The spread of HIV and AIDS has affected millions of people worldwide; According to the "2006 AIDS Epidemic Update", published by the UNAIDS/World Health Organization, there were an estimated 39.5 million people around the world living with HIV, with 4.3 million new HIV infections and 2.9 million deaths from AIDS-related illnesses in 2006. In some regions, there are indications that HIV infection rates have risen by over 50% since 2004. In the wake of this pandemic, a number of misconceptions have arisen surrounding the disease. Below is a list and explanation of some common misconceptions and their rebuttals.
This is false. HIV is an acronym for Human Immunodeficiency Virus, and AIDS (Acquired Immune Deficiency Syndrome) is the collection of symptoms, diseases, and infections associated with an acquired deficiency of the immune system. While HIV is the underlying cause of AIDS, not all HIV-positive individuals have AIDS, as HIV can remain in a latent state for many years.
Highly Active Anti-Retroviral Therapy (HAART) in many cases allows the stabilization of the patient's symptoms, partial recovery of CD4+ T-cell levels, and reduction in viremia (the level of virus in the blood) to low or near-undetectable levels. Disease-specific drugs can also alleviate symptoms of AIDS and even cure specific AIDS-defining conditions in some cases. Medical treatment can reduce HIV infection in many cases to a survivable chronic condition, analogous to diabetes. However, these advances do not constitute a cure, since current treatment regimens cannot eradicate latent HIV from the body.
High levels of HIV-1 (often HAART-resistant) develop if treatment is stopped, if compliance with treatment is inconsistent, or if the virus spontaneously develops resistance to an individual's regimen. Antiretroviral treatment known as post-exposure prophylaxis reduces the chance of acquiring an HIV infection when administered within 72 hours of exposure to HIV. These problems mean that while HIV-positive people with low viremia are less likely to infect others, the chance of transmission always exists. In addition, people on HAART may still become sick.
Virgin cleansing is a myth that has occurred since at least the sixteenth century, when Europeans believed that they could rid themselves of a sexually transmitted disease by transferring it to a virgin through sexual intercourse. Although the exact prevalence of this belief is unclear, it is believed to occur worldwide; however, the majority of modern reported cases of this event have occurred in sub-Saharan Africa. Sex with an uninfected virgin does not cure an HIV-infected person, and such contact will expose the uninfected individual to HIV, potentially further spreading the disease. This myth has gained considerable notoriety as the perceived reason for certain sexual abuse and child molestation occurrences, especially in Africa.
The National Council of Societies for the Prevention of Cruelty to Animals (NSPCA) in Johannesburg, South Africa, has recorded in 2002 beliefs amongst youths that sex with animals is a means to avoid AIDS or cure it if infected. As with "virgin cure" beliefs, there is no scientific evidence suggesting a sexual act can actually cure AIDS. The risk of contracting HIV via sex with animals is small, but the practice has its own health risks.
Diagnosis of infection using antibody testing is a well-established technique in medicine. HIV antibody tests exceed the performance of most other infectious disease tests in both sensitivity (the ability of the screening test to give a positive finding when the person tested truly has the disease) and specificity (the ability of the test to give a negative finding when the subjects tested are free of the disease under study). Many current HIV antibody tests have sensitivity and specificity in excess of 96% and are therefore extremely reliable.
Progress in testing methodology has enabled detection of viral genetic material, antigens, and the virus itself in body fluids and cells. While not widely used for routine testing due to high cost and requirements in laboratory equipment, these direct testing techniques have confirmed the validity of the antibody tests.
Positive HIV antibody tests are usually followed up by retests and tests for antigens, viral genetic material and the virus itself, providing confirmation of actual infection.
