died in Kinshasa in what was then the Belgian Congo. When I went to school for my nursing degree, HIV was determined to by the cause of AIDS. The way I understood it at the time, that when the individual with HIV came down with pneumocystis carinii pneumoniae (PCP), (caused by the fungus Pneumocystis jiroveci) they were now diagnosed with AIDS. Eventually the diagnosis was broadened to include Kaposi’s sarcoma, Hodgkin’s disease, Burkitt’s lymphoma, isosporiasis and Salmonella septicemia. It was almost like the stages of cancer, where stages three and four are the stages where symptoms are debilitating. In the case of HIV, the immune system becomes increasingly compromised, so that the individual eventually succumbs to opportunistic infections. AIDS was more of a classification than a distinct disease process. I may be wrong but this is the statement that I want to make. Not all people with HIV have AIDS, but all people with AIDS have HIV. This is the premise that we we will start this investigation under. So the onus of this discussion is to dispprove this assumption.

HIV Does Not Cause AIDS in the Way We Thought

Research Reveals Why Vaccines Fail to Prevent Infection

For decades, it was believed that HIV progressed to AIDS in a pretty straightforward manner: spreading through the body as a free-circulating virus, attaching itself to immune cells (predominately CD4+ T-cells) and hijacking their genetic machinery in order to create multiple copies of itself. By doing so, HIV is able to disseminate throughout the entire system, expanding in numbers until enough T-cells are killed to fully compromise a person’s immune defenses (the clinical definition of AIDS).

Emerging research suggests that this is probably not the case, or at least not the disease pathway we had long presumed. In fact, since as far back as the late-1990s, scientists had begun to observe that HIV can also spread directly from cell to cell without creating any free-circulating virus.

This secondary mode of transmission, according to research from the San Francisco-based Gladstone Institute of Virology and Immunologyis between 100 and 1,000 times more efficient in depleting CD4 cells than a free-circulating virus and may help explain, in part, why current vaccine models are unable to adequately prevent or neutralize HIV.

By transmitting itself from cell to cell, HIV can cause a cellular chain reaction in which the immune cells literally commit suicide in mass volumes. Research suggests that as much as 95% of CD4 cell death is caused in this manner, as opposed to only 5% with the free virus.

Explaining Cell-to-Cell Transmission

Cell-to-cell transfer of HIV occurs through so-called “virological synapses,” in which the infected cell adheres to a “resting” host cell and employs viral proteins to breach the cellular membrane.

Once invaded, the host reacts to the fragments of deposited viral DNA, triggering a process called pyroptosis wherein the cell recognizes the danger signals and gradually swells and explodes, killing itself. When this occurs, the burst cell releases inflammatory proteins called cytokines which signal other immune cells to the attack—cells that are then actively targeted for HIV infection.

The Gladstone researchers were able to show that by preventing cell-to-cell contact—through chemical inhibitors, synaptic blockers, or even physically separating the cells—CD4 cell death was effectively stopped. They concluded that cell-to-cell contact was “absolutely required” in order for cell death (and disease progression) to take place.

Implications of the Research

What makes these findings particularly important is that they not only explain the mechanisms for CD4 cell depletion, they also spotlight inherent weaknesses in current vaccine design.

By and large, HIV vaccine models have focused on priming the immune system to recognize and attack surface proteins on free-circulating virus. When HIV is transmitted from cell to cell, however, it is essentially impervious to attack, shielded from detection from within the very construct of the infected cell.

In order to overcome this, newer models will need to help the immune system better target proteins vital to the synaptic formation and/or to create antiviral agents that can inhibit the synaptic process. If this can be achieved, the ability of HIV to progress to AIDS could be profoundly limited or even stopped.

While the mechanisms for cell-to-cell transmission are not yet fully understood, the findings represent a profound change in our understanding of how HIV progresses to AIDS and provides us a glimpse into the possible strategies for HIV eradication

The AIDS establishments have spent the last twenty years focusing on
the HIV and not on the real causes of AIDS. The correct approach for
investigating the cause(s) of a disease is by evaluating all medical
evidence that considers infectious, chemical, nutritional, and metabolic
factors. As a pathologist and a toxicologist, I evaluated the published
literature on the worldwide AIDS epidemic and found that HIV does not
cause AIDS. In my book “Get All the Facts: HIV Does Not Cause AIDS”, I
described the multifactorial causes of AIDS in the world and explained the
pathogenesis of AIDS in different risk groups [Mohammed Ali Al-Bayati,
‘Get All The Facts: HIV does not cause AIDS’ Toxi-Health International,
Dixon CA 1999, 183 pages ISBN 0-9673536-0-2]. My findings include:

1) The
HIV-hypothesis is not supported. HIV is a harmless virus in both the in
vivo and the in vitro settings.

2) AIDS in drug users and homosexuals in
the U.S. and Europe is actually caused by the heavy ancillary use of
glucocorticoids and other immunosuppressive agents to medically treat the
wide range of chronic serious illnesses of the respiratory system,
gastrointestinal system, and other organs, malnutrition, release of
endogenous cortisol, and opportunistic infections in these persons. The
appearance of “AIDS” in the U.S. and Europe has coincided with the
approval of glucocorticoid aerosoll use in 1976, the introduction of crack
cocaine, the use of heroin by inhalation, and the use of alkyl nitrites by
homosexuals to enhance sexual activities.

3) AIDS in hemophiliacs is
related to the use of corticosteroids and other immunosuppressive agents
to prevent the development of antibodies for factors VIII and IX and to
treat other chronic illnesses such as joint disease.

4) AIDS in people
receiving blood and/or tissue is related to the use of glucocorticoids to
prevent reactions of transfusion and tissue rejection, and to treat other

5) AIDS in infants and children is caused by their exposure to
drugs and corticosteroids in utero and their exposure to corticosteroids
used after birth to treat their chronic illnesses.

6) AIDS in Africa is
caused by malnutrition, release of endogenous cortisol, and opportunistic
diseases. Atrophy in the lymphoid tissue in people suffering from
malnutrition has been known since 1925. Malnutrition causes severe atrophy
in the thymus and lymphoid organs and impairs the function of the T cells.
These changes are reversible by feeding. The size of the thymus in
malnourished children increased from 20% of normal to 107% of normal,
following nine weeks of feeding.

7) Kaposi’s sarcoma (KS) and lymphoma are
induced by the use of steroids and drugs, and the release of endogenous
cortisol. They are not caused by a slow virus. KS is reversible upon the
termination of treatment with immunosuppressive agents prior to

8) The medications currently used to treat patients with AIDS,
such as AZT, protease inhibitors, and glucocorticoids, are highly toxic.
They can even cause AIDS in asymptomatic patients, and make the disease
worse in patients with AIDS. These drugs do not have any therapeutic
value, and their use must be discontinued immediately.

9) Damage to the
immune system is rapidly reversible after removal of the true insulting
agent or treatment of the true causes. For example. a) The CD4+ T cells of
1075 HIV+ pregnant women increased from 426/uL to 596/uL in six months by
giving these women a balanced diet. This also improved the outcome of
their pregnancy; and b) The reduction in CD4+ T cells in HIV+ homosexuals
was also reversed by the cessation of treatment with glucocorticoids.

What Is the Main Cause of HIV?

HIV (human immunodeficiency virus) is a virus that attacks the body’s immune system, which is responsible for fighting infections. If HIV infection is not treated, the body does not fight infections or cancer as well as healthy people and people who have HIV can become sick easily. 

Acquired immune deficiency syndrome (AIDS) is the late stage of HIV infection. HIV medicines are available that can stop the progression of the disease so most people infected with HIV in the U.S. do not develop AIDS.

How Do You Get HIV?

HIV infection is caused by exposure to the human immunodeficiency virus. The virus is transmitted via blood or through sexual intercourse and exposure to bodily fluids (such as semen or vaginal fluids) from a person with HIV. HIV infection is NOT spread by casual contact.

Main Causes of HIV

HIV infection can occur through:

Sexual contact – HIV is spread most commonly by sexual contact with an infected partner. The virus enters the body through the lining of the vagina, vulva, penis, rectum, or mouth during sexual activity.

Blood contamination – HIV may also be spread through contact with infected blood. However, due to the screening of blood for evidence of HIV infection, the risk of acquiring HIV from blood transfusions is extremely low.

Needles – HIV is frequently spread by sharing needles, syringes, or drug use equipment with someone who is infected with the virus. Transmission from patient to healthcare worker, or vice-versa through accidental sticks with contaminated needles or other medical instruments, is rare.

Mother-infant – HIV also can be spread to babies born to, or breastfed by, mothers infected with the virus.

HIV/AIDS cannot be spread through:

Risk factors for getting infected with HIV include:

What Are Symptoms of HIV?

Early Signs of HIV

Early symptoms of HIV (human immunodeficiency virus), referred to as primary or acute HIV infection, usually occur two to four weeks after infection with the virus and include: 

Early symptoms last about two weeks, are usually mild, and people often don’t even realize they have HIV yet. 

Late-Stage Symptoms of HIV

After several years, if HIV is not treated, other symptoms may develop, including:

How Is HIV Diagnosed?

What Is the Treatment for HIV?

HIV (human immunodeficiency virus) is treated with different combinations of antiretroviral medicines to control the infection.

Early HIV infection is usually treated with one of the following antiretroviral therapy (ART) regimens: 

What Is Acquired Immune Deficiency Syndrome (AIDS)?

Human immunodeficiency virus (HIV) is a virus that attacks the body’s immune system, which is responsible for fighting infections. Acquired immune deficiency syndrome (AIDS) is the late stage of HIV infection. 

In the U.S., most people infected with HIV do not go on to develop AIDS because HIV medications are available to stop disease progression.

What Are Symptoms of Acquired Immune Deficiency Syndrome (AIDS)?

