Immunology => Acquired Immune Deficiency Syndrome (AIDS)
Acquired Immune Deficiency Syndrome (AIDS)
Acquired Immune Deficiency Syndrome (AIDS), specific group of diseases or conditions that result from suppression of the immune system, related to infection with the human immunodeficiency virus (HIV). A person infected with HIV gradually loses immune function along with certain immune cells called CD4 T-lymphocytes or CD4 T-cells, causing the infected person to become vulnerable to pneumonia, fungus infections, and other common ailments. With the loss of immune function, a clinical syndrome (a group of various illnesses that together characterize a disease) develops over time and eventually results in death due to opportunistic infections (infections by organisms that do not normally cause disease except in people whose immune systems have been greatly weakened) or cancers.
In the early 1980s deaths by opportunistic infections, previously observed mainly in organ transplant recipients receiving therapy to suppress their immune responses, were recognized in otherwise healthy homosexual men. In 1983 French cancer specialist Luc Montagnier and scientists at the Pasteur Institute in Paris isolated what appeared to be a new human retrovirus-a special type of virus that reproduces differently from other viruses-from the lymph node of a man at risk for AIDS. Nearly simultaneously, scientists working in the laboratory of American research scientist Robert Gallo at the National Cancer Institute in Bethesda, Maryland, and a group headed by American virologist Jay Levy at the University of California at San Francisco isolated a retrovirus from people with AIDS and from individuals having contact with people with AIDS. All three groups of scientists isolated what is now known as human immunodeficiency virus (HIV), the virus that causes AIDS.
Infection with HIV does not necessarily mean that a person has AIDS, although people who are HIV-positive are often mistakenly said to have AIDS. In fact, a person can remain HIV-positive for more than ten years without developing any of the clinical illnesses that define and constitute a diagnosis of AIDS. In 1998 an estimated 33.4 million people worldwide were living with HIV or AIDS-32.2 million adults and 1.2 million children. The World Health Organization (WHO) estimates that between 1981, when the first AIDS cases were reported, and the end of 1998, HIV has cost the lives of more than 13.9 million people. More than 430,000 of these deaths occurred in the United States.
CLINICAL PROGRESSION OF AIDS
The progression from the point of HIV infection to the clinical diseases that define AIDS may take six to ten years or more. This progression can be monitored using surrogate markers (laboratory data that correspond to the various stages of disease progression) or clinical endpoints (illnesses associated with more advanced disease). Surrogate markers for the various stages of HIV infection include the declining number of CD4 T-cells, the major type of white blood cell lost because of HIV infection. In general, the lower the infected person's CD4 T-cell count, the weaker the person's immune system and the more advanced the disease state. In 1996 it became evident that the actual amount of HIV in a person's blood-the so-called viral burden-could be used to predict the progression to AIDS, regardless of a person's CD4 T-cell count. With advancing technology, viral burden determinations are quickly becoming a standard means of patient testing.
An infected person's immune response to the virus-that is, the person's ability to produce antibodies against HIV-can also be used to determine the progression of AIDS; however, this surrogate marker is less precise during more advanced stages of AIDS because of the overall loss of immune function.
Within one to three weeks after infection with HIV, most people experience nonspecific flulike symptoms such as fever, headache, skin rash, tender lymph nodes, and a vague feeling of discomfort. These symptoms last about one to two weeks. During this phase, known as the acute retroviral syndrome phase, HIV reproduces to very high concentrations in the blood, mutates (changes its genetic nature) frequently, circulates through the blood, and establishes infections throughout the body, especially in the lymphoid organs. The infected person's CD4 T-cell count falls briefly but then returns to near normal levels as the person's immune system responds to the infection.
Individuals are thought to be highly infectious during this phase.
Following the acute retroviral syndrome phase, infected individuals enter a prolonged asymptomatic phase-a symptom-free phase that can last ten years or more. Persons with HIV remain in good health during this period, with levels of CD4 T-cells ranging from low to normal (500 to 750 cells per cubic mm of blood). Nevertheless, HIV continues to replicate during the asymptomatic phase, causing progressive destruction of the immune system.
