Course Objectives

1.  Identify the psychosocial and cultural considerations necessary when working with HIV positive patients.

2.  Describe the stigma associated with the HIV virus.

3.  Describe counseling techniques that can be used before and after HIV testing.

4.  Identify the treatment protocol most often used with HIV/AIDS patients.

5.  Describe the tests most often used to detect the HIV virus.

6.  Describe the risks and benefits of drug treatment for pregnant women.


Where did HIV come from?

The earliest known case of HIV-1 in a human was from a blood sample collected in 1959 from a man in Kinshasa, Democratic Republic of Congo. (How he became infected is not known.) Genetic analysis of this blood sample suggested that HIV-1 may have stemmed from a single virus in the late 1940s or early 1950s.

We know that the virus has existed in the United States since at least the mid- to late 1970s. From 1979-1981 rare types of pneumonia, cancer, and other illnesses were being reported by doctors in Los Angeles and New York among a number of male patients who had sex with other men. These were conditions not usually found in people with healthy immune systems.

In 1982 public health officials began to use the term "acquired immunodeficiency syndrome," or AIDS, to describe the occurrences of opportunistic infections, Kaposi's sarcoma (a kind of cancer), and Pneumocystis carinii pneumonia in previously healthy people. Formal tracking (surveillance) of AIDS cases began that year in the United States.

In 1983, scientists discovered the virus that causes AIDS. The virus was at first named HTLV-III/LAV (human T-cell lymphotropic virus-type III/lymphadenopathy- associated virus) by an international scientific committee. This name was later changed to HIV (human immunodeficiency virus).

For many years scientists theorized as to the origins of HIV and how it appeared in the human population, most believing that HIV originated in other primates. Then in 1999, an international team of researchers reported that they had discovered the origins of HIV-1, the predominant strain of HIV in the developed world. A subspecies of chimpanzees native to west equatorial Africa had been identified as the original source of the virus. The researchers believe that HIV-1 was introduced into the human population when hunters became exposed to infected blood.

Scientists Discover Origin of HIV-1

Today scientists reported that they have discovered the origin of HIV-1, the virus responsible for the global AIDS pandemic. A subspecies of chimpanzees native to west equatorial Africa has been identified as the original source of the virus.

Beatrice H. Hahn, M.D., of the University of Alabama at Birmingham, a grantee of the National Institute of Allergy and Infectious Diseases (NIAID), led the international team of investigators. They describe their findings in the February 4 issue of Nature. The journal moved the normal press embargo ahead to coincide with Dr. Hahn’s presentation of the study details on the opening night of the 6th Conference on Retroviruses and Opportunistic Infections in Chicago.

"This is an important finding with significant potential," notes Anthony S. Fauci, M.D., NIAID director. "We now have chimpanzee isolates of simian immunodeficiency virus [SIVcpz] that have been shown by careful molecular analysis to be closely related to HIV-1. Furthermore, this virus infects a primate species that is 98 percent related to humans. This may allow us – if done carefully and in collaboration with primatologists working to protect this endangered species – to study infected chimpanzees in the wild to find out why these animals don’t get sick, information that may help us better protect humans from developing AIDS."

Until now, HIV-1’s origin had been unclear. Although most scientists suspected that the virus descended from a primate species, only three chimpanzees infected with viruses related to HIV-1 had been documented, and one of these viruses correlated only weakly with HIV-1.

When Dr. Hahn and her collaborators recently identified a fourth chimpanzee infected with SIVcpz, they decided to use this opportunity to carefully examine all four viruses and the animals from which they were derived. With sophisticated genetic techniques, they analyzed the four SIVcpz isolates and compared them with various HIV-1 viruses taken from humans. They also determined the subspecies identity of the chimpanzees: three belonged to a subspecies native to west equatorial Africa, Pan troglodytes troglodytes. The fourth, the chimpanzee infected with a virus most unlike HIV-1, belonged to an east African subspecies known as Pan troglodytes schweinfurthii.

As it turns out, the three isolates from the Pan troglodytes troglodytes chimpanzees strongly resemble the different subgroups of HIV-1, namely groups M (responsible for the pandemic), N and O (both found only in west equatorial Africa). Their investigation also revealed that some of the viruses resulted from genetic recombination in the chimpanzees before they infected humans.

Their other significant find, Dr. Fauci notes, is that the natural habitat of these chimpanzees directly coincides with the pattern of the HIV-1 epidemic in this area of Africa. Putting all these pieces of the puzzle together, Dr. Hahn and her colleagues conclude that Pan troglodytes troglodytes is the natural reservoir of HIV-1 and has been the source of at least three independent occurrences of cross-species virus transmission events from chimpanzees to humans.

The authors believe that HIV-1 was introduced into the human population when hunters became exposed to infected blood. Furthermore, they speculate that humans might still be at risk for cross-species transmission because the bushmeat trade – the hunting and killing of chimpanzees and other endangered animals for human consumption – is still common practice in west equatorial Africa.

This new report suggests that preserving the wild chimpanzee populations will be crucial for further carefully designed studies to better understand how cross-species virus transmission occurs and how infected chimpanzees resist disease, studies that in turn may lead to new strategies for designing HIV drugs and vaccines.

A positive HIV test result means that the person has been infected with HIV (Human Immunodeficiency Virus), the vi type of whrus that causes AIDS (Acquired Immune Deficiency Syndrome). HIV disease progresses to AIDS when the CD4+ T cell count drops below 200 cells/mm, and/or you develop an AIDS-defining condition. CD4+ T cells are aite blood cell that fights infections. When HIV enters a person’s CD4+ T cell, it uses the cell to make copies of itself. This process destroys the CD4+ T cells, weakening the immune system and making it harder for the body to fight infections.The AIDS Surveillance Case Definition of the U.S. Centers for Disease Control and Prevention

A diagnosis of AIDS is made whenever a person is HIV-positive and:

he or she has a CD4+ cell count below 200 cells per micro liter OR his or her CD4+ cells account for fewer than 14 percent of all lymphocytes OR that person has been diagnosed with one or more of the AIDS-defining illnesses listed below.
AIDS is caused by infection with a virus called human immunodeficiency virus (HIV). This virus is passed from one person to another through blood-to-blood and sexual contact. In addition, infected pregnant women can pass HIV to their babies during pregnancy or delivery, as well as through breast feeding.

White blood cells of the immune system provide a first line of defense against viruses and cancers. White blood cells affected with the HIV virus resist treatment by disguising themselves as protease inhibitors. Other cells of the immune system that get infected with AIDS are CD4-possitive T-cells, which orchestrate the immune response, and monocyte macrophage cells, which collect infected cells.

Body fluids that pass the Virus: blood, semen, vaginal fluid, breast milk other body fluids containing blood. There are additional body fluids that may transmit the virus that health care workers may come into contact with: cerebrospinal fluid surrounding the brain and the spinal cord, synovial fluid surrounding bone joints and amniotic fluid surrounding a fetus.

