HIV and AIDS misconceptions

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Overview

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.[1] 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.

The relationship between HIV and AIDS

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

HIV does not cause AIDS

See below.

HIV/AIDS treatment

A cure for AIDS?

See also AIDS Treatment and HIV Treatment.

There is currently no known cure for AIDS, nor a vaccine for HIV.

Highly Active Anti-Retroviral Therapy (HAART) allows the stabilization of the patient's symptoms and viremia, but it does 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.[2] Antiretroviral treatment known as post-exposure prophylaxis reduces the chance of acquiring an HIV infection when administered within 72 hours of exposure to HIV.[3]

It is true that in some cases HIV has been reduced to a survivable chronic condition (an analogy can be made with diabetes—patients with either condition may be treated, leading to a normal quality of life, but this does not constitute a cure). There have been a very small number of cases in which 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.

Sexual intercourse with a virgin will cure AIDS

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.[4][5] 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.[4]

Sexual intercourse with an animal will avoid or cure AIDS

The National 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.[6] As with "virgin cure" beliefs, no 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. Additionally, sexual intercourse with animals is a criminal offense in a number of countries.

(Note: HIV can survive in primates, and is not believed to survive long in other species. Should more than one person engage sexually with an animal, there is a risk that HIV may survive long enough in the fluids from an infected person to infect the second person.)

HIV antibody testing is unreliable

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.[7]

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.[8][9][10][11][12][13]

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.

HIV infection

AIDS can be spread through casual contact with an HIV infected individual

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.[14][15] 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 HIV transmission through kissing,

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.

HIV cannot be transmitted through oral sex

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,[16] when there is contact between semen and the mucous membranes of the mouth. The risk of infection from a single encounter is small, but it increases with frequency of activity according to binomial probability theory.

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 or saliva and breaks in the skin or surface of the mouth.

Not sharing hypodermic needles with a seropositive person means one is safe from HIV

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, not just the needles themselves.

HIV is transmitted by mosquitoes

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.[17] 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,[18] though this risk is very small, and no cases have yet been identified through this route.

HIV survives for only a short time outside the body

HIV in trace amounts of blood survives at room temperature outside the body for hours if dry,[19] and for weeks if wet.[20]

HIV can infect only homosexual men and drug users

HIV can infect anybody, regardless of any age, sex, ethnicity, or sexual orientation.[21][22][23][24][25][26] 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.

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.[23][27]

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 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.[28]

HIV has a well-recognized capacity to mutate to evade the ongoing immune response of the host.[29]

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

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.[30]

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 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.[31] This "bystander killing" effect shows that great harm can be caused to the immune system even with a limited number of infected cells.

History of HIV/AIDS

HIV was introduced to North America by a Canadian flight attendant

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 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 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.[32]

Alternative theories

HIV is a man-made weapon of racial warfare

Infamous examples of real racism in the past such as Tuskegee Study of Untreated Syphilis in the Negro Male (1932-1972) have injured the level of trust in the black community towards public health efforts. The Tuskegee study deliberately left black men diagnosed with syphilis untreated for 40 years. It was the longest non-therapeutic experiment on human beings in medical history. The AIDS epidemic has exposed the Tuskegee study as a historical marker for the legitimate discontent of blacks with the public health system. The belief that AIDS is a form of genocide is rooted in recent experiences of racism. These theories range from the belief that governments promote drug abuse in black communities to the belief that HIV is a man-made weapon of racial warfare. Researchers in public health hope that open and honest conversations about racism in the past can help rebuild trust and improve the health of people in these communities.[33]

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.

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.[34]

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.[35] 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.[36] Elsewhere in Africa, findings are similar.

HIV is not the cause of AIDS

Main article: AIDS reappraisal

There is broad scientific consensus that HIV is the cause of AIDS, but there have been notable groups, past and present, that have rejected this consensus, including Peter Duesberg, PhD, David Rasnick, PhD, Celia Farber, Robert Root-Bernstein, MD, Joseph Sonnabend, MD, Tom Bethell, and Phillip E. Johnson.