One cannot become infected with HIV through day-to-day contact in social settings, schools, or in the workplace. One cannot be infected by shaking someone's hand, by hugging or "dry" kissing someone, by using the same toilet or drinking from the same glass as an HIV-infected person, or by being exposed to coughing or sneezing by an infected person. Saliva carries a negligible viral load, so even open-mouthed kissing is considered a low risk. However, if the infected partner or both of the performers have blood in their mouth due to cuts, open sores, or gum disease, the risk is higher. The CDC has only recorded one case of possible HIV transmission through kissing (involving an HIV-infected man with significant gum disease and a sexual partner also with significant gum disease), and the Terence Higgins Trust says that this is essentially a no-risk situation.
Other interactions that could theoretically result in person-to-person transmission include caring for nose bleeds, biting, and home health care procedures, yet there are very few recorded incidents of transmission occurring in this way.
While it is agreed that oral sex has a much lower HIV-infection risk than vaginal and anal sex, HIV can be transmitted through both insertive and receptive oral sex, when there is contact between semen or vaginal fluid and the mucous membranes of the mouth. The risk of infection from a single encounter is small, but it increases with frequency of activity. To date the CDC lists no documented cases of transmission to the insertive partner of such activities.
Transmission risk may be elevated in the case of open sores on the genitals and/or mouth, or significant gum disease or bleeding, i.e., when there is direct contact between semen and breaks in the skin or surface of the mouth.
Using previously contaminated hypodermic needles or other "works" to divide a drug solution among drug injection partners can spread HIV. Studies in the early- and mid-1980s focused only on sharing needles, but studies beginning in the late-1980s have shown that this message can lead to increased HIV risk of infection because they fail to highlight the risks of infection from sharing the same prep equipment (cotton filters, cookers, and rinse water), not just the needles themselves.
When mosquitoes bite a person, they do not inject the blood of a previous victim into the person they bite next. Mosquitoes do, however, inject their saliva into their victims, which may carry diseases such as dengue fever, malaria, yellow fever, or West Nile virus and can infect a bitten person with these diseases. HIV is not transmitted in this manner. On the other hand, a mosquito may have HIV-infected blood in its gut, and if swatted on the skin of a human who then scratches it, transmission may be possible, though this risk is very small, and no cases have yet been identified through this route.
In November 2005, Jacob Zuma, Deputy President of South Africa, drew widespread condemnation from AIDS activists when he revealed that he had unprotected intercourse with the plaintiff in his rape trial, whom he knew to be HIV-positive, and that he had showered after sex, believing that this would reduce his chances of contracting AIDS.
HIV can survive at room temperature outside the body for hours if dry (provided that initial concentrations are high), and for weeks if wet (in used syringes/needles). However, the amounts typically present in bodily fluids do not survive nearly as long outside the body—generally no more than a few minutes if dry. Again, the amount of time is longer if wet, especially in syringes/needles and related equipment.
HIV can infect anybody, regardless of any age, sex, ethnicity, or sexual orientation. It is true that anal sex (regardless of the gender of the receptive partner) carries a higher risk of infection than most sex acts, but most penetrative sex acts between any individuals carry some risk. Properly used condoms can reduce this risk.
HIV-infected women are still fertile, although in late stages of HIV disease a pregnant woman may have a higher risk of spontaneous miscarriage. Normally, the risk of transmitting HIV to the unborn child is between 15-30%. However, this may be reduced to just 2-3% if patients carefully follow medical guidelines.
This reasoning ignores numerous examples of viruses other than HIV that can be pathogenic after evidence of immunity appears. Measles virus may persist for years in brain cells, eventually causing a chronic neurologic disease despite the presence of antibodies. Viruses such as cytomegalovirus, Herpes simplex virus, and Varicella zoster may be activated after years of latency even in the presence of abundant antibodies. In animals, viral relatives of HIV with long and variable latency periods, such as visna virus in sheep, cause central nervous system damage even after the production of antibodies.
Techniques such as polymerase chain reaction (PCR) have enabled scientists to demonstrate that a much larger proportion of CD4+ T cells are infected than previously realized, particularly in lymphoid tissues. Robert Gallo, a preeminent HIV virologist, suggests that as many as 3% of CD4+ T cells show signs of HIV invasion. Macrophages and other cell types are also infected with HIV and serve as reservoirs for the virus.