How HIV Causes AIDS

A significant component of the research effort of the National Institute of Allergy and Infectious Diseases (NIAID) is devoted to the pathogenesis of HIV (human immunodeficiency virus) disease. Studies on pathogenesis address the complex mechanisms that result in the destruction of the immune system of an HIV-infected person. A detailed understanding of HIV and how it establishes infection and causes AIDS (acquired immunodeficiency syndrome) is crucial to identifying and developing effective drugs and vaccines to fight HIV and AIDS. This fact sheet summarizes the state of knowledge in this area.


Untreated HIV disease is characterized by a gradual deterioration of immune function. Most notably, crucial immune cells called CD4 positive (CD4+) T cells are disabled and killed during the typical course of infection. These cells, sometimes called "T-helper cells," play a central role in the immune response, signaling other cells in the immune system to perform their special functions.

A healthy, uninfected person usually has 800 to 1,200 CD4+ T cells per cubic millimeter (mm3) of blood. During untreated HIV infection, the number of these cells in a person's blood progressively declines. When the CD4+ T cell count falls below 200/mm3, a person becomes particularly vulnerable to the opportunistic infections and cancers that typify AIDS, the end stage of HIV disease. People with AIDS often suffer infections of the lungs, intestinal tract, brain, eyes, and other organs, as well as debilitating weight loss, diarrhea, neurologic conditions, and cancers such as Kaposi's sarcoma and certain types of lymphomas.

Most scientists think that HIV causes AIDS by directly inducing the death of CD4+ T cells or interfering with their normal function, and by triggering other events that weaken a person's immune function. For example, the network of signaling molecules that normally regulates a person's immune response is disrupted during HIV disease, impairing a person's ability to fight other infections. The HIV-mediated destruction of the lymph nodes and related immunologic organs also plays a major role in causing the immunosuppression seen in people with AIDS. Immunosuppression by HIV is confirmed by the fact that medicines, which interfere with the HIV lifecycle, preserve CD4+ T cells and immune function as well as delay clinical illness.


Although HIV was first identified in 1983, studies of previously stored blood samples indicate that the virus entered the U.S. population sometime in the late 1970s. In the United States, 886,575 cases of AIDS, and 501,669 deaths among people with AIDS had been reported to the Centers for Disease Control and Prevention (CDC) by the end of 2002. Approximately 40,000 new HIV infections occur each year in the United States, 70 percent of them among men and 30 percent among women. Of the new infections, approximately 40 percent are from male-to-male contact, 30 percent from heterosexual contact, and 25 percent from injection drug use. Minority groups in the United States have also been disproportionately affected by the epidemic.

Worldwide, an estimated 38 million people were living with HIV/AIDS as of December 2003, according to the Joint United Nations Programme on HIV/AIDS (UNAIDS) . Through 2003, cumulative AIDS-associated deaths worldwide numbered more than 20 million. Globally, approximately 5 million new HIV infections and approximately 3 million AIDS-related deaths, including an estimated 490,000 children under 15 years old, occurred in the year 2003 alone.


HIV belongs to a class of viruses called retroviruses. Retroviruses are RNA (ribonucleic acid) viruses, and in order to replicate (duplicate). they must make a DNA (deoxyribonucleic acid) copy of their RNA. It is the DNA genes that allow the virus to replicate.

Like all viruses, HIV can replicate only inside cells, commandeering the cell's machinery to reproduce. Only HIV and other retroviruses, however, once inside a cell, use an enzyme called reverse transcriptase to convert their RNA into DNA, which can be incorporated into the host cell's genes.

Slow viruses

HIV belongs to a subgroup of retroviruses known as lentiviruses, or "slow" viruses. The course of infection with these viruses is characterized by a long interval between initial infection and the onset of serious symptoms.

Other lentiviruses infect nonhuman species. For example, the feline immunodeficiency virus (FIV) infects cats and the simian immunodeficiency virus (SIV) infects monkeys and other nonhuman primates. Like HIV in humans, these animal viruses primarily infect immune system cells, often causing immune deficiency and AIDS-like symptoms. These viruses and their hosts have provided researchers with useful, albeit imperfect, models of the HIV disease process in people.


The viral envelope

HIV has a diameter of 1/10,000 of a millimeter and is spherical in shape. The outer coat of the virus, known as the viral envelope, is composed of two layers of fatty molecules called lipids, taken from the membrane of a human cell when a newly formed virus particle buds from the cell. Evidence from NIAID-supported research indicates that HIV may enter and exit cells through special areas of the cell membrane known as "lipid rafts." These rafts are high in cholesterol and glycolipids and may provide a new target for blocking HIV.

Embedded in the viral envelope are proteins from the host cell, as well as 72 copies (on average) of a complex HIV protein (frequently called "spikes") that protrudes through the surface of the virus particle (virion). This protein, known as Env, consists of a cap made of three molecules called glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure in the viral envelope. Much of the research to develop a vaccine against HIV has focused on these envelope proteins.

The viral core

Within the envelope of a mature HIV particle is a bullet-shaped core or capsid, made of 2,000 copies of another viral protein, p24. The capsid surrounds two single strands of HIV RNA, each of which has a copy of the virus's nine genes. Three of these genes, gag, pol, and env, contain information needed to make structural proteins for new virus particles. The env gene, for example, codes for a protein called gp160 that is broken down by a viral enzyme to form gp120 and gp41, the components of Env.

Six regulatory genes, tat, rev, nef, vif, vpr, and vpu, contain information necessary to produce proteins that control the ability of HIV to infect a cell, produce new copies of virus, or cause disease. The protein encoded by nef, for instance, appears necessary for the virus to replicate efficiently, and the vpu-encoded protein influences the release of new virus particles from infected cells. Recently, researchers discovered that Vif (the protein encoded by the vif gene) interacts with an antiviral defense protein in host cells (APOBEC3G), causing inactivation of the antiviral effect and enhancing HIV replication. This interaction may serve as a new target for antiviral drugs.

The ends of each strand of HIV RNA contain an RNA sequence called the long terminal repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell.

The core of HIV also includes a protein called p7, the HIV nucleocapsid protein. Three enzymes carry out later steps in the virus's life cycle: reverse transcriptase, integrase, and protease. Another HIV protein called p17, or the HIV matrix protein, lies between the viral core and the viral envelope.


Entry of HIV into cells

Infection typically begins when an HIV particle, which contains two copies of the HIV RNA, encounters a cell with a surface molecule called cluster designation 4 (CD4). Cells carrying this molecule are known as CD4+ cells.

One or more of the virus's gp120 molecules binds tightly to CD4 molecule(s) on the cell's surface. The binding of gp120 to CD4 results in a conformational change in the gp120 molecule allowing it to bind to a second molecule on the cell surface known as a co-receptor. The envelope of the virus and the cell membrane then fuse, leading to entry of the virus into the cell. The gp41 of the envelope is critical to the fusion process. Drugs that block either the binding or the fusion process are being developed and tested in clinical trials. The Food and Drug Administration (FDA) has approved one of the so-called fusion inhibitors, T20, for use in HIV-infected people.

