Common misconceptions about HIV and AIDS

From Free net encyclopedia

Because the worldwide spread of AIDS has had such a tragic effect on millions of people worldwide, a number of misconceptions have arisen surrounding the disease. Below is a list and explanation of some common misconceptions and their rebuttals.

Contents

Sexual intercourse with a virgin will cure AIDS

Virgin cleansing is a myth that has occurred since at least the 16th 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 is unclear, it is believed to occur worldwide (Meel, 2003; Groce et al., 2004). Doing so does not cure the infected person, but it will expose the victim to HIV infection, spreading the disease further. This myth has gained considerable notoriety as the perceived reason for certain recent sexual abuse and child molestation occurrences (Meel, 2003).

HIV was introduced to North America by a Canadian flight attendant

A Canadian airline steward named Gaëtan Dugas was referred to as "Patient O" (for "Out of California") in an early AIDS study by Dr William Darrow of the Centers for Disease Control. He was responsible for infecting several of the first few hundred victims of the disease, but he was not the first person to bring or spread AIDS to North America. This rumor may have started with Randy Shilts' 1987 book And The Band Played On (and the movie based on it, where 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 had sexual intercourse with him.

However, four years after the publication of Shilts' article, Dr. Darrow repudiated his study, admitting its methods were flawed and that Shilts' had misrepresented its conclusions.

HIV is transmitted by mosquitoes

There is no evidence for this. Therefore, there is no need to fear catching HIV from a mosquito bite. 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 saliva into their victims, which may carry diseases such as dengue, malaria, yellow fever or the West Nile virus, thus infecting the person being bitten. However, HIV is not transmitted this way (Webb et al., 1989). On the other hand, a mosquito may have HIV-infected blood in her gut, and if swatted on the skin of a human who then scratches it, transmission may occur (Siemens, 1987). This risk is very small, and no cases have yet been identified through this route.

HIV cannot be transmitted through oral sex

While it is agreed that oral sex is a very much lower risk activity than vaginal and anal sex, it has been established that HIV can be transmitted through both insertive and receptive oral sex (Rothenberg et al., 1998), when there is contact between the semen and the mouth membranes. While the risk of infection from a single encounter is extremely small, it increases with frequency of activity.

You can get AIDS through casual contact with an HIV infected individual

You cannot become infected with HIV through day-to-day contact in social settings, schools or in the workplace. You 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 (Madhok et al., 1986; Courville et al., 1998). Saliva carries a negligible viral load, so even open-mouthed kissing is considered safe in most cases. 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. It must be stressed, however, that the CDC has only recorded one case of HIV transmission through kissing, 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, but, again, there are very few recorded incidents of transmission occurring in this way.

HIV can only infect gay men and drug users

HIV does not discriminate. It can infect anybody, including babies (Ammann et al., 1984; Clumeck et al., 1983 ; Groginsky et al., 1998 ; Oxtoby, 1990 ; Ryder et al., 1988 ; Piot et al., 1987; Ryder and Hassig, 1988; van der Graaf and Diepersloot, 1986). It is true that anal sex (regardless of the gender of the receptive partner) carries a higher risk of infection than some other sex acts, but most sex acts between any individuals carry at least some risk unless adequate protection is used. It is also true that HIV is more prevalent in Western societies at this time among gay men and drug users.

An HIV-infected mother cannot have children

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 (Groginsky et al., 1998; WHO, 2005).

AIDS can be cured

HAART allows the stabilization of the patient’s symptoms and viremia, but they do not cure the patient of HIV or of the symptoms of AIDS. High levels of HIV-1 (often HAART-resistant) return once treatment is stopped (Becker et al., 2002). There is no HIV vaccine at this time, although research continues in this area. It is true, however, that in some cases, HIV has been reduced to a survivable chronic condition. There have been a very small number of cases where an individual has definitively tested positive and subsequently become negative through treatment or otherwise, but even if these cases are accepted (and there remains debate over their legitimacy) it is not known how this occurred, and it is an extremely rare event in the context of almost fifty million cases of HIV infection worldwide.