Eventually, the immune system weakens to the point that the person enters the early symptomatic phase. This phase can last from a few months to several years and is characterized by rapidly falling levels of CD4 T-cells (500 to 200 cells per cubic mm of blood) and opportunistic infections that are not life threatening.
Following the early symptomatic phase, the infected person experiences the extensive immune destruction and serious illness that characterize the late symptomatic phase. This phase can also last from a few months to years, and the affected individual may have CD4 T-cell levels below 200 per cubic mm of blood along with certain opportunistic infections that define AIDS. A wasting syndrome of progressive weight loss and debilitating fatigue occurs in a large proportion of people in this stage. The immune system is in a state of severe failure. The person eventually enters the advanced AIDS phase, in which CD4 T-cell numbers are below 50 per cubic mm of blood. Death due to severe life-threatening opportunistic infections and cancers usually occurs within one to two years.
Death from AIDS is generally due not to HIV infection itself, but to opportunistic infections that occur when the immune system can no longer protect the body against agents normally found in the environment. The appearance of any one of more than 25 different opportunistic infections, called AIDS-defining illnesses, along with a CD4 T-cell count of less than 200 cells per cubic millimeter of blood provides the clinical diagnosis of AIDS in HIV-infected individuals.
The most common opportunistic infection seen in AIDS is Pneumocystis carinii pneumonia (PCP), which is caused by a fungus that normally exists in the airways of all people. Bacterial pneumonia and tuberculosis are also commonly associated with AIDS. In the late symptomatic phase of AIDS, bacterial infection by Mycobacterium avium can cause fever, weight loss, anemia, and diarrhea. Additional bacterial infections of the gastrointestinal tract commonly cause diarrhea, weight loss, loss of appetite, and fever. Also, during advanced AIDS, diseases caused by protozoal parasites, especially toxoplasmosis of the nervous system, are common.
In addition to PCP, people with AIDS often develop other fungal infections. Thrush, an infection of the mouth by the fungus Candida albicans, is common in the early symptomatic phase of AIDS. Other infectious fungi include species of the genus Cryptococcus, a major cause of meningitis in up to 13 percent of people with AIDS. Also, infection by the fungus Histoplasma capsulatum affects up to 10 percent of people with AIDS, causing general weight loss, fever, and respiratory complications or severe central nervous system complications if the infection reaches the brain.
Viral opportunistic infections, especially with members of the herpes virus family, are common in people with AIDS. One herpes family member, cytomegalovirus (CMV), infects the retina of the eye and can result in blindness. Another herpes virus, Epstein-Barr virus (EBV), may result in a cancerous transformation of blood cells. Infections with herpes simplex virus (HSV) types 1 and 2 are also common and result in progressive sores around the mouth and anus.
Many people with AIDS develop cancers, the most common types being B-cell lymphoma and Kaposi's sarcoma (KS). Kaposi's sarcoma-a cancer of blood vessels that results in purple lesions on the skin that can spread to internal organs and cause death-occurs mainly in homosexual and bisexual men. Although the cause of KS is unknown, a link between KS and a new type of herpes virus was discovered in 1994.
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
The causative agent of AIDS is HIV, a human retrovirus. Researchers have known since 1984 that HIV enters human cells by binding with a receptor protein known as CD4, located on human immune-cell surfaces. HIV carries on its surface a viral protein known as gp120, which specifically recognizes and binds to the CD4 protein molecules on the outer surface of human immune cells. However, in 1984 researchers found that CD4 by itself was not sufficient for HIV infection to take place. Some other unknown factor, found only in human cells, was also required. After much research, in 1996 scientists discovered that HIV must also bind to chemokine receptors, small proteins also found on the surface of human immune cells, to enter the cells. The first chemokine receptor linked to HIV entry was CXCR4 (originally called fusin), which is bound by HIV strains that dominate during the latter stages of the disease. Researchers then determined that another chemokine receptor, CCR5, bound HIV strains that dominate in the early stages of the disease. Researchers are continuously discovering more chemokine receptors.