Studies have identified multiple coreceptors for different types of HIV strains. These coreceptors are promising targets for new anti-HIV drugs, some of which are now being tested in preclinical and clinical studies. Agents that block the co-receptors are showing particular promise as potential microbicides that could be used in gels or creams to prevent HIV transmission. In the early stage of HIV disease, most people harbor viruses that use, in addition to CD4, a receptor called CCR5 to enter their target cells. With disease progression, the spectrum of co-receptor usage expands in approximately 50 percent of patients to include other receptors, notably a molecule called CXCR4. Virus that uses CCR5 is called R5 HIV and virus that uses CXCR4 is called X4 HIV.

Although CD4+ T cells appear to be the main targets of HIV, other immune system cells with and without CD4 molecules on their surfaces are infected as well. Among these are long-lived cells called monocytes and macrophages , which apparently can harbor large quantities of the virus without being killed, thus acting as reservoirs of HIV. CD4+ T cells also serve as important reservoirs of HIV; a small proportion of these cells harbor HIV in a stable, inactive form. Normal immune processes may activate these cells, resulting in the production of new HIV virions.

Cell-to-cell spread of HIV also can occur through the CD4-mediated fusion of an infected cell with an uninfected cell.

Reverse transcription

In the cytoplasm of the cell, HIV reverse transcriptase converts viral RNA into DNA, the nucleic acid form in which the cell carries its genes. Fifteen of the 26 antiviral drugs approved in the United States for treating people with HIV infection work by interfering with this stage of the viral life cycle.


The newly made HIV DNA moves to the cell's nucleus, where it is spliced into the host's DNA with the help of HIV integrase. HIV DNA that enters the DNA of the cell is called a provirus. Several drugs that target the integrase enzyme are in the early stages of development and are being investigated for their potential as antiretroviral agents.


For a provirus to produce new viruses, RNA copies must be made that can be read by the host cell's protein-making machinery. These copies are called messenger RNA (mRNA), and production of mRNA is called transcription, a process that involves the host cell's own enzymes. Viral genes in concert with the cellular machinery control this process; the tat gene, for example, encodes a protein that accelerates transcription. Genomic RNA is also transcribed for later incorporation in the budding virion.

Cytokines, proteins involved in the normal regulation of the immune response, also may regulate transcription. Molecules such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, secreted in elevated levels by the cells of HIV-infected people, may help to activate HIV proviruses. Other infections, by organisms such as Mycobacterium tuberculosis , also may enhance transcription by inducing the secretion of cytokines.


After HIV mRNA is processed in the cell's nucleus, it is transported to the cytoplasm. HIV proteins are critical to this process; for example, a protein encoded by the rev gene allows mRNA encoding HIV structural proteins to be transferred from the nucleus to the cytoplasm. Without the rev protein, structural proteins are not made. In the cytoplasm, the virus co-opts the cell's protein-making machinery-including structures called ribosomes-to make long chains of viral proteins and enzymes, using HIV mRNA as a template. This process is called translation.

Assembly and budding

Newly made HIV core proteins, enzymes, and genomic RNA gather inside the cell and an immature viral particle forms and buds off from the cell, acquiring an envelope that includes both cellular and HIV proteins from the cell membrane. During this part of the viral life cycle, the core of the virus is immature and the virus is not yet infectious. The long chains of proteins and enzymes that make up the immature viral core are now cut into smaller pieces by a viral enzyme called protease.

This step results in infectious viral particles. Drugs called protease inhibitors interfere with this step of the viral life cycle. FDA has approved eight such drugs-saquinavir, ritonavir, indinavir, amprenavir, nelfinavir, fosamprenavir, atazanavir, and lopinavir-for marketing in the United States. Recently, an HIV inhibitor that targets a unique step in the viral life cycle, very late in the process of viral maturation, has been identified and is currently undergoing further development.

Recently, researchers have discovered that virus budding from the host cell is much more complex than previously thought. Binding between the HIV Gag protein and molecules in the cell directs the accumulation of HIV components in special intracellular sacks, called multivesicular bodies (MVB), that normally function to carry proteins out of the cell. In this way, HIV actively hitch-hikes out of the cell in the MVB by hijacking normal cell machinery and mechanisms. Discovery of this budding pathway has revealed several potential points for intervening in the viral replication cycle.


Among adults, HIV is spread most commonly during sexual intercourse with an infected partner. During intercourse, the virus can enter the body through the mucosal linings of the vagina, vulva, penis, or rectum or, rarely, via the mouth and possibly the upper gastrointestinal tract after oral sex. The likelihood of transmission is increased by factors that may damage these linings, especially other sexually transmitted infections that cause ulcers or inflammation.

Research suggests that immune system cells of the dendritic cell type, which live in the mucosa, may begin the infection process after sexual exposure by binding to and carrying the virus from the site of infection to the lymph nodes where other immune system cells become infected. A molecule on the surface of dendritic cells, DC-SIGN, may be critical for this transmission process.

HIV also can be transmitted by contact with infected blood, most often by the sharing of needles or syringes contaminated with minute quantities of blood containing the virus. The risk of acquiring HIV from blood transfusions is extremely small in the United States, as all blood products in this country are screened routinely for evidence of the virus.

Almost all HIV-infected children in the United States get the virus from their mothers before or during birth. In the United States, approximately 25 percent of pregnant HIV-infected women not receiving antiretroviral therapy have passed on the virus to their babies. In 1994, researchers showed that a specific regimen of the drug AZT (zidovudine) can reduce the risk of transmission of HIV from mother to baby by two-thirds. The use of combinations of antiretroviral drugs and simpler drug regimens has further reduced the rate of mother-to-child HIV transmission in the United States.

In developing countries, cheap and simple antiviral drug regimens have been proven to significantly reduce mother-to-child transmission at birth in resource-poor settings. Unfortunately, the virus also may be transmitted from an HIV-infected mother to her infant via breastfeeding. Moreover, due to the use of medicines to prevent transmission at delivery, breastfeeding may become the most common mode of HIV infection in infants. Thus, development of affordable alternatives to breastfeeding is greatly needed.


Once it enters the body, HIV infects a large number of CD4+ cells and replicates rapidly. During this acute or primary phase of infection, the blood contains many viral particles that spread throughout the body, seeding various organs, particularly the lymphoid organs.

Two to 4 weeks after exposure to the virus, up to 70 percent of HIV-infected people suffer flu-like symptoms related to the acute infection. Their immune system fights back with killer T cells (CD8+ T cells) and B-cell-produced antibodies , which dramatically reduce HIV levels. A person's CD4+ T cell count may rebound somewhat and even approach its original level. A person may then remain free of HIV-related symptoms for years despite continuous replication of HIV in the lymphoid organs that had been seeded during the acute phase of infection.