Early symptoms of human immunodeficiency virus (HIV) are referred to as primary or acute HIV infection. These symptoms usually occur two to four weeks after a person is infected with the virus and include: 

Painful open sores or ulcers that can develop in the mouth, the esophagus, the anus, or the penis (only occurs in a small proportion of those exposed to the virus)

After several years, if HIV is not treated, symptoms of AIDS may occur and include:

What Causes Acquired Immune Deficiency Syndrome (AIDS)?

Human immunodeficiency virus (HIV) infection is caused by exposure to the human immunodeficiency virus. The virus is transmitted via blood or through sexual intercourse and exposure to other bodily fluids (such as semen or vaginal fluids) from a person with HIV. It is NOT spread by casual contact.

Untreated HIV infection can progress to become acquired immune deficiency syndrome (AIDS).

HIV infection can occur if a person:

People who may have an increased risk of contracting human immunodeficiency virus (HIV) include:

How Is Acquired Immune Deficiency Syndrome (AIDS) Diagnosed?

Human immunodeficiency virus (HIV) is diagnosed with either a blood test or a saliva (spit) test. 

Rapid HIV test results are available in minutes, though some test results can take days.

Patients are diagnosed with acquired immune deficiency syndrome (AIDS) when their CD4 cell count drops below 200 cells/mm, or if they develop certain opportunistic infections.

What Is the Treatment for Acquired Immune Deficiency Syndrome (AIDS)?

Human immunodeficiency virus (HIV) is usually treated with different combinations of antiretroviral medicines to help control HIV infection.

Early HIV infection is often treated with one of the following antiretroviral therapy (ART) regimens: 

There is no cure for acquired immune deficiency syndrome (AIDS) but medications are used to reduce the amount of HIV virus in the body, keep the immune system healthy, and decrease the complications of the disease that can occur.

Types of medication used to treat AIDS include: 

The Discovery of HIV as the Cause of AIDS

Progress in scientific research rarely follows a straight path. Generally, it entails many unexpected meanderings, with a mix of good and bad ideas, good and bad luck. The discovery of the human immunodeficiency virus (HIV) as the cause of AIDS did not avoid this pattern.

The story began in an unfavorable environment: during the late 1970s, many people thought that epidemic diseases caused by microbes, including viruses, no longer posed a threat in industrialized countries. Other prevailing beliefs were that viruses did not cause any human cancers and that there was no such thing as a retrovirus that infected humans. Some of these beliefs were justified, since attempts to find tumor viruses and, in particular, retroviruses in cancers or other diseases in humans had a troubled history, and many of the groups that had the greatest expertise in the study of retroviruses had turned their efforts toward research on oncogenes. Luckily and rather amazingly, however, the conceptual and technical tools arrived in our hands just before the first patients with AIDS were identified in 1981. In addition, there remained a few heretical or “old-fashioned” groups — among which were our two laboratories — that persisted in searching for retroviruses in human cancers, particularly breast cancers and leukemias. This search finally paid off with the discovery of human T-cell leukemia virus types 1 and 2 (HTLV-1 and HTLV-2), the first of which was shown to cause an unusual T-cell leukemia. This discovery was made possible by 15 years of basic research on leukemogenic retroviruses in animals, including the design and development of highly sensitive biochemical assays that were based on reverse transcriptase — the enzyme that is present in all retroviruses, which was discovered in 1970 by Temin and Baltimore.

An additional important contributor was the development of methods for growing T lymphocytes in culture for a period sufficient to allow the expression of putative latent retroviruses. This effort was helped greatly by the isolation of specific factors — in particular, the T-cell growth factor (now called interleukin-2) in Bethesda, Maryland. The role of interferon in repressing the production of retroviruses in mouse cells was demonstrated in Paris, and this discovery led to the use of anti-interferon serum in the search for human retroviruses. Thus, at the beginning of the 1980s, we had the essential tools required to search for a retrovirus in this new and menacing disease called AIDS. But why search for a virus, and specifically a retrovirus, in AIDS? The answer was far from obvious in 1982.

At that time, AIDS had already appeared as a long-lasting disease, with an extremely long lag time between exposure to the agent (through blood or sexual activity) and the profound state of immune suppression characterized by the occurrence of opportunistic infections or cancers. Many factors — fungi, chemicals, and even an autoimmunity to leukocytes — were invoked at that time as possible causes. However, for us, there were clues. First, the various manifestations of AIDS were unified by a biologic marker: a decrease in the levels of a specific subgroup of T cells that harbored the CD4 surface antigen. CD4 and other CDs had been identified only a few years earlier with the use of specific monoclonal antibodies, thanks to the work of Milstein and Kohler. The findings regarding the T-cell subgroup suggested an agent that specifically targeted CD4+ T cells, and HTLV was one such agent. Moreover, there were animal models in which lymphotropic retroviruses caused not only leukemias or lymphomas, but also an AIDS-like wasting syndrome. Furthermore, HTLV was transmitted through blood and sexual activity, as well as from mother to infant, which was consistent with some of what we learned early on about the epidemiology of AIDS. Finally, the Centers for Disease Control and Prevention (CDC) reported cases of AIDS in patients with hemophilia who had received only filtered clotting factors, which seemed to eliminate the possibility that the agent was a microorganism larger than a virus.

This set of arguments convinced us, as well as Max Essex in Boston, each independently to start a search for an HTLV-like virus in patients with AIDS. We began conducting this research at the National Institutes of Health in Bethesda and at the Pasteur Institute in Paris. The theory that a retrovirus caused AIDS was correct, but the hypothesis that it was a close relative of HTLV proved to be wrong. In Bethesda, an earlier survey involving the use of molecular and immunologic probes seemed to favor a variant similar to HTLV-1. In fact, some patients with AIDS were doubly infected with HTLV-1 and the new agent, which complicated the interpretation of the nature of the virus causing AIDS.

In early 1983, a clear-cut isolate was obtained in Paris, with the help of interleukin-2 and anti-interferon serum, from cultured T lymphocytes derived from a lymph-node–biopsy specimen from a patient with lymphadenopathy, a syndrome that was considered to be a precursor of AIDS. This virus proved to be different from HTLV in terms of antigenicity and morphology, but it could be propagated only in fresh cultures of T lymphocytes and not in permanent T-cell lines, which impeded its full characterization. The idea that the causative agent of AIDS should be sought in swollen lymph nodes was partly right, since we now know that lymph nodes are the main site where the virus hides during the presymptomatic phase. At this early stage, it seemed more likely that the isolate was causative than that it was opportunistic, since the immunosuppression was very mild. In some ways, however, it was also a misleading idea that delayed the full characterization of the virus and its mass production for seroepidemiologic studies, because only some viral isolates from patients with fully developed AIDS grow quickly in permanent cell lines, as we would soon learn.

This technical breakthrough was first achieved in late 1983 in Bethesda. Among a few strains in the Bethesda laboratory that grew in continuous cell lines, one came, unbeknownst to both of us, from the third isolate from a patient with Kaposi’s sarcoma in Paris. The origin of the HIV strain with a very high capacity for growth that could readily overcome other HIV strains in culture — and which contaminated cell cultures in several laboratories, beginning with both of ours — was unraveled only in 1991, thanks to the use of the polymerase-chain-reaction technique.

The year 1984 was a time of both intense excitement and harsh discussions between members of our two groups. Identifying the cause of AIDS presented a unique challenge, because unlike other viral diseases responsible for past epidemics (or, more recently, the severe acute respiratory syndrome), AIDS was characterized by clinical signs that developed years after the infection had occurred, and by then, patients usually had numerous other infections. Thus, an exceptional linkage of agent to disease had to be established. This linkage was made (particularly in Bethesda) through the repeated isolation of HIV from patients with AIDS and, more important, through the development of a readily reproducible blood test. The growth of the putative virus in T-cell lines was an enormous step, facilitating the development of a blood test for HIV, which became available in blood-transfusion centers in 1985 and produced convincing evidence of the association between HIV infection and AIDS. The blood test also helped in the cloning and molecular characterization of the genetic material of the virus at the end of 1984, which clearly proved that the new virus belonged to the subfamily of lentiretroviruses; this finding, in turn, opened the way for the design of specific drugs and vaccines.

Other indirect evidence that HIV was the cause of AIDS came from the demonstration, in 1984, of its high degree of tropism for the subgroup of CD4+ T cells, its consistent isolation from patients of different origins who had AIDS, and the isolation of similar viruses that cause AIDS in nonhuman primates (specifically, macaques). Thus, the causative relation between HIV and AIDS was accepted by the scientific and medical community in 1984 and was further verified through the later isolation of HIV type 2 in West African patients with AIDS. The relation was also supported by the clinical efficacy of drugs that specifically inhibit HIV enzymes and the demonstration that mutations in one of the coreceptors for HIV (CCR5) make some persons highly resistant to HIV infection and AIDS.

Many lessons can be drawn from this early intense period, and most suggest that science requires greater modesty. Our experience with AIDS underscores the importance of basic research, which gave us the technical and conceptual tools to find the cause less than three years after the disease was first described. The work of numerous researchers is required for such efforts, and we have described the contributions of many scientists in other publications.1,2 It has also become clear that finding the cause of an infectious disease is the alpha but not the omega of its eradication. The identification of HIV has allowed us to eliminate transmission of the disease through the transfusion of blood and blood products, create rational policies for prevention, and design efficient antiretroviral therapies. These therapies are not a cure, however, and the epidemic is still growing in many countries for lack of accessible treatments and preventive vaccines. Moreover, we must recognize that we are still far from having exhausted the list of potential new pathogens. Finally, one lesson that should be clear is that effective collaboration among groups of scientists and clinicians is essential — and that it is possible to achieve such collaboration without excluding a certain dose of the competitive spirit as a stimulant.

The Evidence That HIV Causes AIDS


The acquired immunodeficiency syndrome (AIDS) was first recognized in 1981 and has since become a major worldwide pandemic. AIDS is caused by the human immunodeficiency virus (HIV). By leading to the destruction and/or functional impairment of cells of the immune system, notably CD4+ T cells, HIV progressively destroys the body’s ability to fight infections and certain cancers.