Any human cell that has the correct binding molecules on its surface is a potential target for HIV infection. However, it is the specific class of human white blood cells called CD4 T-cells that are most affected by HIV because these cells have numerous CD4 molecules on their outer surfaces. HIV replication in CD4 T-cells can kill the cells directly; however, the cells also may be killed or rendered dysfunctional by indirect means without ever having been infected with HIV. CD4 T-cells are critical in the normal immune system because they help other types of immune cells respond to invading organisms. As CD4 T-cells are specifically killed during HIV infection, no help is available for immune responses. General immune system failure results, permitting the opportunistic infections and cancers that characterize clinical AIDS.
Although it is generally agreed that HIV is the virus that causes AIDS and that HIV replication can directly kill CD4 T-cells, the large variation among individuals in the amount of time between infection with HIV and a diagnosis of AIDS has led to speculation that other cofactors-that is, factors acting along with HIV-may influence the course of disease. The exact nature of these cofactors is uncertain-it is believed that they may include genetic, immunologic, and environmental factors or other diseases. However, it is clear that HIV must be present for the development of AIDS.
For years scientists have speculated that HIV spread from chimpanzees to humans, but no conclusive evidence for this pattern of infection existed. Moreover, scientists did not know when the virus first infected humans; HIV could have been passed to humans centuries ago, or decades ago. Two discoveries provide clues that may help solve these mysteries. In 1998 a team of researchers identified what is believed to be the oldest known case of AIDS, an African man who died in 1959. Scientists believe that the form of HIV that killed this man, which probably first infected him in the 1940s or early 1950s, is the close ancestor of the HIV strains infecting more than 33.4 million people today. Then, in early 1999, a team of researchers found the first conclusive evidence that HIV spread from chimpanzees to humans on at least three separate occasions in central Africa, probably beginning in the 1940s or 1950s.
MODES OF TRANSMISSION
HIV is spread through the exchange of body fluids, primarily semen, blood, and blood products. It is most commonly spread by sexual contact with an infected person. The virus is present in the sexual secretions of infected men and women and gains access to the bloodstream of the uninfected person by passing between the cells of a protective tissue layer or by way of small abrasions that may occur as a consequence of sexual intercourse.
HIV is also spread by any sharing of needles or syringes that results in direct exposure to the blood of an infected individual. This method of exposure occurs most commonly among people abusing intravenous (IV) drugs (drugs injected into the veins).
HIV transmission through blood transfusions or use of blood-clotting factors is now extremely rare because of extensive screening of the blood supply; it is estimated that undetected HIV is present in fewer than 1 in 450,000 to 600,000 units of blood.
HIV can be transmitted from an infected mother to her baby, either before or during childbirth, or through breast-feeding. Although only about 25 to 35 percent of babies born to HIV-infected mothers worldwide actually become infected, this mode of transmission accounts for 90 percent of all cases of AIDS in children. In addition, even uninfected children born to HIV-infected mothers have an incidence of heart problems 12 times that of children in the general population.
In the health care setting, workers have been infected with HIV after being stuck with needles containing HIV-infected blood or, less frequently, after infected blood contacts the worker's open cut or splashes into a mucous membrane (for example, the eyes or the inside of the nose). There has been only one demonstrated instance of patients being infected by a health-care worker; this involved HIV transmission from an infected dentist to six patients. In general, infected health-care workers pose no risk to their patients. There is also no risk of contracting HIV infection while donating blood.
The routes of HIV transmission are well known, but unfounded fear continues concerning the potential for transmission by other means, such as casual contact in a household, school, workplace, or food-service setting. No scientific evidence to support any of these fears has been found. HIV does not survive well when exposed to the environment. Drying of HIV-infected human blood or other body fluids reduces the theoretical risk of environmental transmission to essentially zero. Additionally, HIV is unable to reproduce outside its living host; therefore, it does not spread or maintain infectiousness outside its host.