AZT and other antiretroviral drugs, not HIV, cause AIDS

Main article: Duesberg hypothesis

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.[37]

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.[28]

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.[38] 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.[39][40][41][42][43][44][45][46][47][48]

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, but the pathogens responsible are very well established.

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.[49][50]

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).[51]

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.[52]

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.[53]

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 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.[54][55]

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.[56] 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.[57]

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.[58]

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.[59] Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs.[60]

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 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.[61]

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.[62]

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.[61] 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.[63]

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.[64]

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.[65][29][66]

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 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.[34][28]

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 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 is 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.[67]

HIV is the underlying cause of the condition named AIDS, but the additional conditions that may affect an AIDS patient is dependent upon the endemic pathogens to which the patient may be exposed.

Related Chapters

External links

References

  1. "Global AIDS epidemic continues to grow", November 21, 2006, World Health Organization
  2. Becker, S., Dezii, C. M., Burtcel, B., Kawabata, H. and Hodder, S. (2002) Young HIV-infected adults are at greater risk for medication nonadherence. MedGenMed 4, 21 PMID 12466764
  3. (2005) in Fan, H., Conner, R. F. and Villarreal, L. P. eds: AIDS : science and society, 4th edition, Boston, MA: Jones and Bartlett Publishers. ISBN 0-7637-0086-X. 
  4. 4.0 4.1 Meel BL (2003) 1. The myth of child rape as a cure for HIV/AIDS in Transkei: a case report. Med. Sci. Law 43, 85-88 PMID 12627683
  5. Groce NE, Trasi R. (2004) Rape of individuals with disability: AIDS and the folk belief of virgin cleansing. Lancet 363, 1663-1664 PMID 15158626
  6. "Bestiality new Aids myth - SPCA", March 25, 2002; retrieved February 22, 2007
  7. "HIV ASSAYS: OPERATIONAL CHARACTERISTICS", World Health Organization, 2004
  8. Jackson JB, Kwok SY, Sninsky JJ, Hopsicker JS, Sannerud KJ, Rhame FS, Henry K, Simpson M, Balfour HH Jr. (1990) Human immunodeficiency virus type 1 detected in all seropositive symptomatic and asymptomatic individuals. J. Clin. Microbiol. 28, 16-19 PMID 2298875
  9. Busch MP, Eble BE, Khayam-Bashi H, Heilbron D, Murphy EL, Kwok S, Sninsky J, Perkins HA, Vyas GN. (1991) Evaluation of screened blood donations for human immunodeficiency virus type 1 infection by culture and DNA amplification of pooled cells. N. Engl. J. Med. 325, 1-5 PMID 2046708