One reason that HIV is unique is the fact that despite the body's aggressive immune responses, which are sufficient to clear most viral infections, some HIV invariably escapes. This is due in large part to the high rate of mutations that occur during the process of HIV replication. Even when the virus does not avoid the immune system by mutating, the body's best soldiers in the fight against HIV-certain subsets of killer T cells that recognize HIV-may be depleted or become dysfunctional.

In addition, early in the course of HIV infection, people may lose HIV-specific CD4+ T cell responses that normally slow the replication of viruses. Such responses include the secretion of interferons and other antiviral factors, and the orchestration of CD8+ T cells.

Finally, the virus may hide within the chromosomes of an infected cell and be shielded from surveillance by the immune system. Such cells can be considered as a latent reservoir of the virus. Because the antiviral agents currently in our therapeutic arsenal attack actively replicating virus, they are not effective against hidden, inactive viral DNA (so-called provirus). New strategies to purge this latent reservoir of HIV have become one of the major goals for current research efforts.

HIV/AIDS and Stigma

 HIV-related stigma refers to all unfavorable attitudes, beliefs, and policies directed toward people perceived to have HIV/AIDS as well as toward their significant others and loved ones, close associates, social groups, and communities. Patterns of prejudice, which include devaluing, discounting, discrediting, and discriminating against these groups of people, play into and strengthen existing social inequalities—especially those of gender, sexuality, and race—that are at the root of HIV-related stigma.

Erving Goffman is widely credited for conceptualizing and creating a framework for the study of stigma. His work was seminal in creating an environment for ongoing academic research on the topic. In his landmark book Stigma: Notes on the Management of Spoiled Identity (1963), Goffman described stigma as “an attribute that is deeply discrediting within a particular social interaction” (p. 3). His explanation of stigma focuses on the public’s attitude toward a person who possesses an attribute that that falls short of societal expectations. The person with the attribute is “reduced in our minds from a whole and usual person to a tainted, discounted one” (p. 3). Goffman further explained that stigma falls into three categories:

1.   Abominations of the body—various physical deformities.

2.   Blemishes of individual character—weak will, domineering or unnatural passions, treacherous and rigid beliefs, or dishonesty. Blemishes of character are inferred from, for example, mental disorder, imprisonment, addiction, alcoholism, homosexuality, unemployment, suicidal attempts, or radical political behavior.

3.  Tribal stigma of race, nation, and religion—beliefs that are transmitted through lineages and equally contaminate all members of a family (Goffman, 1963).

The stigma concept has been applied to myriad circumstances (Link and Phelan, 2001). Goffman’s ideas are a common thread in much of the published research and provide the theoretical underpinnings for much of the literature on stigma and stereotyping.

According to Goffman and other researchers, diseases associated with the highest degree of stigma share common attributes:

  • The person with the disease is seen as responsible for having the illness
  • The disease is progressive and incurable
  • The disease is not well understood among the public
  • The symptoms cannot be concealed.

HIV infection fits the profile of a condition that carries a high level of stigmatization (Goffman, 1963; Herek, 1999; Jones et al., 1988). First, people infected with HIV are often blamed for their condition and many people believe HIV could be avoided if individuals made better moral decisions. Second, although HIV is treatable, it is nevertheless a progressive, incurable disease (Herek, 1999; Stoddard, 1994). Third, HIV transmission is poorly understood by some people in the general population, causing them to feel threatened by the mere presence of the disease. Finally, although asymptomatic HIV infection can often be concealed, the symptoms of HIV-related illness cannot. HIV-related symptoms may be considered repulsive, ugly, and disruptive to social interaction (Herek, 1999).

The discrimination and devaluation of identity associated with HIV-related stigma do not occur naturally. Rather, they are created by individuals and communities who, for the most part, generate the stigma as a response to their own fears. HIV-related stigma manifests itself in various ways. HIV-positive individuals, their loved ones, and even their caregivers are often subjected to rejection by their social circles and communities when they need support the most. They may be forced out of their homes, lose their jobs, or be subjected to violent assault. For these reasons, HIV-related stigma must be recognized and addressed as a life-altering phenomenon. Hiv Aids continuing education, aids ceus for psychologists, psychologist ceu

HIV-related stigma has been further divided into the following categories:

Instrumental HIV-related stigma—a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness (Herek, 1999)

Symbolic HIV-related stigma—the use of HIV/AIDS to express attitudes toward the social groups or “lifestyles” perceived to be associated with the disease (Herek, 1999)

Courtesy HIV-related stigma—stigmatization of people connected to the issue of HIV/AIDS or HIV- positive people (Snyder, 1999, based on Goffman, 1963).

Stigma and Access to Care

The literature devoted to stigma and access to care falls roughly into three categories. Most of the literature deals with barriers to care that HIV-positive individuals encounter across the continuum from HIV diagnosis to end of life. The next largest category of studies documents the reluctance of health care providers to treat individuals with HIV infection. Finally, a few studies cover the stigma experienced by providers of ancillary and support services to people living with HIV/AIDS.


HIV/AIDS-related stigma affects issues related to HIV testing including delays in testing, the effect of delay on further transmission of HIV, and individuals’ responses to testing positive (Chesney and Smith, 1999). Early detection of HIV infection is important. Knowledge of one’s HIV seropositivity can lead to earlier treatment and improved outcomes (Herek, 1990). Knowledge of seropositivity also can lead to changes in risk behaviors that can reduce or eliminate the risk of HIV transmission. A Kaiser Health Poll report (2000) suggested that fear of being stigmatized by HIV/AIDS has some relationship to people’s decisions about getting tested for HIV. One-third of survey respondents said that if they were tested for HIV, they would be “very” or “somewhat” concerned that people would think less of them if they discovered that they had been tested. In addition, 8 percent of people who had never been tested for HIV said that worries about confidentiality played a part in their decision not to have the test.

Studies provide evidence that stigma is associated with delays in HIV testing among individuals who are at high risk of being infected with HIV (Myers et al., 1993; Stall et al., 1996). In a study of gay and bisexual men who were unaware of their HIV status, two-thirds of the participants expressed a fear of discrimination against people with HIV and said it was a reason for not getting tested (Stall et al., 1996). Earlier in the epidemic, HIV stigmatization was shown to influence the way in which at-risk populations approached HIV testing. People at risk for HIV infection were more likely to seek testing that was offered anonymously (i.e., no names were recorded) than testing that was offered confidentially (i.e., names were kept in confidential files) (Fehrs et al., 1988; Johnson et al., 1988).

HIV/AIDS-related stigma also influences individuals’ responses to testing positive: It aggravates the psychological burden of receiving a positive HIV test (Chesney and Smith, 1999). Earlier in the epidemic, there were reports of severe psychological responses to notification, including denial, anxiety, depression, and suicidal ideation (Coates et al., 1987; Ostrow et al., 1989). Over time, studies have shown a decrease in severe reactions to being notified of positive test results; however, research continues to show that notification is associated with high distress. Distress is greatest immediately after notification and typically declines within 2 to 10 weeks (Ironson et al., 1990; Perry et al., 1990). Stigma also affects the care of HIV-positive individuals. After a person tests positive, he or she faces decisions that include how to enter and adhere to care and whether to disclose HIV seropositivity to partners, friends, family, colleagues, employers, and health care providers (Chesney and Smith, 1999). At each level, a decision to disclose seropositivity may either enhance access to support and care or expose the individual to stigmatization and potential discrimination.