No cases of HIV transmission through the air, by casual contact, or even by kissing an infected individual have been documented. A protein in saliva, known as secretory leukocyte protease inhibitor (SLPI), prevents HIV from infecting white blood cells. However, practices that increase the likelihood of contact with the blood of an infected individual, such as open-mouth kissing or sharing toothbrushes or razors, should be avoided. There is also no known risk of HIV transmission to coworkers, clients, or consumers from contact in food-service establishments.
Studies have shown no evidence of HIV transmission through insects-even in areas where there are many cases of AIDS and large populations of insects such as mosquitoes. HIV lives for only a short time inside an insect and does not reproduce. Thus, even if the virus enters a mosquito or another sucking or biting insect, the insect does not become infected and cannot transmit HIV to the next human it feeds on or bites.
The nature of the AIDS epidemic is constantly evolving. In the United States, HIV infection was initially concentrated in the homosexual community-where widespread transmission occurred because of high-risk sexual behavior-and in people with hemophilia and other individuals receiving blood products. HIV infection then became established among people who abuse intravenous (IV) drugs and was spread by heterosexual contact (sexual relations between partners of the opposite sex) into all groups of society, especially through prostitution and other forms of high-risk sexual practices. Currently, male homosexual interactions (sexual relations between men) account for about 48 percent of AIDS cases, and practices involving IV drug abuse account for about 26 percent. The heterosexual spread of AIDS in the United States, especially from infected males to previously uninfected females, is increasing rapidly and now accounts for 10 percent of transmissions.
Of the more than 665,000 AIDS cases reported in the United States between 1981 and 1998, about 45 percent have been in Caucasians, 36 percent in blacks, 18 percent in Hispanics, and 1 percent in Asians. Adult males make up about 83 percent of these cases and adult females 16 percent. Children account for the remaining 1 percent of AIDS cases. Women and children constitute one of the fastest-growing groups of people with AIDS. Through June 1998, 54 documented cases and 133 possible cases of occupational transmission of AIDS/HIV infection had been reported in health-care workers.
On a global scale, the AIDS epidemic is rapidly expanding. Of the estimated 33.4 million people worldwide living with HIV or AIDS in 1998, a full 68 percent were living in sub-Saharan Africa, yet inhabitants of this continent constitute just 10 percent of the global population. Since the start of the epidemic, 83 percent of all AIDS deaths have been in Africa. The hardest hit region is sub-Saharan Africa: In some urban areas, one in four people have HIV, and 70 percent of the people who became infected with HIV this year live there.
Infection rates in other regions, while low compared with those of sub-Saharan Africa, also increase each year. Twenty-two percent of the 33.4 million people living with AIDS or HIV live in southern and eastern Asia and the Pacific, 4 percent in Latin America, 4 percent in North America and the Caribbean, and 2 percent in Europe and Central Asia. In Asia, Africa, and most countries of the Caribbean, the vast majority of people contract the disease through heterosexual contact.
The major strain of HIV in the United States, Europe, and central Africa is known as HIV-1. In western Africa, AIDS is also caused by HIV-2, a strain of HIV closely related to HIV-1. Other distantly related strains of HIV-1 have been identified in various areas of the world. Although some of these strains cannot be detected with current blood-screening methods, there is little risk of these viruses spreading to the United States because of their geographic isolation. Even in the case of HIV-2, spread outside Africa is rare. Only 64 cases of HIV-2 have been documented in the United States, and transmission in these cases was linked directly to western Africa.
DETECTION AND DIAGNOSIS
Although AIDS has been tracked in the United States since 1981, the identification of HIV as the causative agent was not made until 1983. In 1985 the first blood test for HIV, developed by the research group led by Robert Gallo, was approved for use in blood banks. This test can detect whether a person's blood contains antibodies against HIV, an indication of exposure to the virus. However, for about four to eight weeks after exposure to HIV, an individual will continue to test negative for HIV infection because the immune system has not had enough time to make antibodies against HIV. In 1996 an additional blood test was approved for use in blood banks. This test can detect HIV antigens-proteins produced by the virus itself. The test can thus identify HIV even before the donor's immune system has had a chance to make antibodies. New, more sensitive tests, which detect the viral genetic material, are being evaluated for their ability to detect the virus even earlier. An estimated 50 million blood samples are tested each year in the United States by blood banks, plasma centers, reference laboratories, private clinics, and health departments. Due to the major differences in the protein components of HIV-1 and HIV-2, separate tests were developed to detect these two related viruses. As new strains of HIV are identified from around the world, they will need to be evaluated for detection by these tests.
The Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, has established an authoritative definition for the diagnosis of AIDS: In an HIV-positive individual, the CD4 T-cell count must be below 200 cells per cubic mm of blood, or there must be the clinical appearance of an initial AIDS-defining opportunistic infection, such as PCP (Pneumocystis carinii pneumonia), oral candidiasis (thrush), pulmonary tuberculosis, or invasive cervical carcinoma (cancer of the cervix in women).
Antiviral drugs that attack HIV exploit vulnerable spots in the viral replication cycle. One target is the process of reverse transcription-that is, the conversion of the viral ribonucleic acid (RNA) into deoxyribonucleic acid (DNA)-that HIV must undergo to be infectious. Reverse transcription is a process unique to retroviruses and is performed by the viral enzyme reverse transcriptase (RT). One class of anti-HIV drugs, known as nucleosides, are all RT inhibitors. Five nucleosides are currently licensed by the U.S. Food and Drug Administration (FDA): zidovudine (Retrovir, AZT), didanosine (Videx, ddI), zalcitabine (Hivid, ddC), stavudine (Zerit, d4T), lamivudine (Epivir, 3TC), and abacavir (Ziagen, ABC). These drugs work as DNA-chain terminators. Because the drug appears to be a normal nucleotide base (the building block of DNA), the RT enzyme mistakenly inserts the drug into the growing viral DNA chain. Once the drug is inserted, no additional DNA bases can be added, and therefore viral DNA synthesis is terminated.
Although the nucleosides are more likely to interact with the viral RT enzyme, they also can be incorporated by the enzyme responsible for normal cellular DNA synthesis in the person receiving the drug, leading to toxicity (poisoning) and side effects. Such drug incorporation is usually observed in rapidly dividing cell types, such as the cells of the bone marrow, spongy tissue filling the cavities within bones.
A second problem is the emergence of drug-resistant forms of HIV in people receiving these drugs. Studies on early treatment of HIV infection with AZT have presented contradictory results as to whether such early treatment prolongs life. Because HIV replicates rapidly and mutates frequently during the earliest period of infection, an HIV-infected person carries many different strains of HIV, some of which may be drug-resistant. The limited variety of HIV in the early stage is thought to make it more susceptible to AZT and related drugs.
Although RT inhibitors were never considered a cure for HIV infection, it was hoped that they would slow the progression of AIDS, and AZT has been shown effective in reducing HIV transmission from pregnant women to their babies. However, the clinical benefit of RT inhibitors when used alone has been largely disappointing; they have extended the lives of people with AIDS by only about six months. When taken in conjunction with other RT inhibitors, however, they have been more effective. For example, AZT combined with lamivudine prevents the AIDS virus from developing resistance to AZT even though the virus quickly develops resistance to lamivudine. The combination also has been shown to boost CD4 T-cell counts and to lower levels of HIV in the blood.
RT inhibitors are also effective when used with a new class of anti-HIV drugs known as protease inhibitors, approved by the FDA in December 1995. Protease inhibitors work by crippling a key viral enzyme called protease, which is vital to the reproduction of HIV in the later stages of its replication cycle.After HIV replicates-that is, makes copies of its own protein components-these proteins must be cut to specific sizes before they can assemble into a mature virus. Protease is responsible for trimming the new HIV proteins to their required dimensions. When protease is blocked-or inhibited-the proteins are not cut and the defective HIV cannot infect new cells. The first protease inhibitor drug, saquinavir (Invirase), was approved for use in combination with nucleoside drugs such as AZT. In March 1996 two additional drugs, ritonavir (Norvir) and indinavir (Crivaxin), were rapidly approved for use alone or in combination with nucleosides. Nelfinavir (Viracept), was approved by the FDA in March 1997 and a fifth protease inhibitor, amprenavir (Angenerase), was approved in April 1999.