  10. Silvester C, Healey DS, Cunningham P, Dax EM. (1995) Multisite evaluation of four anti-HIV-1/HIV-2 enzyme immunoassays. Australian HIV Test Evaluation Group. J Acquir Immune Defic Syndr Hum Retrovirol. 8, 411-419 PMID 7882108
  11. Urassa W, Godoy K, Killewo J, Kwesigabo G, Mbakileki A, Mhalu F, Biberfeld G. (1999) The accuracy of an alternative confirmatory strategy for detection of antibodies to HIV-1: experience from a regional laboratory in Kagera, Tanzania. J. Clin. Virol. 14, 25-29 PMID 10548127
  12. Nkengasong JN, Maurice C, Koblavi S, Kalou M, Yavo D, Maran M, Bile C, N'guessan K, Kouadio J, Bony S, Wiktor SZ, Greenberg AE. (1999) Evaluation of HIV serial and parallel serologic testing algorithms in Abidjan, Cote d'Ivoire. AIDS 13, 109-117 PMID 10207552
  13. Samdal HH, Gutigard BG, Labay D, Wiik SI, Skaug K, Skar AG. (1996) Comparison of the sensitivity of four rapid assays for the detection of antibodies to HIV-1/HIV-2 during seroconversion. Clin. Diagn. Virol. 7, 55-61 PMID 9077430
  14. Madhok R, Gracie JA, Lowe GD, Forbes CD. (1986) Lack of HIV transmission by casual contact. Lancet 328, 863
  15. MCourville TM, Caldwell B, Brunell PA. (1998) Lack of evidence of transmission of HIV-1 to family contacts of HIV-1 infected children. Clin Pediatr (Phila) 37, 175-178 PMID 9545605
  16. Rothenberg RB, Scarlett M, del Rio C, Reznik D, O'Daniels C. (1998) Oral transmission of HIV. AIDS 12, 2095-2105 PMID 9833850
  17. Webb PA, Happ CM, Maupin GO, Johnson BJ, Ou CY, Monath TP. (1989) Potential for insect transmission of HIV: experimental exposure of Cimex hemipterus and Toxorhynchites amboinensis to human immunodeficiency virus. J. Infect. Dis. 160, 970-977 PMID 2479697
  18. Siemens DF (1987) AIDS Transmission and Insects. Science 238, 143 PMID 2889266
  19. Resnick L, Veren K, Salahuddin SZ, Tondreau S, Markham PD. (1986) Stability and inactivation of HTLV-III/LAV under clinical and laboratory environments. JAMA 255, 1887-1991 PMID 2419594
  20. Heimer R, Abdala N. (2000) Viability of HIV-1 in syringes: implications for interventions among injection drug users AIDS Reader 10, 410-417 PMID 10932845
  21. Ammann AJ, Wara DW, Cowan MJ (1984) Pediatric acquired immunodeficiency syndrome Ann N Y Acad Sci 437, 340-349 PMID 6242000
  22. Clumeck N, Mascart-Lemone F, de Maubeuge J, Brenez D, Marcelis L (1983) Acquired immune deficiency syndrome in Black Africans. Lancet 321, 642 PMID 613131
  23. 23.0 23.1 Groginsky E, Bowdler N, Yankowitz J. (1998) Update on vertical HIV transmission. J Reprod Med 43, 637-646 PMID 9749412
  24. Oxtoby MJ. (1990) Perinatally acquired human immunodeficiency virus infection. Pediatr Infect Dis J. 9, 609-19 PMID 2235185
  25. Ryder RW, Hassig SE. (1988) The epidemiology of perinatal transmission of HIV. AIDS 2 Suppl 1, S83-S89 PMID 3147684
  26. van der Graaf M, Diepersloot RJ. (1986) Transmission of human immunodeficiency virus (HIV/HTLV-III/LAV): a review. Infection 14, 203-11 PMID 3539811
  27. WHO, 2005
  28. 28.0 28.1 28.2 "DISEASE PROGRESSION DESPITE ANTIBODIES", "The Relationship Between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome", National Institute of Allergy and Infectious Diseases, September, 1995
  29. 29.0 29.1 Levy JA (1993) Pathogenesis of human immunodeficiency virus infection. Microbiol Rev. 57, 183-289 PMID 8464405