Accessing health care can be a challenge for people who are HIV positive, because the health care system itself is often a source of stigma. Health care professionals, particularly those who infrequently encounter HIV-positive people, can be insensitive to their patients’ concerns about stigma. In addition, health care professionals are not always knowledgeable about appropriate procedures for maintaining patient confidentiality (Herek et al., 1998).

The literature on caregiving reveals that stigmatization is evident among health care providers. Fear of contagion and fear of death have clear negative effects on health care providers’ attitudes toward and treatment of HIV-positive patients (Gerbert et al., 1991; Weinberger et al., 1992).  Health care providers also may fear stigmatization themselves because of their work with HIV-positive patients (Durham, 1994). Caregivers, whether professionals or volunteers, risk what Goffman called “courtesy stigma,” in which they are stigmatized as a result of their association with HIV/AIDS and people living with HIV disease. That stigma may influence their willingness to work with people with HIV or may make their work more difficult (Snyder et al., 1999). Isolation is a significant issue for seropositive clients. Hiv Aids continuing education, aids ceus for psychologists, psychologist ceu


United States:  Through December 2001, a total of 816,149 cases of AIDS had been reported to the CDC.

Worldwide: Based on estimates from the United Nations AIDS program (UNAIDS), approximately 65 million people have been infected with HIV since the start of the global epidemic. At the end of 2002, an estimated 42 million people were living with HIV infection or AIDS.

UNAIDS estimates 5.0 million new HIV infections occurred in 2002. This represents about 14,000 new cases per day. An estimated 3.1 million adults and children died of HIV/AIDS in 2002.


Among people enrolled in large epidemiologic studies in Western countries, the median time from infection with HIV to the development of AIDS-related symptoms has been approximately 10 to 12 years in the absence of antiretroviral therapy. Researchers, however, have observed a wide variation in disease progression. Approximately 10 percent of HIV-infected people in these studies have progressed to AIDS within the first 2 to 3 years following infection, while up to 5 percent of individuals in the studies have stable CD4+ T cell counts and no symptoms even after 12 or more years.

Factors such as age or genetic differences among individuals, the level of virulence of an individual strain of virus, and co-infection with other microbes may influence the rate and severity of disease progression. Drugs that fight the infections associated with AIDS have improved and prolonged the lives of HIV-infected people by preventing or treating conditions such as Pneumocystis carinii pneumonia, cytomegalovirus disease, and diseases caused by a number of fungi.

HIV co-receptors and disease progression

Recent research has shown that most infecting strains of HIV use a co-receptor molecule called CCR5, in addition to the CD4 molecule, to enter certain of its target cells. HIV-infected people with a specific mutation in one of their two copies of the gene for this receptor may have a slower disease course than people with two normal copies of the gene. Rare individuals with two mutant copies of the CCR5 gene appear, in most cases, to be completely protected from HIV infection. Mutations in the gene for other HIV co-receptors also may influence the rate of disease progression.

Viral burden and disease progression

Numerous studies show that people with high levels of HIV in their bloodstream are more likely to develop new AIDS-related symptoms or die than those with lower levels of virus. For instance, in the Multicenter AIDS Cohort Study (MACS), investigators showed that the level of HIV in an untreated person's plasma 6 months to a year after infection-the so-called viral "set point"-is highly predictive of the rate of disease progression; that is, patients with high levels of virus are much more likely to get sicker faster than those with low levels of virus. The MACS and other studies have provided the rationale for providing aggressive antiretroviral therapy to HIV-infected people, as well as for routinely using newly available blood tests to measure viral load when initiating, monitoring, and modifying anti-HIV therapy.

Potent combinations of three or more anti-HIV drugs known as highly active antiretroviral therapy, or HAART, can reduce a person's "viral burden" (amount of virus in the circulating blood) to very low levels and in many cases delay the progression of HIV disease for prolonged periods. Before the introduction of HAART therapy, 85 percent of patients survived an average of 3 years following AIDS diagnosis. Today, 95 percent of patients who start therapy before they get AIDS survive on average 3 years following their first AIDS diagnosis. For those who start HAART after their first AIDS event, survival is still very high at 85 percent, averaging 3 years after AIDS diagnosis.

Antiretroviral regimens, however, have yet to completely and permanently suppress the virus in HIV-infected people. Recent studies have shown that, in addition to the latent HIV reservoir discussed above, HIV persists in a replication-competent form in resting CD4+ T cells even in people receiving aggressive antiretroviral therapy who have no readily detectable HIV in their blood. Investigators around the world are working to develop the next generation of anti-HIV drugs that can stop HIV, even in these biological scenarios.

A treatment goal, along with reduction of viral burden, is the reconstitution of the person's immune system, which may have become sufficiently damaged that it cannot replenish itself. Various strategies for assisting the immune system in this regard are being tested in clinical trials in tandem with HAART, such as the Evaluation of Subcutaneous Proleukin in a Randomized International Trial (ESPRIT) trial exploring the effects of the T cell growth factor, IL-2.


Although HIV-infected people often show an extended period of clinical latency with little evidence of disease, the virus is never truly completely latent although individual cells may be latently infected. Researchers have shown that even early in disease, HIV actively replicates within the lymph nodes and related organs, where large amounts of virus become trapped in networks of specialized cells with long, tentacle-like extensions. These cells are called follicular dendritic cells (FDCs). FDCs are located in hot spots of immune activity in lymphoid tissue called germinal centers. They act like flypaper, trapping invading pathogens (including HIV) and holding them until B cells come along to start an immune response.

Over a period of years, even when little virus is readily detectable in the blood, significant amounts of virus accumulate in the lymphoid tissue, both within infected cells and bound to FDCs. In and around the germinal centers, numerous CD4+ T cells are probably activated by the increased production of cytokines such as TNF-alpha and IL-6 by immune system cells within the lymphoid tissue. Activation allows uninfected cells to be more easily infected and increases replication of HIV in already infected cells.

While greater quantities of certain cytokines such as TNF-alpha and IL-6 are secreted during HIV infection, other cytokines with key roles in the regulation of normal immune function may be secreted in decreased amounts. For example, CD4+ T cells may lose their capacity to produce IL-2, a cytokine that enhances the growth of other T cells and helps to stimulate other cells' response to invaders. Infected cells also have low levels of receptors for IL-2, which may reduce their ability to respond to signals from other cells.

Breakdown of lymph node architecture

Ultimately, with chronic cell activation and secretion of inflammatory cytokines, the fine and complex inner structure of the lymph node breaks down and is replaced by scar tissue. Without this structure, cells in the lymph node cannot communicate and the immune system cannot function properly. Investigators also have reported recently that this scarring reduces the ability of the immune system to replenish itself following antiretroviral therapy that reduces the viral burden.