Preliminary results from four American and European studies indicate that these drugs cause dramatic increases in the number of CD4 T-cells and decreases in the amount of virus in the blood. These results are about two to three times more powerful than those seen with the nucleoside drugs. However, HIV can quickly develop resistance to these new drugs, at least when they are used alone. Resistance can be delayed when the agents are combined with other anti-HIV drugs-for example, the nucleosides.
In fact, the most effective treatment against HIV is now considered to be a combination of three drugs taken together-two nucleoside RT inhibitors and one protease inhibitor. Although these drug combinations, commonly called antiviral cocktails, may cause severe side effects (such as diarrhea, abdominal cramps, and anemia), when taken properly they can reduce blood levels of the virus to undetectable levels. Each drug must be taken according to specific guidelines, however, and one missed dose can allow the virus to quickly mutate to a strain that resists the drugs.
These drug combinations can also consist of two nucleoside RT inhibitors and one non-nucleoside RT inhibitor, a new class of anti-HIV drug first recommended for approval by the FDA in June 1996. These drugs work similarly to nucleoside RT inhibitors in that they bind to the HIV reverse transcriptase enzyme. However, they do not compete with other nucleosides for binding sites. The first drug of this type to be developed was nevirapine (Viramune), which was appproved by the FDA in April 1997. Two other non-nucleoside RT inhibitors, delavirdine (Rescriptin) and efavirenz (Sustiva), followed in 1997 and 1998, respectively. All three drugs are effective only when taken with nucleoside RT inhibitors; they should not be used with protease inhibitors.
The benefits of combination treatment have been extraordinary. Some patients who appeared near death are now back at work. Mortality rates from AIDS in the United States have declined significantly in recent years. For those aged 25 to 44, HIV-infection dropped from the leading cause of death in 1995 to third-leading in 1996 and the fifth-leading in 1997, the most recent year for which statistics are available. This newfound optimism must be tempered with caution, however, as drug combination treatment is still relatively new and little is known about its long-term success rate. Moreover, outside of industrialized nations, combination therapy is prohibitively expensive. The cost of treating a single patient ranges from $10,000 to $12,000 yearly, an unattainable sum in most regions of the world.
The development of antiviral therapies for HIV is complex, and each new approach and drug must be extensively evaluated for safety and effectiveness. The general perception that this evaluation process causes unnecessary delays in providing therapies spurred public demonstrations against the FDA. These demonstrations have resulted in policy changes that make experimental drugs and approaches more readily available to people with AIDS, even before the drugs or approaches are approved. Although early availability of a drug entails the risk that it may be used in people before its toxicity and side effects are fully understood, many people with AIDS are willing to take this risk with the hope that the drug may prove effective.
Effective drug treatments are available to fight many AIDS-associated opportunistic infections, and these treatments have provided clinical benefit and prolonged survival for individuals with AIDS. Recent drug treatments for PCP have dramatically decreased illness and death due to this opportunistic infection. Antifungal drugs such as amphotericin B and fluconazole are effective against AIDS-related fungal infections. The antiherpes drugs ganciclovir and foscarnet are used to treat CMV retinitis and other herpes diseases. Because these therapies require medical supervision and are often needed on an extended basis, a network of community hospices has been established to provide low-cost outpatient care for individuals with AIDS. Some hospices provide shelter and compassionate support for people living with AIDS.
Gene therapy, an approach that involves altering the genes of the infected person to help prevent the virus from spreading to uninfected cells, might someday be used to treat HIV infection. Gene therapy has been used in clinical trials to inhibit HIV by introducing into cells a new gene that interferes with the viral regulatory proteins. In other trials, gene therapy has been used to introduce a new gene that protects the cells from becoming infected by HIV.