Although the fraction of CD4+ T cells that is infected with HIV at any given time is never high (only a small subset of activated cells serve as ideal targets of infection), several groups have shown that rapid cycles of death of infected cells and infection of new target cells occur throughout the course of disease.
Furthermore, like other viruses, HIV is able to suppress the immune system by secreting proteins that interfere with it. For example, HIV's coat protein, gp120, sheds from viral particles and binds to the CD4 receptors of otherwise healthy T cells; this interferes with the normal function of these signalling receptors. Another HIV protein, Tat, has been demonstrated to suppress T cell activity. This behavior is not significantly different in quality from, say, the influenza viruses, which are well-known to secrete immunosuppressive proteins which can slow down the antiviral immune response.
Infected lymphocytes express the Fas ligand, a cell-surface protein that triggers the death of neighboring uninfected T cells expressing the Fas receptor. This "bystander killing" effect shows that great harm can be caused to the immune system even with a limited number of infected cells.
A Canadian airline steward named Gaëtan Dugas was referred to as "Patient 0" in an early AIDS study by Dr. William Darrow of the Centers for Disease Control. Many people consider Dugas to be responsible for bringing HIV to North America. This is considered inaccurate, as HIV had spread long before Dugas began his career. This rumor may have started with Randy Shilts' 1987 book And the Band Played On (and the movie based on it, in which Dugas is referred to as AIDS' Patient Zero), but neither the book nor the movie state him to have been the first to bring the virus to North America. He was called "Patient Zero" because at least 40 of the 248 people known to be infected by AIDS in 1983 had had sexual intercourse with him, or with someone who had sexual intercourse with him.
However, four years after the publication of Shilts' book, Dr. Darrow repudiated his study, saying that its methods were flawed and claiming that Shilts had misrepresented its conclusions.
The current consensus is that HIV was introduced to North America by a Haitian immigrant who contracted it while working in the Democratic Republic of the Congo in the early 1960s, or from another person who worked there during that time.
While HIV is most likely a mutated form of Simian Immunodeficiency Virus, a disease present only in chimpanzees and African monkeys, it is extremely unlikely that the zoonosis (inter-species transfer of a disease) of HIV occurred through sexual intercourse. The African chimpanzees and monkeys which carry SIV are often hunted for food, and epidemiologists theorize that the disease appeared in humans after hunters came into blood-contact with monkeys infected with SIV that they had killed. The first known instance of HIV in a human was found in a person who died in the Democratic Republic of the Congo in 1959, and a recent study dates the last common ancestor of HIV and SIV to between 1884 and 1914 by using a molecular clock approach.
The diseases that have come to be associated with AIDS in Africa, such as wasting syndrome, diarrheal diseases and tuberculosis, have long been severe burdens there. However, high rates of mortality from these diseases, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people, including well-educated members of the middle class.
For example, in a study in Côte d'Ivoire, HIV-seropositive individuals with pulmonary tuberculosis were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary tuberculosis. In Malawi, mortality over three years among children who had received recommended childhood immunizations and who survived the first year of life was 9.5 times higher among HIV-seropositive children than among HIV-seronegative children. The leading causes of death were wasting and respiratory conditions. Elsewhere in Africa, findings are similar.
There is broad scientific consensus that HIV is the cause of AIDS, but some individuals reject this consensus, including biologist Peter Duesberg, biochemist David Rasnick, journalist/activist Celia Farber, conservative writer Tom Bethell, and intelligent design advocate Phillip E. Johnson. (Some one-time skeptics have since rejected AIDS denialism, including physiologist Robert Root-Bernstein, and physician and AIDS researcher Joseph Sonnabend.)
A great deal is known about the pathogenesis of HIV disease, even though important details remain to be elucidated. However, a complete understanding of the pathogenesis of a disease is not a prerequisite to knowing its cause. Most infectious agents have been associated with the disease they cause long before their pathogenic mechanisms have been discovered. Because research in pathogenesis is difficult when precise animal models are unavailable, the disease-causing mechanisms in many diseases, including tuberculosis and hepatitis B, are poorly understood, but the pathogens responsible are very well established.