CD8+ T cells are critically important in the immune response to HIV. These cells attack and kill infected cells that are producing virus. Thus, vaccine efforts are directed toward eliciting or enhancing these killer T cells, as well as eliciting antibodies that will neutralize the infectivity of HIV.

CD8+ T cells also appear to secrete soluble factors that suppress HIV replication. Several molecules, including RANTES, MIP-1alpha, MIP-1beta, and MDC appear to block HIV replication by occupying the coreceptors necessary for many strains of HIV to enter their target cells. There may be other immune system molecules-including the so-called CD8 antiviral factor (CAF), the defensins (type of antimicrobials), and others yet undiscovered-that can suppress HIV replication to some degree.


HIV replicates rapidly; several billion new virus particles may be produced every day. In addition, the HIV reverse transcriptase enzyme makes many mistakes while making DNA copies from HIV RNA. As a consequence, many variants or strains of HIV develop in a person, some of which may escape destruction by antibodies or killer T cells. Additionally, different strains of HIV can recombine to produce a wide range of variants.

During the course of HIV disease, viral strains emerge in an infected person that differ widely in their ability to infect and kill different cell types, as well as in their rate of replication. Scientists are investigating why strains of HIV from people with advanced disease appear to be more virulent and infect more cell types than strains obtained earlier from the same person. Part of the explanation may be the expanded ability of the virus to use other co-receptors, such as CXCR4.


Researchers around the world are studying how HIV destroys or disables CD4+ T cells, and many think that a number of mechanisms may occur simultaneously in an HIV-infected person. Data suggest that billions of CD4+ T cells may be destroyed every day, eventually overwhelming the immune system's capacity to regenerate.

Direct cell killing

Infected CD4+ T cells may be killed directly when large amounts of virus are produced and bud out from the cell surface, disrupting the cell membrane, or when viral proteins and nucleic acids collect inside the cell, interfering with cellular machinery.


Infected CD4+ T cells may be killed when the regulation of cell function is distorted by HIV proteins, probably leading to cell suicide by a process known as programmed cell death or apoptosis. Recent reports indicate that apoptosis occurs to a greater extent in HIV-infected people, both in their bloodstream and lymph nodes. Apoptosis is closely associated with the aberrant cellular activation seen in HIV disease.

Uninfected cells also may undergo apoptosis. Investigators have shown in cell cultures that the HIV envelope alone or bound to antibodies sends an inappropriate signal to CD4+ T cells causing them to undergo apoptosis, even if not infected by HIV.

Innocent bystanders

Uninfected cells may die in an innocent bystander scenario: HIV particles may bind to the cell surface, giving them the appearance of an infected cell and marking them for destruction by killer T cells after antibody attaches to the viral particle on the cell. This process is called antibody-dependent cellular cytotoxicity.

Killer T cells also may mistakenly destroy uninfected cells that have consumed HIV particles and that display HIV fragments on their surfaces. Alternatively, because HIV envelope proteins bear some resemblance to certain molecules that may appear on CD4+ T cells, the body's immune responses may mistakenly damage such cells as well.


Researchers have shown in cell cultures that CD4+ T cells can be turned off by activation signals from HIV that leaves them unable to respond to further immune stimulation. This inactivated state is known as anergy.

Damage to precursor cells

Studies suggest that HIV also destroys precursor cells that mature to have special immune functions, as well as the microenvironment of the bone marrow and the thymus needed for developing such cells. These organs probably lose the ability to regenerate, further compounding the suppression of the immune system.


Although monocytes and macrophages can be infected by HIV, they appear to be relatively resistant to being killed by the virus. These cells, however, travel throughout the body and carry HIV to various organs, including the brain, which may serve as a hiding place or "reservoir" for the virus that may be relatively resistant to most anti-HIV drugs.

Neurologic manifestations of HIV disease are seen in up to 50 percent of HIV-infected people, to varying degrees of severity. People infected with HIV often experience

1. Cognitive symptoms, including impaired short-term memory, reduced concentration, and mental slowing
2. Motor symptoms such as fine motor clumsiness or slowness, tremor, and leg weakness
3. Behavioral symptoms including apathy, social withdrawal, irritability, depression, and personality change
4. More serious neurologic manifestations in HIV disease typically occur in patients with high viral loads, generally when a person has advanced HIV disease or AIDS.

Neurologic manifestations of HIV disease are the subject of many research projects. Current evidence suggests that although nerve cells do not become infected with HIV, supportive cells within the brain, such as astrocytes and microglia (as well as monocyte/macrophages that have migrated to the brain) can be infected with the virus. Researchers postulate that infection of these cells can cause a disruption of normal neurologic functions by altering cytokine levels, by delivering aberrant signals, and by causing the release of toxic products in the brain. The use of anti-HIV drugs frequently reduces the severity of neurologic symptoms, but in many cases does not, for reasons that are unclear. The impact of long-term therapy and long-term HIV disease on neurologic function is also unknown and under intensive study.

During a normal immune response, many parts of the immune system are mobilized to fight an invader. CD4+ T cells, for instance, may quickly multiply and increase their cytokine secretion, thereby signaling other cells to perform their special functions. Scavenger cells called macrophages may double in size and develop numerous organelles , including lysosomes that contain digestive enzymes used to process ingested pathogens. Once the immune system clears the foreign antigen, it returns to a relative state of quiescence.

Paradoxically, although it ultimately causes immune deficiency, HIV disease for most of its course is characterized by immune system hyperactivation, which has negative consequences. As noted above, HIV replication and spread are much more efficient in activated CD4+ cells. Chronic immune system activation during HIV disease also may result in a massive stimulation of B cells, impairing the ability of these cells to make antibodies against other pathogens.

Chronic immune activation also can result in apoptosis, and an increased production of cytokines that not only may increase HIV replication but also have other deleterious effects. Increased levels of TNF-alpha, for example, may be at least partly responsible for the severe weight loss or wasting syndrome seen in many HIV-infected people.

The persistence of HIV and HIV replication plays an important role in the chronic state of immune activation seen in HIV-infected people. In addition, researchers have shown that infections with other organisms activate immune system cells and increase production of the virus in HIV-infected people. Chronic immune activation due to persistent infections, or the cumulative effects of multiple episodes of immune activation and bursts of virus production, likely contribute to the progression of HIV disease.


The clinical spectrum of disease among people with HIV has changed dramatically in the era of HAART. NIAID and its grantees are actively studying the new clinical syndrome of disease among persons on long term-therapy. Research is concentrating on the impact of HIV over the long term, the toxicity of the medicines used to control HIV, and the effects of aging on HIV disease progression. People with HIV have a variety of conditions including diabetes, heart disease, neurocognitive decline, and cancers that may, or may not, be directly due to HIV or its treatment. Long-term studies of people with HIV in the United States and abroad are underway.