  30. Richman DD. (2000) Normal physiology and HIV pathophysiology of human T-cell dynamics. J. Clin. Invest. 105, 565-566 PMID 10712427
  31. Xu XN, Laffert B, Screaton GR, Kraft M, Wolf D, Kolanus W, Mongkolsapay J, McMichael AJ, Baur AS. (1999) Induction of Fas ligand expression by HIV involves the interaction of Nef with the T cell receptor zeta chain.J Exp Med. 189, 1489-96. PMID 10224289
  32. Zhu T, Korber BT, Nahmias AJ, Hooper E, Sharp PM, Ho DD. (1998) An African HIV-1 sequence from 1959 and implications for the origin of the epidemic. Nature 391, 594-597 PMID 9468138
  33. The Tuskegee Syphilis Study, 1932 to 1972: implications for HIV education and AIDS risk education programs in the black community. Am J Public Health. 1991 November; 81(11): 1498–1505.
  34. 34.0 34.1 UNAIDS, 2000
  35. Ackah AN, Coulibaly D, Digbeu H, Diallo K, Vetter KM, Coulibaly IM, Greenberg AE, De Cock KM. (1995) Response to treatment, mortality, and CD4 lymphocyte counts in HIV-infected persons with tuberculosis in Abidjan, Cote d'Ivoire. Lancet 345, 607-610 PMID 7898177
  36. Taha TE, Kumwenda NI, Broadhead RL, Hoover DR, Graham SM, Van Der Hoven L, Markakis D, Liomba GN, Chiphangwi JD, Miotti PG. (1999) Mortality after the first year of life among human immunodeficiency virus type 1-infected and uninfected children. Pediatr Infect Dis J. 18, 689-694 PMID 10462337
  37. UNAIDS, 2003
  38. HHS, 2005
  39. Palella FJ Jr, Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, Aschman DJ, Holmberg SD. (1998) Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators. N. Engl. J. Med. 338, 853-860 PMID 9516219
  40. Mocroft A, Vella S, Benfield TL, Chiesi A, Miller V, Gargalianos P, d'Arminio Monforte A, Yust I, Bruun JN, Phillips AN, Lundgren JD. (1998) Changing patterns of mortality across Europe in patients infected with HIV-1. EuroSIDA Study Group. Lancet 352, 1725-1730 PMID 9848347
  41. Mocroft A, Katlama C, Johnson AM, Pradier C, Antunes F, Mulcahy F, Chiesi A, Phillips AN, Kirk O, Lundgren JD. (2000) AIDS across Europe, 1994-98: the EuroSIDA study. Lancet 356, 291-296 PMID 11071184
  42. Vittinghoff E, Scheer S, O'Malley P, Colfax G, Holmberg SD, Buchbinder SP. (1999) Combination antiretroviral therapy and recent declines in AIDS incidence and mortality. J. Infect. Dis. 179, 717-720 PMID 9952385
  43. Detels R, Munoz A, McFarlane G, Kingsley LA, Margolick JB, Giorgi J, Schrager LK, Phair JP. (1998) Effectiveness of potent antiretroviral therapy on time to AIDS and death in men with known HIV infection duration. Multicenter AIDS Cohort Study Investigators. JAMA 280, 1497-1503 PMID 9809730
  44. de Martino M, Tovo PA, Balducci M, Galli L, Gabiano C, Rezza G, Pezzotti P. (2000) Reduction in mortality with availability of antiretroviral therapy for children with perinatal HIV-1 infection. Italian Register for HIV Infection in Children and the Italian National AIDS Registry. JAMA 284, 190-197 PMID 10889592
  45. Hogg RS, Yip B, Kully C, Craib KJ, O'Shaughnessy MV, Schechter MT, Montaner JS. (1999) Improved survival among HIV-infected patients after initiation of triple-drug antiretroviral regimens. CMAJ 160, 659-665 PMID 10102000
  46. Schwarcz SK, Hsu LC, Vittinghoff E, Katz MH. (2000) Impact of protease inhibitors and other antiretroviral treatments on acquired immunodeficiency syndrome survival in San Francisco, California, 1987-1996. Am J Epidem 152, 178-185 PMID 10909955