There is a treatment known as Post-exposure prophylaxis that reduces the chance of getting infected when administered within 72 hours of exposure to HIV.

The AIDS epidemic began when a human male had sexual intercourse with African monkeys, transmitting the virus to modern humans

While it is true that HIV is most likely a mutated form of SIV (the Simian Immunodeficiency Virus), a disease present only in African monkeys, it is extremely unlikely that the zoonosis (inter-species transfer of a disease) of HIV occurred through sexual intercourse. The African 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 Congo in 1959 (Zhu et al., 1998).

AIDS was created by the CIA

This rumor started when an article in the Soviet newspaper Literary Gazette in 1985 claimed that AIDS was the product of U.S. germ warfare experiments. They claimed that the AIDS virus was created in Fort Detrick, Maryland, at a supersecret US Army research laboratory. Their only source was the Patriot, a leftist Indian newspaper that, U.S. experts charged, was a favored conduit of the KGB for its disinformation campaigns. Other reports claim that an operation known as the Special Virus Cancer Program run by Litton Bionetics developed AIDS. This was apparently accomplished under a US government contract tasked with creating a lethal biological warfare entity that was refractory to the human immune system.

HIV is the same as AIDS

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 virtually universally acknowledged as the underlying cause of AIDS, not all HIV positive individuals have AIDS, as the HIV virus can remain in a latent state for many years.

HIV antibody testing is unreliable

Diagnosis of infection using antibody testing is one of the best-established concepts in medicine. HIV antibody tests exceed the performance of most other infectious disease tests in both sensitivity (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). All current HIV antibody tests have sensitivity and specificity in excess of 96% (except the HIV-TEK G by Sorin Biomedica) and are therefore extremely reliable (WHO, 2004).

Progress in testing methodology has also enabled detection of viral genetic material, antigens and the virus itself in body fluids and cells. While not widely used for routine testing due to high cost and requirements in laboratory equipment, these direct testing techniques have confirmed the validity of the antibody tests (Jackson et al., 1990; Busch et al., 1991; Silvester et al., 1995; Urassa et al., 1999; Nkengasong et al., 1999; Samdal et al., 1996).

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

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 (UNAIDS, 2000).

For example, in a study in Côte d'Ivoire, HIV-seropositive individuals with pulmonary tuberculosis (TB) were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary TB (Ackah et al. 1995). 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 (Taha et al., 1999). Elsewhere in Africa, findings are similar.

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

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

AZT and other antiretroviral drugs, not HIV, cause AIDS

The vast majority of people with AIDS never received antiretroviral drugs, including those in developed countries prior to the licensure of AZT in 1987, and people in developing countries today where very few individuals have access to these medications (UNAIDS, 2003).

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 (NIAID, 1995).

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 (HHS, 2005). Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which clearly would not be seen if antiretroviral drugs caused AIDS (Palella et al., 1998; Mocroft et al., 1998; Mocroft et al., 2000; Vittinghoff et al., 1999; Detels et al., 1998; de Martino et al., 2000; Hogg et al., 1999; Schwarcz et al., 2000; Kaplan et al., 2000, McNaghten et al., 1999).

Behavioral factors such as recreational drug use and multiple sexual partners, not HIV, account for 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 (NIAID, 1995a; NIAID, 1995b).

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

For example, in a prospectively studied cohort in Vancouver, 715 homosexual men were followed for a median of 8.6 years. Among 365 HIV-positive individuals, 136 developed AIDS. No AIDS-defining illnesses occurred among 350 seronegative men despite the fact that these men reported appreciable use of inhalable nitrites ("poppers") and other recreational drugs, and frequent receptive anal intercourse (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 (Vermund et al., 1993).

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 (Des Jarlais et al., 1993).

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

This notion is contradicted by a report by the Transfusion Safety Study Group (TSSG), which compared HIV-negative and HIV-positive blood recipients who had been given transfusions for similar diseases. Approximately 3 years after the transfusion, the mean CD4+ T-cell count in 64 HIV-negative recipients was 850/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 (Donegan et al., 1990; Cohen. 1994).

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

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 (Hasset et al., 1993). 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 (Aledort et al., 1993).