United States Statistics

HIV ranks 5th among the leading causes of death for all persons between the ages of 35 and 44, but 2nd among Hispanic males of that age group and 1st among African-American males of that age.

HIV/AIDS was the 5th leading cause of death for U.S. women aged 25-44. Among African American women in this same age group, HIV/AIDS was the third leading cause of death in 1999.

Men Who Have Sex with Men

In the United States, HIV-related illness and death historically have had a tremendous impact on men who have sex with men. Even with the increase among drug users, men having sex with men continues to account for the largest number of people reported with AIDS each year.

HIV Testing


In the early 1980s when the epidemic began, AIDS (acquired immunodeficiency disease) patients were not likely to live longer than a few years. With the development of safe and effective drugs, however, people infected with HIV (human immunodeficiency virus) now have longer and healthier lives.

The discovery and development of new therapeutic strategies against HIV is one of the highest priorities for the National Institute of Allergy and Infectious Diseases (NIAID). Research supported by NIAID has already greatly advanced our understanding of HIV and how it causes AIDS. This knowledge provides the foundation for NIAID’s HIV/AIDS research effort and continues to support studies designed to further extend and improve the quality of life of those infected with HIV.


Currently, there are 26 antiretroviral drugs approved by the Food and Drug Administration to treat individuals infected with HIV. These drugs fall into three major classes.

  1. Reverse transcriptase (RT) inhibitors interfere with the critical step during the HIV life cycle known as reverse transcription. During this step, reverse transcriptase, an HIV enzyme, converts HIV RNA to HIV DNA. There are two main types of RT inhibitors.

  2. Nucleoside/nucleotide RT inhibitors are faulty DNA building blocks. When these faulty pieces are incorporated into the HIV DNA (during the process when the HIV RNA is converted to HIV DNA), the DNA chain cannot be completed, thereby blocking HIV from replicating in a cell.

    • Non-nucleoside RT inhibitors bind to reverse transcriptase, interfering with its ability to convert the HIV RNA into HIV DNA.

  3. Protease inhibitors (PI) interfere with the protease enzyme that HIV uses to produce infectious viral particles.

  4. Fusion inhibitors interfere with the virus’ ability to fuse with the cellular membrane, thereby blocking entry into the host cell.


Currently available drugs do not cure HIV infection or AIDS. They can suppress the virus, even to undetectable levels, but are unable to completely eliminate HIV from the body. Hence, infected patients still need to take antiretroviral drugs.


As HIV reproduces itself, different strains of the virus emerge, some that are resistant to antiretroviral drugs. Therefore, doctors recommend patients infected with HIV take a combination of antiretroviral drugs known as HAART. This strategy, which typically combines drugs from at least two different classes of antiretroviral drugs, has been shown to effectively suppress the virus when used properly. Developed by NIAID-supported researchers, HAART has revolutionalized how we treat people infected with HIV by successfully suppressing the virus and decreasing the rate of opportunistic infections.


Although the use of HAART has greatly reduced the number of deaths due to HIV/AIDS, this powerful combination of drugs cannot suppress the virus completely. Therefore, people infected with HIV who take antiretroviral drugs can still transmit HIV to others through unprotected sex and needle sharing.


People infected with HIV have impaired immune systems that can leave them susceptible to opportunistic infections (OIs) and AIDS-associated co-infections, caused by a wide range of microorganisms such as protozoa, viruses, fungi, and bacteria. One example is hepatitis C virus (HCV) infection which can lead to liver cancer.

Potent HIV therapies such as HAART, however, have produced dramatic responses in patients by suppressing HIV and slowing the progression of OIs and AIDS-associated co-infections. These therapies allow the immune system to recover, sustain, and protect the body from other infections. Hence, antiretroviral drugs provide a way for the immune system to remain intact and effective, thereby improve the quality and duration of life for people with HIV.


People taking antiretroviral drugs often have low adherence to complicated drug regimens. The current recommended regimen involves taking several antiretroviral drugs each day from at least two different classes, some of which may require fasting and cause unpleasant side effects such as nausea and vomiting. In addition, antiretroviral drugs may cause more serious medical problems, including metabolic changes such as abnormal fat distribution, abnormal lipid and glucose metabolism, and bone loss. Therefore, NIAID is investigating simpler, less toxic, and more effective drug regimens.


NIAID supports the development and testing of new therapeutic agents, classes, and combinations of antiretroviral drugs that will be able to continuously suppress the virus with few side effects. Through clinical trials involving volunteers, NIAID-supported studies will provide accurate and extensive information about the safety and efficacy of the new drug candidates and combinations, and will identify potential uncommon, but important, toxicities of newly approved agents. Studies are also underway to assess rare toxicities of older approved agents, especially as a result of long-term use.

Through the Multicenter AIDS Cohort Study and Women’s Interagency HIV Study, NIAID supports long-term studies of HIV disease and its treatment in both men and women. Since their inception, these cohort studies have enrolled and collected data from more than 10,000 people. In addition, NIAID supports treatment studies conducted through three HIV/AIDS clinical trials networks: Adult AIDS Clinical Trials Groups, Pediatric AIDS Clinical Trials Groups, and the Terry Beirn Community Programs for Clinical Research on AIDS.

To expand upon and better coordinate the global HIV/AIDS research activities, NIAID is restructuring all of its HIV clinical trials research networks to increase collaboration, efficiency, harmonization, and flexibility. This new structure is designed to encourage greater integration of vaccine, prevention, and treatment research; to improve upon research efforts; and to address high priority research questions, particularly in resource-limited settings where AIDS is most devastating.


NIAID supports studies aimed at understanding the side effects of antiretroviral drugs as well as strategies to reduce exposure to potentially toxic drug regimens, such as

  • Structured treatment interruption (STI) protocols

  • Use of immune-based therapies with HAART

  • Studies to compare different dosing schedules

  • Studies to compare early versus delayed treatment

NIAID also supports projects evaluating regimens containing agents associated with toxicities. For example, NIAID-funded researchers are conducting studies to evaluate treatments for several drug-associated metabolic complications, including fat redistribution, lipid and glucose abnormalities, and bone loss. In addition, researchers are studying the long-term metabolic effects of various antiretroviral regimens in pregnant women and their infants and in HIV-infected children and adolescents.


The Pharmaceutical Research and Manufacturers Association of America maintains a database of new drugs in development to treat HIV infection. They include new protease inhibitors and more potent, less toxic RT inhibitors, as well as other drugs that interfere with entirely different steps in the virus’ lifecycle. These new categories of drugs include

  • Entry inhibitors that interfere with HIV's ability to enter cells

  • Integrase inhibitors that interfere with HIV's ability to insert its genes into a cell's normal DNA

  • Assembly and budding inhibitors that interfere with the final stage of the HIV life cycle, when new virus particles are released into the bloodstream

  • Cellular metabolism modulators that interfere with the cellular processes needed for HIV replication

  • Gene therapy that uses modified genes inserted directly into cells to suppress HIV replication. These cells are designed to produce T cells that are genetically resistant to HIV infection.