An HIV-infected person is diagnosed with AIDS when his or her immune system is seriously compromised and manifestations of HIV infection are severe. The U.S. Centers for Disease Control and Prevention (CDC) currently defines AIDS in an adult or adolescent age 13 years or older as the presence of one of 26 conditions indicative of severe immunosuppression associated with HIV infection, such as Pneumocystis carinii pneumonia (PCP), a condition extraordinarily rare in people without HIV infection. Most other AIDS-defining conditions are also “opportunistic infections” which rarely cause harm in healthy individuals. A diagnosis of AIDS also is given to HIV-infected individuals when their CD4+ T-cell count falls below 200 cells/cubic millimeter (mm3) of blood. Healthy adults usually have CD4+ T-cell counts of 600-1,500/mm3 of blood. In HIV-infected children younger than 13 years, the CDC definition of AIDS is similar to that in adolescents and adults, except for the addition of certain infections commonly seen in pediatric patients with HIV.

In many developing countries, where diagnostic facilities may be minimal, healthcare workers use a World Health Organization (WHO) AIDS case definiton based on the presence of clinical signs associated with immune deficiency and the exclusion of other known causes of immunosuppression, such as cancer or malnutrition. An expanded WHO AIDS case definition, with a broader spectrum of clinical manifestations of HIV infection, is employed in settings where HIV antibody tests are available.

As of the end of 2000, an estimated 36.1 million people worldwide – 34.7 million adults and 1.4 million children younger than 15 years – were living with HIV/AIDS. Through 2000, cumulative HIV/AIDS-associated deaths worldwide numbered approximately 21.8 million – 17.5 million adults and 4.3 million children younger than 15 years. In the United States, an estimated 800,000 to 900,000 people are living with HIV infection. As of December 31, 1999, 733,374 cases of AIDS and 430,441 AIDS-related deaths had been reported to the CDC. AIDS is the fifth leading cause of death among all adults aged 25 to 44 in the United States. Among African-Americans in the 25 to 44 age group, AIDS is the leading cause of death for men and the second leading cause of death for women.

This document summarizes the abundant evidence that HIV causes AIDS. Questions and answers at the end of this document address the specific claims of those who assert that HIV is not the cause of AIDS.


HIV fulfills Koch’s postulates as the cause of AIDS.

Among many criteria used over the years to prove the link between putative pathogenic (disease-causing) agents and disease, perhaps the most-cited are Koch’s postulates, developed in the late 19th century. Koch’s postulates have been variously interpreted by many scientists, and modifications have been suggested to accommodate new technologies, particularly with regard to viruses. However, the basic tenets remain the same, and for more than a century Koch’s postulates, as listed below, have served as the litmus test for determining the cause of any epidemic disease:

  1. Epidemiological association: the suspected cause must be strongly associated with the disease.
  2. Isolation: the suspected pathogen can be isolated – and propagated – outside the host.
  3. Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host.

With regard to postulate #1, numerous studies from around the world show that virtually all AIDS patients are HIV-seropositive; that is they carry antibodies that indicate HIV infection. With regard to postulate #2, modern culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals with both early- and late-stage disease. In addition, the polymerase chain (PCR) and other sophisticated molecular techniques have enabled researchers to document the presence of HIV genes in virtually all patients with AIDS, as well as in individuals in earlier stages of HIV disease.

Postulate #3 has been fulfilled in tragic incidents involving three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated, cloned HIV in the laboratory. In all three cases, HIV was isolated from the infected individual, sequenced and shown to be the infecting strain of virus. In another tragic incident, transmission of HIV from a Florida dentist to six patients has been documented by genetic analyses of virus isolated from both the dentist and the patients. The dentist and three of the patients developed AIDS and died, and at least one of the other patients has developed AIDS. Five of the patients had no HIV risk factors other than multiple visits to the dentist for invasive procedures.

In addition, through December 1999, the CDC had received reports of 56 health care workers in the United States with documented, occupationally acquired HIV infection, of whom 25 have developed AIDS in the absence of other risk factors. The development of AIDS following known HIV seroconversion also has been repeatedly observed in pediatric and adult blood transfusion cases, in mother-to-child transmission, and in studies of hemophilia, injection-drug use and sexual transmission in which seroconversion can be documented using serial blood samples. For example, in a 10-year study in the Netherlands, researchers followed 11 children who had become infected with HIV as neonates by small aliquots of plasma from a single HIV-infected donor. During the 10-year period, eight of the children died of AIDS. Of the remaining three children, all showed a progressive decline in cellular immunity, and two of the three had symptoms probably related to HIV infection.

Koch’s postulates also have been fulfilled in animal models of human AIDS. Chimpanzees experimentally infected with HIV have developed severe immunosuppression and AIDS. In severe combined immunodeficiency (SCID) mice given a human immune system, HIV produces similar patterns of cell killing and pathogenesis as seen in people. HIV-2, a less virulent variant of HIV which causes AIDS in people, also causes an AIDS-like syndrome in baboons. More than a dozen strains of simian immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in Asian macaques. In addition, chimeric viruses known as SHIVs, which contain an SIV backbone with various HIV genes in place of the corresponding SIV genes, cause AIDS in macaques. Further strengthening the association of these viruses with AIDS, researchers have shown that SIV/SHIVs isolated from animals with AIDS cause AIDS when transmitted to uninfected animals.

AIDS and HIV infection are invariably linked in time, place and population group.

Historically, the occurence of AIDS in human populations around the world has closely followed the appearance of HIV. In the United States, the first cases of AIDS were reported in 1981 among homosexual men in New York and California, and retrospective examination of frozen blood samples from a U.S. cohort of gay men showed the presence of HIV antibodies as early as 1978, but not before then. Subsequently, in every region, country and city where AIDS has appeared, evidence of HIV infection has preceded AIDS by just a few years.

Many studies agree that only a single factor, HIV, predicts whether a person will develop AIDS.

Other viral infections, bacterial infections, sexual behavior patterns and drug abuse patterns do not predict who develops AIDS. Individuals from diverse backgrounds, including heterosexual men and women, homosexual men and women, hemophiliacs, sexual partners of hemophiliacs and transfusion recipients, injection-drug users and infants have all developed AIDS, with the only common denominator being their infection with HIV.

In cohort studies, severe immunosuppression and AIDS-defining illnesses occur almost exclusively in individuals who are HIV-infected.

For example, analysis of data from more than 8,000 participants in the Multicenter AIDS Cohort Study (MACS) and the Women’s Interagency HIV Study (WIHS) demonstrated that participants who were HIV-seropositive were 1,100 times more likely to develop an AIDS-associated illness than those who were HIV-seronegative. These overwhelming odds provide a clarity of association that is unusual in medical research.

In a Canadian cohort, investigators followed 715 homosexual men for a median of 8.6 years. Every case of AIDS in this cohort occurred in individuals who were HIV-seropositive. No AIDS-defining illnesses occurred in men who remained negative for HIV antibodies, despite the fact that these individuals had appreciable patterns of illicit drug use and receptive anal intercourse.

Before the appearance of HIV, AIDS-related diseases such as PCP, KS and MAC were rare in developed countries; today, they are common in HIV-infected individuals.

Prior to the appearance of HIV, AIDS-related conditions such as Pneumocystis carinii pneumonia (PCP), Kaposi’s sarcoma (KS) and disseminated infection with the Mycobacterium avium complex (MAC) were extraordinarily rare in the United States. In a 1967 survey, only 107 cases of PCP in the United States had been described in the medical literature, virtually all among individuals with underlying immunosuppressive conditions. Before the AIDS epidemic, the annual incidence of Kaposi’s sarcoma in the United States was only 0.2 to 0.6 cases per million population, and only 32 individuals with disseminated MAC disease had been described in the medical literature.

By the end of 1999, CDC had received reports of 166,368 HIV-infected patients in the United States with definitive diagnoses of PCP, 46,684 with definitive diagnoses of KS, and 41,873 with definitive diagnoses of disseminated MAC (personal communication).

In developing countries, patterns of both rare and endemic diseases have changed dramatically as HIV has spread, with a far greater toll now being exacted among the young and middle-aged, including well-educated members of the middle class.

In developing countries, the emergence of the HIV epidemic has dramatically changed patterns of disease in affected communities. As in developed countries, previously rare, “opportunistic” diseases such as PCP and certain forms of meningitis have become more commonplace. In addition, as HIV seroprevalence rates have risen, there have been significant increases in the burden of endemic conditions such as tuberculosis (TB), particularly among young people. For example, as HIV seroprevalence increased sharply in Blantyre, Malawi from 1986 to 1995, tuberculosis admissions at the city’s main hospital rose more than 400 percent, with the largest increase in cases among children and young adults. In the rural Hlabisa District of South Africa, admissions to tuberculosis wards increased 360 percent from 1992 to 1998, concomitant with a steep rise in HIV seroprevalence. High rates of mortality due to endemic conditions such as TB, diarrheal diseases and wasting syndromes, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people in many developing countries.

In studies conducted in both developing and developed countries, death rates are markedly higher among HIV-seropositive individuals than among HIV-seronegative individuals.

For example, Nunn and colleagues assessed the impact of HIV infection over five years in a rural population in the Masaka District of Uganda. Among 8,833 individuals of all ages who had an unambiguous result on testing for HIV-antibodies, HIV-seropositive people were 16 times more likely to die over five years than HIV-seronegative people. Among individuals ages 25 to 34, HIV-seropositive people were 27 times more likely to die than HIV-seronegative people.

In another study in Uganda, 19,983 adults in the rural Rakai District were followed for 10 to 30 months. In this cohort, HIV-seropositive people were 20 times more likely to die than HIV-seronegative people during 31,432 person-years of observation.