The vast majority of people with AIDS never received antiretroviral drugs, including those in developed countries prior to the licensure of AZT in 1987. Still, today, very few individuals in developing countries have access to these medications.
In the 1980s, clinical trials enrolling patients with AIDS found that AZT given as single-drug therapy conferred a modest (and short-lived) survival advantage compared to placebo. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. The lack of excess AIDS cases and death in the AZT arms of these placebo-controlled trials effectively counters the argument that AZT causes AIDS.
Subsequent clinical trials found that patients receiving two-drug combinations had up to 50 percent increases in time to progression to AIDS and in survival when compared to people receiving single-drug therapy. In more recent years, three-drug combination therapies have produced another 50 percent to 80 percent improvements in progression to AIDS and in survival when compared to two-drug regimens in clinical trials. Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which would be unlikely if antiretroviral drugs caused AIDS.
The proposed behavioral causes of AIDS, such as multiple sexual partners and long-term recreational drug use, have existed for many years. The epidemic of AIDS, characterized by the occurrence of formerly rare opportunistic infections such as Pneumocystis carinii pneumonia (PCP) did not occur in the United States until a previously unknown human retrovirus—HIV—spread through certain communities.
Compelling evidence against the hypothesis that behavioral factors cause AIDS comes from recent studies that have followed cohorts of homosexual men for long periods of time and found that only HIV-seropositive men develop AIDS. For example, in a prospectively studied cohort in Vancouver, 715 homosexual men were followed for a median of 8.6 years. Among 365 HIV-positive individuals, 136 developed AIDS. No AIDS-defining illnesses occurred among 350 seronegative men, despite the fact that these men reported appreciable use of nitrite inhalants ("poppers") and other recreational drugs, and frequent receptive anal intercourse (Schechter et al., 1993).
Other studies show that among homosexual men and injection-drug users, the specific immune deficit that leads to AIDS—a progressive and sustained loss of CD4+ T cells—is extremely rare in the absence of other immunosuppressive conditions. For example, in the Multicenter AIDS Cohort Study, more than 22,000 T-cell determinations in 2,713 HIV-seronegative homosexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/µl of blood, and this individual was receiving immunosuppressive therapy.
In a survey of 229 HIV-seronegative injection-drug users in New York City, mean CD4+ T-cell counts of the group were consistently more than 1000 cells/µl of blood. Only two individuals had two CD4+ T-cell measurements of less than 300/µl of blood, one of whom died with cardiac disease and non-Hodgkin's lymphoma listed as the cause of death.
This notion is contradicted by a report by the Transfusion Safety Study Group (TSSG), which compared HIV-negative and HIV-positive blood recipients who had been given blood transfusions for similar diseases. Approximately 3 years following blood transfusion, the mean CD4+ T-cell count in 64 HIV-negative recipients was 850/µl of blood, while 111 HIV-seropositive individuals had average CD4+ T-cell counts of 375/µl of blood. By 1993, there were 37 cases of AIDS in the HIV-infected group, but not a single AIDS-defining illness in the HIV-seronegative transfusion recipients.
This view is contradicted by many studies. For example, among HIV-seronegative patients with hemophilia A enrolled in the Transfusion Safety Study, no significant differences in CD4+ T-cell counts were noted between 79 patients with no or minimal factor treatment and 52 with the largest amount of lifetime treatments. Patients in both groups had CD4+ T cell-counts within the normal range. In another report from the Transfusion Safety Study, no instances of AIDS-defining illnesses were seen among 402 HIV-seronegative hemophiliacs who had received factortherapy.