In addition, scientists are learning how immune modulators help boost the immune response to the virus and may make the existing anti-HIV drugs more effective. Therapeutic vaccines also are being evaluated for this purpose and could help reduce the number of anti-HIV drugs needed or the duration of treatment.

HIV TESTING Characteristics and Applications of HIV Test Technologies

Only FDA-approved HIV tests should be used for diagnostic purposes. Routine screening in the United States for HIV-2 and HIV-1 group O infections is not generally recommended unless geographic, behavioral, or clinical information indicates that infection with these strains might be present. Several HIV test technologies have been approved by FDA for diagnostic use in the United States. These tests enable testing of different fluids (i.e., whole blood, serum, plasma, oral fluid, and urine) . The available technologies

  • enable specimen collection procedures that are less invasive and more acceptable than venipuncture, thus helping expand HIV testing into nontraditional settings (with home sample collection tests, oral fluid tests, and urine-based tests);

  • enable provision of HIV test results during a single visit at the time of testing (with rapid tests) ; and

  • increase the convenience of HIV testing (with home sample collection tests).

The decision to adopt a particular test technology in a clinical or nontraditional setting should be based on several factors, including

  • accuracy of the test,

  • client preferences and acceptability,

  • likelihood of client returning for results,

  • cost and mechanism for provider reimbursement,

  • ease of sample collection,

  • complexity of laboratory services required for the test,

  • availability of trained personnel, and

  • FDA approval of the test.

Home Testing Versus Home Sample Collection

FDA has not approved home-use HIV test kits, which allow consumers to purchase a test kit, collect a sample in private, and interpret their own HIV test results in a few minutes. The Federal Trade Commission has warned that some home-use HIV test kits, many of which are available on the Internet and in the "gray" market (i.e., unauthorized imports), supply inaccurate results. These tests are different from FDA-approved home sample collection kits , which allow consumers to purchase test kits, collect a sample in private, send the sample to a laboratory for testing, and telephone for their HIV test result, counseling, and referral.

HIV-2 and HIV-1 Group O Infections

Although most HIV infections in the United States are of HIV-1 group B subtype, current EIAs can accurately identify infections with nearly all non-B subtypes and many infections with group O HIV subtypes. Infections with HIV-2 and HIV-1 group O are rare in the United States, and routine screening for these subtypes is not generally recommended as part of diagnostic testing except in areas where several such infections have been identified. Routine screening for HIV-2 might be appropriate in certain populations where potential risk for HIV-2 infection is higher (e.g., in areas where West African immigrants have settled). Since June 1992, FDA has recommended routine screening for antibody to HIV-2 (in addition to HIV-1) for all blood and plasma donations. Clients with clinical, epidemiologic, or laboratory history that suggests HIV infection and negative or indeterminate HIV-1 screening tests should receive further diagnostic testing to rule out HIV infection, potentially including testing for HIV-1 non-B subtypes and HIV-2. Hiv Aids continuing education, aids ceus for psychologists, psychologist ceu.

Other Test Uses

Viral load and HIV-1 p24 antigen assays are not intended for routine diagnosis but could be used in clinical management of HIV-infected persons in conjunction with clinical signs and symptoms and other laboratory markers of disease progression. Although HIV-1 p24 antigen assays are used for routine screening in blood and plasma centers, routine use for diagnosing HIV infection has been discouraged because the estimated average time from detection of p24 antigen to detection of HIV antibody by standard EIA is 6 days, and not all recently infected persons have detectable levels of p24 antigen .

Interpreting HIV Test Results

Standard Testing Algorithm

HIV-1 testing consists of initial screening with an EIA to detect antibodies to HIV-1. Specimens with a nonreactive result from the initial EIA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive EIA result are retested in duplicate. If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., Western blot or, less commonly, an immunofluorescence assay [IFA]). Only specimens that are repeatedly reactive by EIA and positive by IFA or reactive by Western blot are considered HIV-positive and indicative of HIV infection. Specimens that are repeatedly EIA-reactive occasionally provide an indeterminate Western blot result, which might represent either an incomplete antibody response to HIV in specimens from infected persons or nonspecific reactions in specimens from uninfected persons. Although IFA can be used to resolve an indeterminate Western blot sample, this assay is not widely used. Generally, a second specimen should be collected >1 month later and retested for persons with indeterminate Western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) could also help resolve an initial indeterminate Western blot in certain situations. A small number of tested specimens might provide inconclusive results because of insufficient quantity of specimen for the screening or confirmatory tests. In these situations, a second specimen should be collected and tested for HIV infection. Aids CE Course for Psychologists, APA Approved continuing education, Online Course to meet state and national requirements.

Modified Testing Algorithms

FDA has licensed only one rapid test, but modified testing algorithms are anticipated when additional rapid HIV tests are approved. If >2 sensitive and specific rapid HIV tests became available, one positive rapid test could be confirmed with a different rapid test. This combination has provided positive predictive value compared with the EIA/Western blot or IFA algorithm. However, no such algorithms have been adequately assessed or approved for diagnostic use in the United States.

Positive HIV Test Results

An HIV test should be considered positive only after screening and confirmatory tests are reactive. A confirmed positive test result indicates that a person has been infected with HIV. False-positive results when both screening and confirmatory tests are reactive are rare. However, the possibility of a mislabeled sample or laboratory error must be considered, especially for a client with no identifiable risk for HIV infection. HIV-vaccine--induced antibodies may be detected by current tests and may cause a false-positive result. Persons whose test results are HIV-positive and who are identified as vaccine trial participants should be encouraged to contact or return to their trial site or an associated trial site for HIV CTR services.

Negative HIV Test Results

Because a negative test result likely indicates absence of HIV infection (i.e., high negative predictive value), a negative test need not be repeated in clients with no new exposure in settings with low HIV prevalence. For clients with a recent history of known or possible exposure to HIV who are tested before they could develop detectable antibodies, the possibility of HIV infection cannot be excluded without follow-up testing. A false negative result also should be considered in persons with a negative HIV-1 test who have clinical symptoms suggesting HIV-1 infection or AIDS. Additional testing for HIV-2 and HIV-1 group O infection might be appropriate for these persons.

Indeterminate HIV Test Results

Most persons with an initial indeterminate Western blot result who are infected with HIV-1 will develop detectable HIV antibody within 1 month. Thus, clients with an initial indeterminate Western blot result should be retested for HIV-1 infection >1 month later. Persons with continued indeterminate Western blot results after 1 month are unlikely to be HIV-infected and should be counseled as though they are not infected unless recent HIV exposure is suspected.

Nucleic acid tests for HIV DNA or RNA exist, but are not approved by FDA for diagnostic purposes and are not generally recommended for resolving indeterminate Western blot results. However, in consultation with clinical and laboratory specialists, nucleic acid testing (if available) might also be useful for determining infection status among persons with an initial indeterminate Western blot result.

References: Department of Health and Human Services, Center for Disease Control and Preventions



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