Similar findings have emerged from other studies

Kilmarx and colleagues recently reported data on HIV infection and mortality in a cohort of female commercial sex workers in Chiang Rai, Thailand. Among 500 women enrolled in the study between 1991 and 1994, the mortality rate through October 1998 among women who were HIV-infected at enrollment was 52.7 times higher than among women who remained uninfected with HIV. The mortality rate among women who became infected during the study was 22.5 higher than among persistently uninfected women. Among the HIV-infected women, only 3 of whom received antiretroviral medications, all reported causes of death were associated with immunosuppression, whereas the reported causes of death of the two uninfected women were postpartum amniotic embolism and gunshot wound.

Excess mortality among HIV-seropositive people also has been repeatedly observed in studies in developed countries, perhaps most dramatically among hemophiliacs. For example, Darby et al. studied 6,278 hemophiliacs living in the United Kingdom during the period 1977-91. Among 2,448 individuals with severe hemophilia, the annual death rate was stable at 8 per 1,000 during 1977-84. While death rates remained stable at 8 per 1,000 from 1985-1992 among HIV-seronegative persons with severe hemophilia, deaths rose steeply among those who had become HIV-seropositive following HIV-tainted transfusions during 1979-1986, reaching 81 per 1,000 in 1991-92. Among 3,830 individuals with mild or moderate hemophilia, the pattern was similar, with an initial death rate of 4 per 1,000 in 1977-84 that remained stable among HIV-seronegative individuals but rose to 85 per 1,000 in 1991-92 among seropositive individuals.

Similar data have emerged from the Multicenter Hemophilia Cohort Study. Among 1,028 hemophiliacs followed for a median of 10.3 years, HIV-infected individuals (n=321) were 11 times more likely to die than HIV-negative subjects (n=707), with the dose of Factor VIII having no effect on survival in either group.

In the Multicenter AIDS Cohort Study (MACS), a 16-year study of 5,622 homosexual and bisexual men, 1,668 of 2,761 HIV-seropositive men have died (60 percent), 1,547 after a diagnosis of AIDS. In contrast, among 2,861 HIV-seronegative participants, only 66 men (2.3 percent) have died.

HIV can be detected in virtually everyone with AIDS.

Recently developed sensitive testing methods, including the polymerase chain reaction (PCR) and improved culture techniques, have enabled researchers to find HIV in patients with AIDS with few exceptions. HIV has been repeatedly isolated from the blood, semen and vaginal secretions of patients with AIDS, findings consistent with the epidemiologic data demonstrating AIDS transmission via sexual activity and contact with infected blood.

Numerous studies of HIV-infected people have shown that high levels of infectious HIV, viral antigens, and HIV nucleic acids (DNA and RNA) in the body predict immune system deterioration and an increased risk for developing AIDS. Conversely, patients with low levels of virus have a much lower risk of developing AIDS.

For example, in an anlysis of 1,604 HIV-infected men in the Multicenter AIDS Cohort Study (MACS), the risk of a patient developing AIDS with six years was strongly associated with levels of HIV RNA in the plasma as measured by a sensitive test known as the branched-DNA signal-amplification assay (bDNA):

Plasma RNA concentration
(copies/mL of blood)
Proportion of patients
developing AIDS within six years
501 – 3,000
3,001 – 10,000
10,001 – 30,000

(Source: Mellors et al. Ann Intern Med 1997;126:946)Similar associations between increasing HIV RNA levels and a greater risk of disease progression have been observed in HIV-infected children in both developed and developing countries.

In the very small proportion of untreated HIV-infected individuals whose disease progresses very slowly, the amount of HIV in the blood and lymph nodes is significantly lower than in HIV-infected people whose disease progression is more typical.

The availability of potent combinations of drugs that specifically block HIV replication has dramatically improved the prognosis for HIV-infected individuals. Such an effect would not be seen if HIV did not have a central role in causing AIDS.

Clinical trials have shown that potent three-drug combinations of anti-HIV drugs, known as highly active antiretroviral therapy (HAART), can significantly reduce the incidence of AIDS and death among HIV-infected individuals as compared to previously available HIV treatment regimens.

Use of these potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, among both adults and children.

For example, in a prospective study of more than 7,300 HIV-infected patients in 52 European outpatient clinics, the incidence of new AIDS-defining illnesses declined from 30.7 per 100 patient-years of observation in 1994 (before the availability of HAART) to 2.5 per 100 patient years in 1998, when the majority of patients received HAART.

Among HIV-infected patients who receive anti-HIV therapy, those whose viral loads are driven to low levels are much less likely to develop AIDS or die than patients who do not respond to therapy. Such an effect would not be seen if HIV did not have a central role in causing AIDS.

Clinical trials in both HIV-infected children and adults have demonstrated a link between a good virologic response to therapy (i.e. much less virus in the body) and a reduced risk of developing AIDS or dying.

This effect has also been seen in routine clinical practice. For example, in an analysis of 2,674 HIV-infected patients who started highly active antiretroviral therapy (HAART) in 1995-1998, 6.6 percent of patients who achieved and maintained undetectable viral loads (<400 copies/mL of blood) developed AIDS or died within 30 months, compared with 20.1 percent of patients who never achieved undetectable concentrations.

Nearly everyone with AIDS has antibodies to HIV.

A survey of 230,179 AIDS patients in the United States revealed only 299 HIV-seronegative individuals. An evaluation of 172 of these 299 patients found 131 actually to be seropositive; an additional 34 died before their serostatus could be confirmed.

Numerous serosurveys show that AIDS is common in populations where many individuals have HIV antibodies. Conversely, in populations with low seroprevalence of HIV antibodies, AIDS is extremely rare.

For example, in the southern African country of Zimbabwe (population 11.4 million), more than 25 percent of adults ages 15 to 49 are estimated to be HIV antibody-positive, based on numerous studies. As of November 1999, more than 74,000 cases of AIDS in Zimbabwe had been reported to the World Health Organization (WHO). In contrast, Madagascar, an island country off the southeast coast of Africa (population 15.1 million) with a very low HIV seroprevalence rate, reported only 37 cases of AIDS to WHO through November 1999. Yet, other sexually transmitted diseases, notably syphilis, are common in Madagascar, suggesting that conditions are ripe for the spread of HIV and AIDS if the virus becomes entrenched in that country.

The specific immunologic profile that typifies AIDS – a persistently low CD4+ T-cell count – is extraordinarily rare in the absence of HIV infection or other known cause of immunosuppression.

For example, in the NIAID-supported Multicenter AIDS Cohort Study (MACS), 22,643 CD4+ T-cell determinations in 2,713 HIV-seronegative homosexual and bisexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/mm3 of blood, and this individual was receiving immunosuppressive therapy. Similar results have been reported from other studies.

Newborn infants have no behavioral risk factors for AIDS, yet many children born to HIV-infected mothers have developed AIDS and died.

Only newborns who become HIV-infected before or during birth, during breastfeeding, or (rarely) following exposure to HIV-tainted blood or blood products after birth, go on to develop the profound immunosuppression that leads to AIDS. Babies who are not HIV-infected do not develop AIDS. In the United States, 8,718 cases of AIDS among children younger than age 13 had been reported to the CDC as of December 31, 1999. Cumulative U.S. AIDS deaths among individuals younger than age 15 numbered 5,044 through December 31, 1999. Globally, UNAIDS estimates that 480,000 child deaths due to AIDS occurred in 1999 alone.

Because many HIV-infected mothers abuse recreational drugs, some have argued that maternal drug use itself causes pediatric AIDS. However, studies have consistently shown that babies who are not HIV-infected do not develop AIDS, regardless of their mothers’ drug use.

For example, a majority of the HIV-infected, pregnant women enrolled in the European Collaborative Study are current or former injection drug users. In this ongoing study, mothers and their babies are followed from birth in 10 centers in Europe. In a paper in Lancet, study investigators reported that none of 343 HIV-seronegative children born to HIV-seropositive mothers had developed AIDS or persistent immune deficiency. In contrast, among 64 seropositive children, 30 percent presented with AIDS within 6 months of age or with oral candidiasis followed rapidly by the onset of AIDS. By their first birthday, 17 percent died of HIV-related diseases.

In a study in New York, investigators followed 84 HIV-infected and 248 HIV-uninfected infants, all born to HIV-seropositive mothers. The mothers of the two groups of infants were equally likely to be injection drug users (47 percent vs. 50 percent), and had similar rates of alcohol, tobacco, cocaine, heroin and methadone use. Of the 84 HIV-infected children, 22 died during a median follow-up period of 27.6 months, including 20 infants who died before their second birthday. Twenty-one of these deaths were classified as AIDS-related. Among the 248 uninfected children, only one death (due to child abuse) was reported during a median follow-up period of 26.1 months.

The HIV-infected twin develops AIDS while the uninfected twin does not.

Because twins share an in utero environment and genetic relationships, similarities and differences between them can provide important insight into infectious diseases, including AIDS. Researchers have documented cases of HIV-infected mothers who have given birth to twins, one of whom is HIV-infected and the other not. The HIV-infected children developed AIDS, while the other children remained clinically and immunologically normal.

Studies of transfusion-acquired AIDS cases have repeatedly led to the discovery of HIV in the patient as well as in the blood donor.

Numerous studies have shown an almost perfect correlation between the occurrence of AIDS in a blood recipient and donor, and evidence of homologous HIV strains in both the recipient and the donor.

HIV is similar in genetic structure and morphology to other lentiviruses that often cause immunodeficiency in their animal hosts in addition to slow, progressive wasting disorders, neurodegeneration and death.

Like HIV in humans, animal viruses such as feline immunodeficiency virus (FIV) in cats, visna virus in sheep and simian immunodeficiency virus (SIV) in monkeys primarily infect cells of the immune system such as T cells and macrophages. For example, visna virus infects macrophages and causes a slowly progressive neurologic disease.

HIV causes the death and dysfunction of CD4+ T lymphocytes in vitro and in vivo.

