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Dr Richard Hunt |
BACTERIOLOGY | IMMUNOLOGY | MYCOLOGY | PARASITOLOGY | VIROLOGY | |||||||||||||||
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LINKS TO OTHER HIV AND AIDS SECTIONS ARE AT THE BOTTOM OF THIS PAGE |
VIROLOGY
- CHAPTER SEVEN THE HISTORY OF THE DISEASE HUMAN IMMUNODEFICIENCY VIRUS AND AIDS
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WEB RESOURCES Read the original 1981-1982 MMWR reports on a new immunodeficiency disease in the gay community:A Cluster of Kaposi's Sarcoma and Pneumocystis carinii Pneumonia among Homosexual Male Residents of Los Angeles and Orange Counties, California Diffuse, Undifferentiated Non-Hodgkins Lymphoma among Homosexual Males -- United States The first report of
transfusion-related immune deficiency In December 1982: First
report of hemophilia-related immune deficiency in July 1982: Important
milestones in the epidemiology of AIDS from CDC. Links to many of the
important MMWR papers
History of AIDS
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In 1981, clusters of cases of Kaposi's sarcoma (figure 3B) were reported in patients in San Francisco and New York. This was an unusual occurrence since, in the United States, Kaposi's sarcoma was a rare disease that normally occurred in elderly men of Jewish or Mediterranean ancestry; however, these new clusters of patients were all young male homosexuals and the disease was much more aggressive. Other diseases associated with immuno-compromisation also arose in this same population; particularly of note were the occurrence of Pneumocystis pneumonia (which is an opportunistic infection) and lymphadenopathy (diffuse, undifferentiated non-Hodgkins lymphoma).
Pneumocystis pneumonia, which is caused by a fungal parasite (Pneumocystis carinii - now renamed Pneumocystis jiroveci, Figure 3A), was also a very rare disease in the United States. During the period between 1967 and 1978, only five cases of this disease occurred in Los Angeles; however, in 1981 alone, five cases occurred in the same area. Again, all patients were young male homosexuals. The number of sex partners of these patients appeared to be important in that the disease was particularly prevalent among promiscuous individuals and the partners of those individuals. No cases of diffuse, undifferentiated non-Hodgkins lymphoma were reported in the young male (20 - 39 years old) population of the San Francisco area during the period 1977-1980. However, from March 1981 to January 1982, the unusual occurrence of four cases within 10 months was observed; again, these were in the homosexual male population. During 1982, similar immunodeficiencies were found in hemophiliacs (July), persons who received blood transfusions (December) and intra-venous drug users who shared needles. Moreover, by January 1983, it was clear that the female sex partners of these patients also got the disease. In view of this, it was obvious that an infectious agent was involved; this agent was either passed during sexual intercourse or by receiving blood (or blood products) from another person. At the same time as these events were occurring in western countries, doctors in Uganda were observing a similar fatal wasting syndrome that they called slim disease. The cell picture - the selective loss of T4 helper (CD4+) cells - suggests a virus. But the causative agent was difficult to identify at first because it does not grow on resting T4 cells. The discovery of HIV depended on the ability to grow the virus in vitro and this required the used of activated T4 cells. The disease was originally termed
Kaposi's Sarcoma and Opportunistic Infections (KSOI) and then Gay-Related Immune Deficiency (GRID) but we now know it as Acquired
Immuno-Deficiency Syndrome (AIDS or SIDA in French and Spanish). AIDS is almost always fatal as a result of immuno-suppression and consequent opportunistic infections
(unless chemotherapeutic intervention occurs).
The epidemic has resulted in the deaths of more than half of AIDS patients.
The clue to growing HIV came with the realization that, while it did not grow on resting T4 lymphocytes, it would grow on T4 cells that had been activated with a cytokine called interleukin-1. The virus was isolated in 1984 by Luc Montanier (Pasteur Institute, Paris) and Robert Gallo (NIH, Bethesda, USA). Montanier called the virus lymphadenopathy virus (LAV) and Gallo, who had discovered the first human leukemia virus (HTLV-1), named the virus HTLV-3. Today we know it as human immunodeficiency virus (HIV). A similar cellular picture is seen in some cases of feline leukemia and HTLV-1 infection, i.e. a selective loss of a specific class of cells giving rise to immune suppression, further suggesting that the cause of AIDS is a virus. |
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VIDEO See a 17 minute video looking back 20 years to the early days of CDC's involvement in the AIDS epidemic VIDEO
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Figure 3ACysts of Pneumocystis carinii in AIDS. Methenamine silver stain. Histopathology of lung shows characteristic cysts with cup forms and dot-like cyst wall thickenings. CDC/ Dr. Edwin P. Ewing, Jr. |
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Figure 3B Kaposi's Sarcoma |
The perivenular infiltrate of Kaposi sarcoma shows a mixture of spindle cells, inflammatory cells, and ectatic vascular spaces.
The Johns Hopkins Autopsy Resource
(JHAR). Image Archive.
Skin showing AIDS-associated Kaposi's sarcoma
Bristol
Biomedical Image Archive, University of Bristol. Used with permission |
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Lesions on the
stomach of a patient with Kaposi's sarcoma
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OTHER SECTIONS ON HIV PART I HUMAN IMMUNODEFICIENCY VIRUS AND AIDS PART II HIV AND AIDS, THE DISEASE PART III COURSE OF THE DISEASE PART XI OTHER CELLS INFECTED BY HIV AND POPULATION POLYMORPHISM PART VI SUBTYPES AND CO-RECEPTORS PART VII COMPONENTS AND LIFE CYCLE OF HIV |
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