In a cohort in the United Kingdom, researchers matched 17 HIV-seropositive hemophiliacs with 17 HIV-seronegative hemophiliacs with regard to clotting factorconcentrate 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 (Sabin et al., 1996).

Among HIV-infected hemophiliacs, Transfusion Safety Study investigators found that neither the purity nor the amount of factor VIII therapy had a deleterious effect on CD4+ T cell counts (Gjerset et al., 1994). Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs (Goedert et al., 1989).

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

The distribution of AIDS cases, whether in the United States or elsewhere in the world, invariably mirrors the prevalence of HIV in a population. In the United States, HIV first appeared in populations of homosexual men and injection-drug users, a majority of whom are male. Because HIV is spread primarily through sex or by the exchange of HIV-contaminated needles during intravenous drug use, it is not surprising that a majority of U.S. AIDS cases have occurred in men (U.S. Census Bureau, 1999).

These behaviors also 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.

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

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 (U.S. Census Bureau, 1999). 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. (UNAIDS, 2005).

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

This reasoning ignores numerous examples of viruses other than HIV that can be pathogenic after evidence of immunity appears. Measles virus may persist for years in brain cells, eventually causing a chronic neurologic disease despite the presence of antibodies. Viruses such as cytomegalovirus, herpes simplex and varicella zoster may be activated after years of latency even in the presence of abundant antibodies. In animals, viral relatives of HIV with long and variable latency periods, such as visna virus in sheep, cause central nervous system damage even after the production of antibodies (NIAID, 1995).

Also, HIV is well recognized as being able to mutate to avoid the ongoing immune response of the host (Levy. 1993).

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

New techniques such as the polymerase chain reaction (PCR) have enabled scientists to demonstrate that a much larger proportion of CD4+ T cells are infected than previously realized, particularly in lymphoid tissues. Robert Gallo, who is one of the preeminent HIV virologists, 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 (Richman, 2000).

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 countersurveillance behavior is not significantly different in quality from, say, the influenza viruses, which are well-known to secrete immunosuppressive proteins in an effort to slow down the antiviral immune response.

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

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 (Alcabes et al., 1993).

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 (Evans. 1982; Levy. 1993; Fauci. 1996).

HIV is not the cause of AIDS because some people have symptoms associated with AIDS but are not infected with HIV

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

However, immunosuppression has many other potential causes. Individuals who take glucocorticoids and/or immunosuppressive drugs to prevent transplant rejection or for autoimmune diseases can have increased susceptibility to unusual infections, as do individuals with certain genetic conditions, severe malnutrition and certain kinds of cancers. There is no evidence suggesting that the numbers of such cases have risen, while abundant epidemiologic evidence shows a staggering rise in cases of immunosuppression among individuals who share one characteristic: HIV infection (NIAID, 1995; UNAIDS, 2000).

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

The diseases associated with AIDS, such as PCP and Mycobacterium avium complex (MAC), are not caused by HIV but rather result from the immunosuppression caused by HIV disease. As the immune system of an HIV-infected individual weakens, he or she becomes susceptible to the particular viral, fungal and bacterial infections common in the community. For example, HIV-infected people in certain midwestern and mid-Atlantic regions are much more likely than people in New York City to develop histoplasmosis, which is caused by a fungus. A person in Africa is exposed to different pathogens than is an individual in an American city. Children may be exposed to different infectious agents than adults (USPHS/IDSA, 2001).

It should not be surprising if a person with limited immune function is exposed to the common cold, that he or she will develop a cold instead of some other disease. Similarly, if a person with limited immune function lives in a place where malaria is common, he or she will develop malaria -- but if this person lives in a place where malaria is NOT, then he or she has no appreciable risk of developing malaria, despite the immune suppression. An AIDS patient in a malaria region may develop malaria; if you transport the same person to the U.S., then the chance of developing malaria drops immediately, just as the chance of picking up disease common to the U.S. rises immediately.

In a nutshell, HIV is the underlying cause of the condition named AIDS, but what actually kills an AIDS patient is any combination of whatever other dangerous infectious diseases may be common in that particular place and time.


See also

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