CD4+ T cell dysfunction and depletion are hallmarks of HIV disease. The recognition that HIV infects and destroys CD4+ T cells in vitro strongly suggests a direct link between HIV infection, CD4+ T cell depletion, and development of AIDS. A variety of mechanisms, both directly and indirectly related to HIV infection of CD4+ T cells, are likely responsible for the defects in CD4+ T cell function observed in HIV-infected people. Not only can HIV enter and kill CD4+ T cells directly, but several HIV gene products may interfere with the function of uninfected cells.


MYTH: HIV antibody testing is unreliable.

FACT: Diagnosis of infection using antibody testing is one of the best-established concepts in medicine. HIV antibody tests exceed the performance of most other infectious disease tests in both sensitivity and specificity. Current HIV antibody tests have sensitivity and specificity in excess of 98% and are therefore extremely reliable.

Progress in testing methodology has also enabled detection of viral genetic material, antigens and the virus itself in body fluids and cells. While not widely used for routine testing due to high cost and requirements in laboratory equipment, these direct testing techniques have confirmed the validity of the antibody tests.

MYTH: There is no AIDS in Africa. AIDS is nothing more than a new name for old diseases.

FACT: The diseases that have come to be associated with AIDS in Africa – such as wasting syndrome, diarrheal diseases and TB – have long been severe burdens there. However, high rates of mortality from these diseases, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people, including well-educated members of the middle class.

For example, in a study in Cote d’Ivoire, HIV-seropositive individuals with pulmonary tuberculosis (TB) were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary TB. In Malawi, mortality over three years among children who had received recommended childhood immunizations and who survived the first year of life was 9.5 times higher among HIV-seropositive children than among HIV-seronegative children. The leading causes of death were wasting and respiratory conditions. Elsewhere in Africa, findings are similar.

MYTH: HIV cannot be the cause of AIDS because researchers are unable to explain precisely how HIV destroys the immune system.

FACT: A great deal is known about the pathogenesis of HIV disease, even though important details remain to be elucidated. However, a complete understanding of the pathogenesis of a disease is not a prerequisite to knowing its cause. Most infectious agents have been associated with the disease they cause long before their pathogenic mechanisms have been discovered. Because research in pathogenesis is difficult when precise animal models are unavailable, the disease-causing mechanisms in many diseases, including tuberculosis and hepatitis B, are poorly understood. The critics’ reasoning would lead to the conclusion that M. tuberculosis is not the cause of tuberculosis or that hepatitis B virus is not a cause of liver disease.

MYTH: AZT and other antiretroviral drugs, not HIV, cause AIDS.

FACT: The vast majority of people with AIDS never received antiretroviral drugs, including those in developed countries prior to the licensure of AZT in 1987, and people in developing countries today where very few individuals have access to these medications.

As with medications for any serious diseases, antiretroviral drugs can have toxic side effects. However, there is no evidence that antiretroviral drugs cause the severe immunosuppression that typifies AIDS, and abundant evidence that antiretroviral therapy, when used according to established guidelines, can improve the length and quality of life of HIV-infected individuals.

In the 1980s, clinical trials enrolling patients with AIDS found that AZT given as single-drug therapy conferred a modest (and short-lived) survival advantage compared to placebo. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. Significantly, long-term follow-up of these trials did not show a prolonged benefit of AZT, but also never indicated that the drug increased disease progression or mortality. The lack of excess AIDS cases and death in the AZT arms of these placebo-controlled trials effectively counters the argument that AZT causes AIDS.

Subsequent clinical trials found that patients receiving two-drug combinations had up to 50 percent increases in time to progression to AIDS and in survival when compared to people receiving single-drug therapy. In more recent years, three-drug combination therapies have produced another 50 percent to 80 percent improvements in progression to AIDS and in survival when compared to two-drug regimens in clinical trials. Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which clearly would not be seen if antiretroviral drugs caused AIDS.

MYTH: Behavioral factors such as recreational drug use and multiple sexual partners account for AIDS.

FACT: The proposed behavioral causes of AIDS, such as multiple sexual partners and long-term recreational drug use, have existed for many years. The epidemic of AIDS, characterized by the occurrence of formerly rare opportunistic infections such as Pneumocystis carinii pneumonia (PCP) did not occur in the United States until a previously unknown human retrovirus – HIV – spread through certain communities.

Compelling evidence against the hypothesis that behavioral factors cause AIDS comes from recent studies that have followed cohorts of homosexual men for long periods of time and found that only HIV-seropositive men develop AIDS.

For example, in a prospectively studied cohort in Vancouver, 715 homosexual men were followed for a median of 8.6 years. Among 365 HIV-positive individuals, 136 developed AIDS. No AIDS-defining illnesses occurred among 350 seronegative men despite the fact that these men reported appreciable use of inhalable nitrites (“poppers”) and other recreational drugs, and frequent receptive anal intercourse.

Other studies show that among homosexual men and injection-drug users, the specific immune deficit that leads to AIDS – a progressive and sustained loss of CD4+ T cells – is extremely rare in the absence of other immunosuppressive conditions. For example, in the Multicenter AIDS Cohort Study, more than 22,000 T-cell determinations in 2,713 HIV-seronegative homosexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/mm3 of blood, and this individual was receiving immunosuppressive therapy.

In a survey of 229 HIV-seronegative injection-drug users in New York City, mean CD4+ T-cell counts of the group were consistently more than 1000 cells/mm3 of blood. Only two individuals had two CD4+ T-cell measurements of less than 300/mm3 of blood, one of whom died with cardiac disease and non-Hodgkin’s lymphoma listed as the cause of death.

MYTH: AIDS among transfusion recipients is due to underlying diseases that necessitated the transfusion, rather than to HIV.

FACT: This notion is contradicted by a report by the Transfusion Safety Study Group (TSSG), which compared HIV-negative and HIV-positive blood recipients who had been given transfusions for similar diseases. Approximately 3 years after the transfusion, the mean CD4+ T-cell count in 64 HIV-negative recipients was 850/mm3 of blood, while 111 HIV-seropositive individuals had average CD4+ T-cell counts of 375/mm3 of blood. By 1993, there were 37 cases of AIDS in the HIV-infected group, but not a single AIDS-defining illness in the HIV-seronegative transfusion recipients.

MYTH: High usage of clotting factor concentrate, not HIV, leads to CD4+ T-cell depletion and AIDS in hemophiliacs.

FACT: This view is contradicted by many studies. For example, among HIV-seronegative patients with hemophilia A enrolled in the Transfusion Safety Study, no significant differences in CD4+ T-cell counts were noted between 79 patients with no or minimal factor treatment and 52 with the largest amount of lifetime treatments. Patients in both groups had CD4+ T cell-counts within the normal range. In another report from the Transfusion Safety Study, no instances of AIDS-defining illnesses were seen among 402 HIV-seronegative hemo.

In a cohort in the United Kingdom, researchers matched 17 HIV-seropositive hemophiliacs with 17 HIV-seronegative hemophiliacs with regard to clotting factor concentrate usage over a ten-year period. During this time, 16 AIDS-defining clinical events occurred in 9 patients, all of whom were HIV-seropositive. No AIDS-defining illnesses occurred among the HIV-negative patients. In each pair, the mean CD4+ T cell count during follow-up was, on average, 500 cells/mm3 lower in the HIV-seropositive patient.

Among HIV-infected hemophiliacs, Transfusion Safety Study investigators found that neither the purity nor the amount of Factor VIII therapy had a deleterious effect on CD4+ T cell counts (Gjerset et al., Blood 1994;84:1666). Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs.

MYTH: The distribution of AIDS cases casts doubt on HIV as the cause. Viruses are not gender-specific, yet only a small proportion of AIDS cases are among women.

FACT: The distribution of AIDS cases, whether in the United States or elsewhere in the world, invariably mirrors the prevalence of HIV in a population. In the United States, HIV first appeared in populations of homosexual men and injection-drug users, a majority of whom are male. Because HIV is spread primarily through sex or by the exchange of HIV-contaminated needles during injection-drug use, it is not surprising that a majority of U.S. AIDS cases have occurred in men.

Increasingly, however, women in the United States are becoming HIV-infected, usually through the exchange of HIV-contaminated needles or sex with an HIV-infected male. The CDC estimates that 30 percent of new HIV infections in the United States in 1998 were in women. As the number of HIV-infected women has risen, so too has the number of female AIDS patients in the United States. Approximately 23 percent of U.S. adult/adolescent AIDS cases reported to the CDC in 1998 were among women. In 1998, AIDS was the fifth leading cause of death among women aged 25 to 44 in the United States, and the third leading cause of death among African-American women in that age group.

In Africa, HIV was first recognized in sexually active heterosexuals, and AIDS cases in Africa have occurred at least as frequently in women as in men. Overall, the worldwide distribution of HIV infection and AIDS between men and women is approximately 1 to 1.

MYTH: HIV cannot be the cause of AIDS because the body develops a vigorous antibody response to the virus.

FACT: This reasoning ignores numerous examples of viruses other than HIV that can be pathogenic after evidence of immunity appears. Measles virus may persist for years in brain cells, eventually causing a chronic neurologic disease despite the presence of antibodies. Viruses such as cytomegalovirus, herpes simplex and varicella zoster may be activated after years of latency even in the presence of abundant antibodies. In animals, viral relatives of HIV with long and variable latency periods, such as visna virus in sheep, cause central nervous system damage even after the production of antibodies.

Also, HIV is well recognized as being able to mutate to avoid the ongoing immune response of the host.

MYTH: Only a small number of CD4+ T cells are infected by HIV, not enough to damage the immune system.

FACT: New techniques such as the polymerase chain reaction (PCR) have enabled scientists to demonstrate that a much larger proportion of CD4+ T cells are infected than previously realized, particularly in lymphoid tissues. Macrophages and other cell types are also infected with HIV and serve as reservoirs for the virus. Although the fraction of CD4+ T cells that is infected with HIV at any given time is never extremely high, several groups have shown that rapid cycles of death of infected cells and infection of new target cells occur throughout the course of disease.