In a cohort in the United Kingdom, researchers matched 17 HIV-seropositive hemophiliacs with 17 HIV-seronegative hemophiliacs with regard to clotting factor concentrate usage over a ten-year period. During this time, 16 AIDS-defining clinical events occurred in 9 patients, all of whom were HIV-seropositive. No AIDS-defining illnesses occurred among the HIV-negative patients. In each pair, the mean CD4+ T cell count during follow-up was, on average, 500 cells/µl lower in the HIV-seropositive patient.
Among HIV-infected hemophiliacs, Transfusion Safety Study investigators found that neither the purity nor the amount of factor VIII therapy had a deleterious effect on CD4+ T cell counts. Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs.
The distribution of AIDS cases, whether in the United States or elsewhere in the world, invariably mirrors the prevalence of HIV in a population. In the United States, HIV first appeared in populations of gay men and injection-drug users, a majority of whom are male. HIV is spread primarily through unprotected sex, the exchange of HIV-contaminated needles, or cross-contamination of the drug solution and infected blood during intravenous drug use. Because these behaviors show a gender skew—Western men are more likely to take illegal drugs intravenously than Western women, and men are more likely to report higher levels of the riskiest sexual behaviors, such as unprotected anal intercourse—it is not surprising that a majority of U.S. AIDS cases have occurred in men.[68 ]
Women in the United States, however, are increasingly becoming HIV-infected, usually through the exchange of HIV-contaminated needles or sex with an HIV-infected male. The CDC estimates that 30 percent of new HIV infections in the United States in 1998 were in women. As the number of HIV-infected women has risen, so too has the number of female AIDS patients in the United States. Approximately 23 percent of U.S. adult/adolescent AIDS cases reported to the CDC in 1998 were among women. In 1998, AIDS was the fifth leading cause of death among women aged 25 to 44 in the United States, and the third leading cause of death among African-American women in that age group.[69 ]
In Africa, HIV was first recognized in sexually active heterosexuals, and AIDS cases in Africa have occurred at least as frequently in women as in men. Overall, the worldwide distribution of HIV infection and AIDS between men and women is approximately 1 to 1.[68 ] In sub-Saharan Africa, 57% of adults with HIV are women, and young women aged 15 to 24 are more than three times as likely to be infected as young men.
HIV disease has a prolonged and variable course. The median period of time between infection with HIV and the onset of clinically apparent disease is approximately 10 years in industrialized countries, according to prospective studies of homosexual men in which dates of seroconversion are known. Similar estimates of asymptomatic periods have been made for HIV-infected blood-transfusion recipients, injection-drug users and adult hemophiliacs.
As with many diseases, a number of factors can influence the course of HIV disease. Factors such as age or genetic differences between individuals, the level of virulence of the individual strain of virus, as well as exogenous influences such as co-infection with other microbes may determine the rate and severity of HIV disease expression. Similarly, some people infected with hepatitis B, for example, show no symptoms or only jaundice and clear their infection, while others suffer disease ranging from chronic liver inflammation to cirrhosis and hepatocellular carcinoma. Co-factors probably also determine why some smokers develop lung cancer while others do not.
However, immunosuppression has many other potential causes. Individuals who take glucocorticoids and/or immunosuppressive drugs to prevent transplant rejection or to treat autoimmune diseases can have increased susceptibility to unusual infections, as do individuals with certain genetic conditions, severe malnutrition and certain kinds of cancers. There is no evidence suggesting that the numbers of such cases have risen, while abundant epidemiologic evidence shows a very large rise in cases of immunosuppression among individuals who share one characteristic: HIV infection.
The diseases associated with AIDS, such as Pneumocystis jiroveci pneumonia (PCP) and Mycobacterium avium complex (MAC), are not caused by HIV, but rather result from the immunosuppression caused by HIV disease. As the immune system of an HIV-infected individual weakens, he or she becomes susceptible to the particular viral, fungal, and bacterial infections common in the community. For example, HIV-infected people in the Midwestern United States are much more likely than people in New York City to develop histoplasmosis, which is caused by a fungus. A person in Africa is exposed to different pathogens than individuals in an American city. Children may be exposed to different infectious agents than adults.