  47. Kaplan JE, Hanson D, Dworkin MS, Frederick T, Bertolli J, Lindegren ML, Holmberg S, Jones JL. (2000) Epidemiology of human immunodeficiency virus-associated opportunistic infections in the United States in the era of highly active antiretroviral therapy. Clin Infect Dis. Suppl 1, S5-14 PMID 10770911
  48. McNaghten AD, Hanson DL, Jones JL, Dworkin MS, Ward JW. (1999) Effects of antiretroviral therapy and opportunistic illness primary chemoprophylaxis on survival after AIDS diagnosis. Adult/Adolescent Spectrum of Disease Group. AIDS 13, 1687-1695 PMID 10509570
  49. NIAID, 1995a
  50. NIAID, 1995b
  51. Schechter MT, Craib KJ, Gelmon KA, Montaner JS, Le TN, O'Shaughnessy MV. (1993) HIV-1 and the aetiology of AIDS. Lancet 341, 658-659 PMID 8095571
  52. Vermund SH, Hoover DR, Chen K. (1993) CD4+ counts in seronegative homosexual men. The Multicenter AIDS Cohort Study. N Engl. J. Med. 328, 442 PMID 8093639
  53. Des Jarlais DC, Friedman SR, Marmor M, Mildvan D, Yancovitz S, Sotheran JL, Wenston J, Beatrice S. (1993) CD4 lymphocytopenia among injecting drug users in New York City. J Acquir Immune Defic Syndr. 6, 820-822 PMID 8099613
  54. Donegan E, Stuart M, Niland JC, Sacks HS, Azen SP, Dietrich SL, Faucett C, Fletcher MA, Kleinman SH, Operskalski EA, et al. (1990) Infection with human immunodeficiency virus type 1 (HIV-1) among recipients of antibody-positive blood donations. Ann Intern Med. 113, 733-739 PMID 2240875
  55. Cohen J. (1994) Duesberg and critics agree: hemophilia is the best test. Science 266, 1645-1646 PMID 7992044
  56. Hassett J, Gjerset GF, Mosley JW, Fletcher MA, Donegan E, Parker JW, Counts RB, Aledort LM, Lee H, Pike MC. (1993) Effect on lymphocyte subsets of clotting factor therapy in human immunodeficiency virus-1-negative congenital clotting disorders. The Transfusion Safety Study Group. Blood 82, 1351-1357 PMID 8353293
  57. Aledort LM, Operskalski EA, Dietrich SL, Koerper MA, Gjerset GF, Lusher JM, Lian EC, Mosley JW. (1993) Low CD4+ counts in a study of transfusion safety. The Transfusion Safety Study Group. N. Engl. J. Med. 328, 441-442 PMID 8093638
  58. Sabin CA, Pasi KJ, Phillips AN, Lilley P, Bofill M, Lee CA. (1996) Comparison of immunodeficiency and AIDS defining conditions in HIV negative and HIV positive men with haemophilia A. BMJ 312, 207-210 PMID 8563582
  59. Gjerset GF, Pike MC, Mosley JW, Hassett J, Fletcher MA, Donegan E, Parker JW, Counts RB, Zhou Y, Kasper CK, et al. (1994) Effect of low- and intermediate-purity clotting factor therapy on progression of human immunodeficiency virus infection in congenital clotting disorders. Transfusion Safety Study Group. Blood 84, 1666-1671 PMID 7915149
  60. Goedert JJ, Kessler CM, Aledort LM, Biggar RJ, Andes WA, White GC 2nd, Drummond JE, Vaidya K, Mann DL, Eyster ME, et al. (1989) A prospective study of human immunodeficiency virus type 1 infection and the development of AIDS in subjects with hemophilia. N. Engl. J. Med. 321, 1141-1148 PMID 2477702
  61. 61.0 61.1 U.S. Census Bureau, 1999
  62. NIAID FACT Sheet: HIV/AIDS Statistics
  63. UNAIDS, 2005
  64. Alcabes P, Munoz A, Vlahov D, Friedland GH. (1993) Incubation period of human immunodeficiency virus. Epidemiol Rev. 15, 303-318 PMID 8174659
  65. Evans AS. (1982) The clinical illness promotion factor: a third ingredient. Yale J Biol Med. 55, 193-199 PMID 6295003
  66. Fauci AS. (1996) Host factors and the pathogenesis of HIV-induced disease. Nature 384, 529-534 PMID 8955267
  67. USPHS/IDSA, 2001

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