MYTH: HIV is not the cause of AIDS because many individuals with HIV have not developed AIDS.

FACT: HIV disease has a prolonged and variable course. The median period of time between infection with HIV and the onset of clinically apparent disease is approximately 10 years in industrialized countries, according to prospective studies of homosexual men in which dates of seroconversion are known. Similar estimates of asymptomatic periods have been made for HIV-infected blood-transfusion recipients, injection-drug users and adult hemophiliacs.

As with many diseases, a number of factors can influence the course of HIV disease. Factors such as age or genetic differences between individuals, the level of virulence of the individual strain of virus, as well as exogenous influences such as co-infection with other microbes may determine the rate and severity of HIV disease expression. Similarly, some people infected with hepatitis B, for example, show no symptoms or only jaundice and clear their infection, while others suffer disease ranging from chronic liver inflammation to cirrhosis and hepatocellular carcinoma. Co-factors probably also determine why some smokers develop lung cancer while others do not.

MYTH: Some people have many symptoms associated with AIDS but do not have HIV infection.

FACT: Most AIDS symptoms result from the development of opportunistic infections and cancers associated with severe immunosuppression secondary to HIV.

However, immunosuppression has many other potential causes. Individuals who take glucocorticoids and/or immunosuppressive drugs to prevent transplant rejection or for autoimmune diseases can have increased susceptibility to unusual infections, as do individuals with certain genetic conditions, severe malnutrition and certain kinds of cancers. There is no evidence suggesting that the numbers of such cases have risen, while abundant epidemiologic evidence shows a staggering rise in cases of immunosuppression among individuals who share one characteristic: HIV infection.

MYTH: The spectrum of AIDS-related infections seen in different populations proves that AIDS is actually many diseases not caused by HIV.

FACT: The diseases associated with AIDS, such as PCP and Mycobacterium avium complex (MAC), are not caused by HIV but rather result from the immunosuppression caused by HIV disease. As the immune system of an HIV-infected individual weakens, he or she becomes susceptible to the particular viral, fungal and bacterial infections common in the community. For example, HIV-infected people in certain midwestern and mid-Atlantic regions are much more likely than people in New York City to develop histoplasmosis, which is caused by a fungus. A person in Africa is exposed to different pathogens than is an individual in an American city. Children may be exposed to different infectious agents than adults.


I have checked through all of the reputable sources on the subject that did not require me to spend a fortune. After all I do not make any money on this blog, so I have to watch my expenses. Working under these limitations I was unable to find any conclusive proof that HIV is not the cause of AIDS. What I am likening it to is the ongoing debate about whether the earth is flat. You will never convince true believers of the fact that the earth is indeed round. You will also never convince some that HIV is the cause of AIDS. Sometimes you just have to know when to stop arguing. I will from time to time check up on the subject to see if any new and more difinitive information is available. There is some evidence that the Herpes virus HH-6V could play a role in the progression to AIDS, unfortunately there is little information available, since Dr. Fauci and the NIAID crushed the research on it. There is also rumors that one of the early tratments for AIDS AZT killed more people then the actual disease did. The problem is that the effects of the drug mirrored AIDS as well. Kind of sounds familar to Remdesivir. It is like de javu.

Resources, “Does HIV cause AIDS? An updated response to Duesberg’s theories.” By R. Kurth;, “HIV Does Not Cause AIDS in the Way We Thought: Research Reveals Why Vaccines Fail to Prevent Infection.” By James Myhre & Dennis Sifris, MD;, “HIV Does Not Cause AIDS.” By Mohammed Ali Al-Bayati;, “What Is the Main Cause of HIV?” By John P. Cunha, DO.;, “The Discovery of HIV as the Cause of AIDS.” By Robert C. Gallo, M.D., and Luc Montagnier, M.D.;, “What Causes AIDS?” By John P. Cunha, DO, FACOEP;, “The Evidence That HIV Causes AIDS.”;, “History of AIDS.”;, “HIV as the cause of AIDS.” By Francoise Barre-Sinoussi;


Duesberg’s Hypothesis

In the 80s Peter Duesberg wrote a paper refuting HIV as the cause of AIDS. He stated that it was a harmless retrovirus that had been hitching a genetic ride on the human genome for millions of years. He however , did not leave a void where the HIV was. His hypothesis is based on a multiplicity of environmental exposures. The Gay crowd of the 80s lived a particularly dangerous lifestyle. Their lifestyles involved heavy recreational drug use. They reasoned that the initial signals of AIDS, Kaposi’s sarcoma and Pneumocytis carnii pneumonia (PCP) were strongly linked to amyl nitrite (poppers), a ppular drug among promiscuous gays. Other wasting symptoms were all associated with heavy drug use and lifestyle stressors. Risk factors included promiscuous sex with multiple partners and cumulative toxic exposures from psychoactive drugs including methedrine, cocaine, heorin, LSD, and a cocktail of antibiotics prescribed to treat ubiquitous sexually transmitted diseases.

History of AIDS

In the 1980s and early 1990s, the outbreak of HIV and AIDS swept across the United States and rest of the world, though the disease originated decades earlier. Today, more than 70 million people have been infected with HIV and about 35 million have died from AIDS since the start of the pandemic, according to the World Health Organization (WHO).

What is HIV?

The human immunodeficiency virus, or HIV, is a virus that attacks the immune system, specifically CD4 cells (or T cells).

The virus is transmitted through bodily fluids such as blood, semen, vaginal fluids, anal fluids, and breast milk. Historically, HIV has most often been spread through unprotected sex, the sharing of needles for drug use, and through birth.

Over time, HIV can destroy so many CD4 cells that the body can’t fight infections and diseases, eventually leading to the most severe form of an HIV infection: acquired immunodeficiency syndrome, or AIDS. A person with AIDS is very vulnerable to cancer and to life-threatening infections, such as pneumonia.

Though there is no cure for HIV or AIDS, a person with HIV who receives treatment early can live nearly as long as someone without the virus. And a study in 2019 in the medical journal, Lancet, showed that an anti-viral treatment effectively halted the spread of HIV.

Where Did AIDS Come From?

Scientists have traced the origin of HIV back to chimpanzees and simian immunodeficiency virus (SIV), an HIV-like virus that attacks the immune system of monkeys and apes.

In 1999, researchers identified a strain of chimpanzee SIV called SIVcpz, which was nearly identical to HIV. Chimps, the scientist later discovered, hunt and eat two smaller species of monkeys—red-capped mangabeys and greater spot-nosed monkeys—that carry and infect the chimps with two strains of SIV. These two strains likely combined to form SIVcpz, which can spread between chimpanzees and humans.

SIVcpz likely jumped to humans when hunters in Africa ate infected chimps, or the chimps’ infected blood got into the cuts or wounds of hunters. Researchers believe the first transmission of SIV to HIV in humans that then led to the global pandemic occurred in 1920 in Kinshasa, the capital and largest city in the Democratic Republic of Congo.

The virus spread may have spread from Kinshasa along infrastructure routes (roads, railways, and rivers) via migrants and the sex trade.

In the 1960s, HIV spread from Africa to Haiti and the Caribbean when Haitian professionals in the colonial Democratic Republic of Congo returned home. The virus then moved from the Caribbean to New York City around 1970 and then to San Francisco later in the decade.

International travel from the United States helped the virus spread across the rest of the globe.

The AIDS Epidemic Arises

Though HIV arrived in the United States around 1970, it didn’t come to the public’s attention until the early 1980s.

In 1981, the Centers for Disease Control and Prevention (CDC) published a report about five previously healthy homosexual men becoming infected with Pneumocystis pneumonia, which is caused by the normally harmless fungus Pneumocystis jirovecii. This type of pneumonia, the CDC noted, almost never affects people with uncompromised immune systems.

The following year, The New York Times published an alarming article about the new immune system disorder, which, by that time, had affected 335 people, killing 136 of them. Because the disease appeared to affect mostly homosexual men, officials initially called it gay-related immune deficiency, or GRID.

Though the CDC discovered all major routes of the disease’s transmission—as well as that female partners of AIDS-positive men could be infected—in 1983, the public considered AIDS a gay disease. It was even called the “gay plague” for many years after.

In September of 1982, the CDC used the term AIDS to describe the disease for the first time. By the end of the year, AIDS cases were also reported in a number of European countries.

The AIDS Epidemic Arises

Though HIV arrived in the United States around 1970, it didn’t come to the public’s attention until the early 1980s.

In 1981, the Centers for Disease Control and Prevention (CDC) published a report about five previously healthy homosexual men becoming infected with Pneumocystis pneumonia, which is caused by the normally harmless fungus Pneumocystis jirovecii. This type of pneumonia, the CDC noted, almost never affects people with uncompromised immune systems.

The following year, The New York Times published an alarming article about the new immune system disorder, which, by that time, had affected 335 people, killing 136 of them. Because the disease appeared to affect mostly homosexual men, officials initially called it gay-related immune deficiency, or GRID.

Though the CDC discovered all major routes of the disease’s transmission—as well as that female partners of AIDS-positive men could be infected—in 1983, the public considered AIDS a gay disease. It was even called the “gay plague” for many years after.

In September of 1982, the CDC used the term AIDS to describe the disease for the first time. By the end of the year, AIDS cases were also reported in a number of European countries.

Numerous other medications for HIV are now available, and are typically used together in what’s known as antiretroviral therapy (ART) or highly active antiretroviral treatment (HAART).

The regimes work by preventing the virus from multiplying, giving the immune system a chance to recover and fight off infections and HIV-related cancers. The therapy also helps reduce the risk of HIV transmission, including between an infected mother and her unborn child.