Efforts also are under way to develop an effective immunization that could be either protective, preventing infection if an immunized person is exposed to HIV, or therapeutic, prolonging survival or decreasing immune destruction in people already infected with HIV. The World Health Organization (WHO) is currently sponsoring a large-scale trial of a protective-vaccine candidate in areas of the world where the rate of HIV infection is just beginning to rise dramatically. In 1998 the FDA approved the first large-scale trial of an AIDS vaccine in uninfected volunteers who are at high risk for exposure. The vaccine, made from the viral protein gp120, is designed to stimulate the production of antibodies that could protect against HIV infection. The vaccine is being tested for safety and effectiveness in Thailand and North America.
With the discovery in 1996 that HIV must bind to chemokine receptors as well as CD4 molecules, researchers also began to develop synthetic laboratory agents that might block HIV from attaching to these receptors and casing infection. Individuals who lack CCR5 receptors due to a genetic defect appear to be protected from contracting the disease.
Because there is as yet no successful vaccination against HIV, prevention efforts have focused mainly on educating the public about routes of HIV transmission and about personal measures that reduce the risk of infection. The CDC has established the National AIDS Clearinghouse, a hotline to disseminate educational literature and current statistics on AIDS. Safe-sex campaigns encourage sexual abstinence or monogamy (sexual relations with only one partner) and the use of latex condoms to provide a protective barrier during sexual intercourse. Needle-exchange programs have been implemented to reduce needle sharing and consequent HIV transmission among IV drug abusers. The U.S. government has set strict guidelines for health-care settings, including use of protective clothing and proper instrument disposal, to decrease the risk of transmission to both the patient and the health care provider. On a national scale, screening of the blood supply has greatly reduced the risk of contracting HIV from blood products. However, with the exception of blood screening, these prevention programs have had only limited success.
Many people consider HIV infection and AIDS to be completely preventable because the routes of HIV transmission are so well known. To completely prevent transmission, however, dramatic changes in sexual behavior and drug dependence would have to occur throughout the world. Furthermore, prevention efforts that promote sexual awareness through open discussion and condom distribution in public schools have been opposed because of the fear that these efforts may encourage sexual activity. Similarly, needle exchange programs have been criticized as promoting drug abuse. Prevention programs that identify HIV-infected individuals and notify their sexual partners, as well as programs that promote HIV testing at the time of marriage or pregnancy, have been criticized for invading personal privacy.
Efforts aimed at public awareness have been propelled by community-based organizations such as Project Inform and Act-Up, which provide current information to HIV-infected individuals and to individuals at risk for infection. Public figures and celebrities who are themselves HIV infected or who have died from AIDS-including American basketball player Magic Johnson, American actor Rock Hudson, American diver Greg Louganis, and American tennis player Arthur Ashe-have personalized the disease of AIDS and thereby helped society come to terms with the enormity of the epidemic. As a memorial to people who have died from AIDS, especially in the early years of the epidemic, friends and families of AIDS victims stitched together a giant quilt in which each panel of the quilt was dedicated to the memory of an individual who died from AIDS. This quilt has traveled on display from community to community to promote AIDS awareness.
The U.S. government has also attempted to assist HIV-infected individuals through legislation and additional community-funding measures. In 1990 HIV-infected people were included in the Americans with Disabilities Act, making discrimination against people with AIDS for jobs, housing, and other social benefits illegal. Additionally, the Ryan White Comprehensive AIDS Resources Emergency Act established a community-funding program designed to assist in the daily lives of people living with AIDS. This congressional act was named in memory of a young man who contracted HIV through blood products and became a public figure for his courage in fighting the disease and community prejudice. The act is still in place, although continued funding for such social programs is threatened by opposition in the U.S. Congress.
The lack of effective vaccines and antiviral drugs for AIDS has spurred speculation that the funding for AIDS research is insufficient. Although the actual amount of government funding for AIDS research is large, most of these funds are used for expensive clinical studies to evaluate new drugs. Many scientists believe that not enough is known about the basic biology of HIV and recommend shifting the emphasis of AIDS research to basic research that could ultimately result in more effective medicines.