The World Health Organization (WHO), in 1988, declared December 1st to be World AIDS Day. By the end of the decade, there were at least 100,000 reported cases of AIDS in the United States and WHO estimated 400,000 AIDS cases worldwide.

HIV/AIDS in the 1990s and 2000s

In 1991, the red ribbon became an international symbol of AIDS awareness.

In that year, basketball player Magic Johnson announced he had HIV, helping to further bring awareness to the issue and dispel the stereotype of it being a gay disease. Soon after, Freddie Mercury—lead singer of the band Queen—announced he had AIDS and died a day later.

In 1994, the FDA approved the first oral (and non-blood) HIV test. Two years later, it approved the first home testing kit and the first urine test.

AIDS-related deaths and hospitalizations in developed countries began to decline sharply in 1995 thanks to new medications and the introduction of HAART. Still, by 1999, AIDS was the fourth biggest cause of death in the world and the leading cause of death in Africa.

HIV Treatment Progresses

In 2001, generic drug manufacturers began selling discounted copies of patented HIV drugs to developing countries, leading to several major pharmaceutical manufacturers slashing prices on their HIV drugs. The following year, the Joint United Nations Programme on HIV/AIDS (UNAIDS) reported that AIDS was by far the leading cause of death in sub-Saharan Africa.

In 2009, President Barack Obama lifted a 1987 U.S. ban that prevented HIV-positive people from entering the country.

The FDA approved pre-exposure prophylaxis, or PrEP, for HIV-negative people in 2012. When taken daily, PrEP can reduce the risk of HIV from sex by more than 90 percent and from intravenous drug use by 70 percent, according to the CDC. A major study completed in 2019 showed that over 750 gay men on an anti-viral treatment did not transmit the virus to their partners. “Our findings provide conclusive evidence that the risk of HIV transmission through anal sex when HIV viral load is suppressed is effectively zero,” the paper, published in Lancet, stated.

At the end of 2019, some 38 million people were living with HIV/AIDS worldwide, and 940,000 people died from AIDS-related illnesses that year, according to WHO. Sub-Saharan Africa remains the most severely affected region, accounting for nearly two-thirds of the world’s current HIV cases.

Origins and Silent Spread

Early 20th Century – At some point in the first few decades of the 20th century, Simian Immunodeficiency Virus makes the jump from chimpanzees to humans in Central Africa. Now known as the subtype HIV-1, the virus begins circulating in Léopoldville, now Kinshasa in the Democratic Republic of the Congo—believed to be the first zoonotic transmission of HIV.

1959 – A man dies in the Congo—tests of his blood samples later establish this is the earliest confirmed HIV-related death.

1960s – HIV-2 is believed to have jumped to humans from monkeys in West Africa, likely Guinea-Bisseau, around this time. Studies later reveal that HIV-1 arrived in the Americas during the late 1960s. A significant number of Haitians were working in the Congo at the time, with some likely bringing the virus back to the Caribbean on their return.

December 12, 1977 – Grethe Rask, a Danish physician and surgeon who spent years working in the Congo, dies of pneumonia. Over several years, she suffered from a number of opportunistic infections and severe immunodeficiency. Ten years after her death, a blood test finds she was infected with HIV.

A Gay Men’s Crisis


April 24 – The CDC receives a report on Ken Horne, a gay man living in San Francisco who is suffering from Kaposi’s Sarcoma, a rare and unusually aggressive cancer linked with weakened immunity. Horne dies on November 30, 1981. The same year, the CDC retroactively identifies Horne as the first American patient of the AIDS epidemic. 


May 18  Lawrence Mass, a gay doctor in New York City, writes an article for The New York Native, an LGBT newspaper, titled “Disease Rumors Largely Unfounded.” Although the headline would soon be proven false, his report that a number of gay men have been admitted to New York City intensive care unites with severely compromised immune systems is the first article to mention what soon becomes known as AIDS.

June 5, 1981  The CDC publishes an article describing five cases of a rare lung infection in young, otherwise healthy gay men in Los Angeles, two of whom have died and three of whom die a short time after. The same day, New York City dermatologist Dr. Alvin Friedman-Kien reports a cluster of instances of Kaposi’s Sarcoma in gay men in New York and California. Several major outlets report on the article, and the CDC begins to receive a steady trickle of reports of similar cases. This article is often cited as the official beginning of the AIDS Crisis.

July 1981 – An LGBT newspaper in San Francisco, The Bay Area Reporter, writes about “Gay Men’s Pneumonia” and urges gay men experiencing shortness of breath to see a doctor. The New York Times article “Rare Cancer Seen in 41 Homosexuals” leads to the coining of the term “gay cancer” to describe Kaposi’s Sarcoma.

August 11, 1981  Writer and film producer Larry Kramer hosts a fundraiser in his New York City apartment, at which Dr. Friedman-Kien addresses a crowd of gay men. He raises $6,635 to fund research into the mysterious new illness, the only money raised for the cause in 1981. Kramer soon co-founds the Gay Men’s Health Crisis (GMHC), a community-based non-profit dedicated to serving the community throughout the emerging crisis.


May 11 – In an article titled “New Homosexual Disorder Worries Health Officials,” the New York Times first publishes the phrase Gay-Related Immune Deficiency, or GRID, contributing to the widespread misconception that AIDS only affects gay men.

September 24 – The CDC uses the term “AIDS” for the first time. It defines Acquired Immune Deficiency Syndrome as “A disease at least moderately predictive of a defect in cell-mediated immunity, occurring in a person with no known cause for diminished resistance to that disease.”


January 1 – Ward 86, the world’s first dedicated outpatient clinic for people with AIDS, opens at San Francisco General Hospital. The clinic develops the San Francisco Model of Care, a holistic approach that focuses not only on medical care but also on making patients comfortable, providing them with resources they need to deal with the many challenges of living with AIDS, and allowing patients facing severe social stigma to live, and in many cases die, with dignity. This compassionate model is adopted by medical professionals around the world and sets the standard for excellence in treating HIV-AIDS patients.

January 7 – The CDC reports the first cases of AIDS in women.

March 4 – The CDC publishes an article saying that AIDS is most prevalent “among gay men with multiple sexual partners, people who inject drugs, Haitians, and people with hemophilia.” It suggests that sexual contact and exposure to blood and blood products are the most likely vectors for the disease.

May 20 – Dr. Françoise Barré-Sinoussi and her colleagues at France’s Pasteur Institute report their discovery of a retrovirus believed to be the cause of AIDS. She and a colleague eventually receive the Nobel Prize for their work.

May 25 – The New York Times publishes its first front-page article on AIDS.

June 12 – At the National AIDS Forum in Denver, 11 gay men with AIDS take over the stage. They issue a statement laying out what becomes known as the Denver Principles, asserting the rights of people with AIDS to be protected from discrimination, to have their voices heard by organizations making decisions about AIDS research and treatment, and to respect and dignity. They also demand that the phrase “AIDS victims” be replaced by “people with AIDS.”

September 9 – The CDC rules out the possibility of transmission by casual contact, air, water, food, or environmental services, but misconceptions about the ways AIDS can be spread lingers for years.

November 22 – The World Health Organization convenes its first meeting on AIDS and begins formal surveillance of the illness.

Awareness Spreads, Misconceptions Linger


March 1 – A study in the American Journal of Medicine examines a cluster of 40 patients with KS and other opportunistic illnesses, tracing their sexual contacts. It describes an unidentified flight attendant, “Patient O” (the O standing for “outside Southern California,” where the study was focused), who was known to have hundreds of sexual partners a year. The report states this man had sexual contact with eight of the men in the study, and was the first patient in the study to show the onset of HIV/AIDS symptoms. Misconceptions around the study (and a misreading of Patient O”) give rise to the myth of Patient Zero, a promiscuous or even malicious gay man who single-handedly and knowingly touched off the AIDS pandemic in the United States.

April 23 – The Department of Health and Human Services announces the discovery of a retrovirus they call HTLV-III, the cause of AIDS. They also announce the development of a blood test and raise hopes that a vaccine could be developed in the next two years.

July 13 – The CDC recommends avoiding injection drug use and reducing needle sharing as ways of preventing transmission.


March 2 – The U.S. Food and Drug Administration licenses the first blood test for HIV, and blood banks begin screening the country’s blood supply.

April 22 – The Normal Heart, an autobiographical play about the early days of the crisis by Larry Kramer, opens off-Broadway.

July 25 – Rock Hudson, a legendary actor from the Golden Age of Hollywood whose homosexuality was an open secret in the industry, announces he has AIDS. Media coverage of AIDS increases dramatically in the following months.

August 27 – Ryan White, a teenager who contracted AIDS through donated blood, is barred from attending his middle school in Russiaville, Indiana due to his condition. The ensuing legal battle makes White a national figure, highlighting the stigma of the disease and the misconceptions surrounding how it is spread and who can contract it.

September 17 – President Ronald Reagan mentions AIDS publicly for the first time. He calls it a “top priority” and rebuffs accusations that his administration has not taken it seriously.

October 2 – Rock Hudson dies of an AIDS-related illness. He bequeaths $250,000 to create the American Foundation for AIDS Research.

A Public Health Crisis


January 16 – The CDC reports that 1985 saw an 89 percent increase in AIDS diagnoses from 1984, and predicts that the number will double in 1986.

May 1 – The International Committee on the Taxonomy of Viruses officially gives the name Human Immunodeficiency Virus, or HIV, to the virus that causes AIDS.

July 18 – A group of minority community leaders meet with Surgeon General C. Everett Koop to voice concerns about HIV/AIDS in communities of color, unofficially founding the National Minority AIDS Council.

November – In the Life: A Black Gay Anthology, the first collection of writings about the AIDS crisis from 29 Black, gay authors, is published. The book receives little mainstream attention at publication, but goes down in history as a watershed moment in gay literature.


February – Cleve Jones creates the first panel of the AIDS Memorial Quilt in honor of his friend Marvin Feldman, who died of an AIDS-related illness the previous October. Jones makes the panel three feet by six feet, the standard size of a grave plot, intending it and subsequent panels to serve as a way of remembering, grieving and celebrating the lives of people who have died from AIDS in a society where many families refused to acknowledge their cause of death and some funeral homes and cemeteries refused to handle their remains. The project becomes the NAMES Project.

February 4 – Legendary pianist Liberace dies of an AIDS-related illness. His doctor claims that Liberace, who had long denied rumors that he was gay, died of a heart attack. A week later, the actual cause of his death is revealed.

March 12 – Kramer helps found the AIDS Coalition to Unleash Power, or ACT UP, a direct-action group that pressures officials, governments, pharmaceutical companies, and other institutions to protect those at risk of HIV and those who have contracted it. The organization’s motto is “Silence = Death.” ACT UP begins agitating for increased access to experimental medications, as well as a coordinated national AIDS response.

March 19 – The FDA approves AZT, the first medication for treat AIDS. The treatment does not cure HIV-AIDS, but can be used to slow its progress and prevent transmission in some instances, such as during birth. The FDA also adjusts regulations to expand access to experimental medications.

March 31 – President Reagan and Prime Minister Jacques Chirac of France agree their countries will share credit for the discovery of HIV.

May 15 – The Public Health Service adds HIV to its immigration exclusion list. For the next 23 years, visa applicants are required to take a blood test and may be denied entry to the U.S. if they test positive.

May 31 – Reagan gives his first speech about AIDS. On June 24, he creates the first Presidential Commission on AIDS.

August 5 – A federal judge rules that a Florida school board cannot ban three HIV-positive brothers, Ricky, Robert, and Randy Ray, from attending school. The community of Arcadia, Florida responds with death threats, bomb threats and a school boycott.

August 18 – The FDA green-lights the first human test of a candidate vaccine against HIV.

August 28 – After weeks of threats following a ruling that they could not be banned from school for being HIV-positive, the home of brothers Ricky, Robert, and Randy Ray is burned to the ground while the family is staying elsewhere. The Rays later announce that they will leave Arcadia.

October 1 – The first national AIDS Awareness Month begins, with the CDC launching a massive public education campaign that warns “everyone is at risk.”

October 11  The NAMES Project displays its AIDS Memorial Quilt on the National Mall in Washington, D.C. for the first time. The Quilt bears the names of 1,920 people who died of AIDS-related illnesses when it is first displayed—the number eventually grows to over 10,000, making the Quilt the largest piece of community folk art in the world.

November – San Francisco Chronicle journalist Randy Shilts publishes And the Band Played On, a book about the early years of the AIDS crisis. Shilts traces the story of AIDS from the death of Grethe Rask to the death of Rock Hudson, arguing that the epidemic was allowed to happen thanks to incompetence, apathy, and discrimination against the populations it affected the most. His framing also leads to French Canadian flight attendant Gaëtan Dugas being identified as “Patient Zero.”


May 26 – The Surgeon General releases the nation’s first coordinated HIV/AIDS education strategy, mailing out 107 million copies of a pamphlet titled Understanding AIDS in an attempt to reach every household in America, the largest public mailing in history.

November 4  President Reagan signs the first comprehensive federal AIDS bill, the Health Omnibus Programs Extension (HOPE) Act, establishing the Office of AIDS Research and authorizing federal funds for AIDS prevention, research, and testing.

December 1 – The WHO declares the first World AIDS Day.


February 16 – Keith Haring, a pop artist whose graffiti-inspired works often promoted AIDS-related charities and other social causes, dies of an AIDS-related illness.

April 8 – Ryan White dies of an AIDS-related illness.

June 6 – The International AIDS Conference convenes in San Francisco, but a number of organizations boycott in protest of American immigration restrictions.

July 26 – President George H.W. Bush signs the Ryan White Comprehensive AIDS Resources Emergency Act, allocating over $220 million in federal funds for care and treatment of people with AIDS in its first year. The bill is the result of a bargain—in exchange for instituting “payer of last resort” programs to cover treatment for poor and uninsured people with HIV/AIDS, conservatives won the inclusion of clauses stipulating that certain funds will only be available to states that have passed harsh criminal laws against knowingly transmitting HIV.


May – The Visual AIDS’ Artists Caucus launches the Red Ribbon project, creating small red ribbons for people to wear to raise awareness and fight against the stigma of HIV/AIDS. The ribbons receive widespread attention the following month, when they are worn by a number of attendees and presenters at the 45th Tony Awards.

November 7  Earvin “Magic” Johnson, a future Hall of Fame basketball player and one of the most famous athletes in the country, announces that he has tested positive for HIV and will retire immediately. He does not elaborate on how he contracted the virus, but later acknowledges that he had unprotected sex with many women over the course of his career. The news reverberates around the country, and while rumors spread that Johnson is gay, for many his diagnosis confirms that straight people also face risk of contracting HIV/AIDS.

November 24 – Legendary Queen frontman Freddie Mercury dies of an AIDS-related illness, one day after announcing that he has AIDS. A gay icon and the first rock star known to have died of HIV/AIDS, his death sets of outpourings of grief around the world, as many in the AIDS activist community express their gratitude that he made his diagnosis public.


AIDS becomes the leading cause of death for American men aged 25 to 44.

April 8 – Tennis star Arthur Ashe, the only Black man to win singles titles at Wimbledon, the US Open and the Australian Open, announces that he is HIV-positive. He believes he contracted the virus via a blood transfusion he received during heart surgery.

April 20 – The Freddie Mercury Tribute Concert for AIDS Awareness draws a crowd of 72,000 to London’s Wembley Stadium.

December 13 – Fifteen-year-old Ricky, the oldest of the Ray brothers, dies of an AIDS-related illness.


February 3 – Rudolf Nureyev, a Soviet ballet dancer whose 1961 defection and subsequent performances with London’s Royal Ballet made him an international sensation, dies in Paris of an AIDS-related illness.

February 6 – Arthur Ashe dies of an AIDS-related illness.

June  President Bill Clinton establishes the Office of National AIDS Policy to coordinate federal effort to combat HIV/AIDS.

December 14 – Philadelphia, a major motion picture starring Tom Hanks as a gay man with AIDS and Denzel Washington as his lawyer in an anti-discrimination lawsuit, debuts to rave reviews. One of the first mainstream films to deal with homophobia and HIV/AIDS, it is a box office hit and Hanks wins Best Actor at the 66th Academy Awards.


AIDS becomes the leading cause of death for all Americans aged 25-44.

February 17 – Journalist Randy Shilts dies of an AIDS-related illness.

June – The FDA approves the first protease inhibitor, ushering in the era of highly active antiviral therapy (HAART). Over the next few years, aggressive treatments like this become the new standard in HIV care.

September 22  The National Academy of Sciences concludes that syringe exchange programs are effective in preventing the spread of HIV/AIDS.

November – The number of total AIDS cases reported in the United States passes 500,000.

November 11 – Pedro Zamora dies of an AIDS-related illness. The 22-year-old broke many barriers as a contestant on MTV’s The Real World, in which he discussed living with AIDS with his housemates, dispelled many misconceptions, and began a relationship with another contestant, with whom he shared the first same-sex commitment ceremony to be aired on American television.


February 23 – Greg Louganis, who swept the diving events at the 1984 and 1988 Olympics and is considered by many the greatest American diver ever, announces that he is HIV-positive. First diagnosed six months before the 1988 games, Louganis had kept his diagnosis and treatment a secret, even after coming out as gay in 1994.

READ MORE: How Greg Louganis’ Olympic Diving Accident Forced a Conversation About AIDS


The number of AIDS cases diagnosed annually in the U.S. declines for the first time since the pandemic began. AIDS ceases to be the leading cause of death for all Americans aged 25-44, although it remains the leading case of death among African Americans aged 25-44.


November 21 – The Food and Drug Administration Modernization Act institutes an accelerated drug-approval process, enshrining in law a demand frequently made by activists.


President Clinton declares HIV/AIDS a “severe and ongoing health crisis” in African American and Hispanic communities, after community leaders develop a “Call to Action” to address the dramatically disproportionate amount of cases in their communities. Congress soon allocates $156 million for the Minority AIDS initiative.


Despite declining numbers in the United States, the WHO announces that AIDS has become the fourth-leading cause of death worldwide and the number one killer in Africa.

HIV as the cause of AIDS

HIV/AIDS denialism is the belief that human immunodeficiency virus (HIV) does not cause acquired immune deficiency syndrome (AIDS), despite conclusive evidence to the contrary. Some of its proponents reject the existence of HIV, while others accept that HIV exists but argue that it is a harmless passenger virus and not the cause of AIDS. Insofar as they acknowledge AIDS as a real disease, they attribute it to some combination of sexual behaviorrecreational drugsmalnutrition, poor sanitationhaemophilia, or the effects of the medications used to treat HIV infection (antiretrovirals).

The scientific consensus is that the evidence showing HIV to be the cause of AIDS is conclusive and that HIV/AIDS denialist claims are pseudoscience based on conspiracy theories, faulty reasoning, cherry picking, and misrepresentation of mainly outdated scientific data. With the rejection of these arguments by the scientific community, HIV/AIDS denialist material is now targeted at less scientifically sophisticated audiences and spread mainly through the Internet.

Despite its lack of scientific acceptance, HIV/AIDS denialism has had a significant political impact, especially in South Africa under the presidency of Thabo Mbeki. Scientists and physicians have raised alarm at the human cost of HIV/AIDS denialism, which discourages HIV-positive people from using proven treatments. Public health researchers have attributed 330,000 to 340,000 AIDS-related deaths, along with 171,000 other HIV infections and 35,000 infant HIV infections, to the South African government’s former embrace of HIV/AIDS denialism. The interrupted use of antiretroviral treatments is also a major global concern as it potentially increases the likelihood of the emergence of antiretroviral-resistant strains of the virus.

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