When Did AIDS Begin?
By
Malise Cross

The earliest reported case of AIDS was believed to have been in a seaman from Manchester England in 1959. (Kuby & Auleb)

The man died of an immunodeficiency associated infection. Some tissue from the dead seaman, which had been preserved in paraffin blocks, showed that DNA from HIV was in cells from his bone marrow, spleen, kidney and pharyngeal mucosa. In 1998 it was determined that the specimen had been contaminated during the investigation. However, there is another case of HIV infection dating back to 1959. In scanning 1200-stored plasma samples from various parts of Africa, one tested positive for HIV antibodies. The sample came from an HIV-infected Bantu man in Kinshasa (Congo). They were able to detect HIV DNA in the sample as well. The earliest known presence of HIV in the US was in 1969 in a teenager whose cause of death involved immune deficiency. The earliest case in Europe was in a Danish surgeon who had worked in Zaire and died in 1976.

There are many theories of how HIV developed, ranging from plausible and worthy notions to wacky inconceivable ideas. One notion conceives HIV as human made--for conspiracy theories, such as: the US Government created HIV and Ebola virus; it was a Soviet plot; or the CIA developed it. A different opinion accepts HIV as an animal-origin virus, which came from cats or evolved from monkey viruses. Another notion is that it existed in rural populations, subsequently evolving and spreading with urbanization. With urbanization there is an increase in the transmission of many diseases (including STDs), and in the importance of transmission through drug use.

Many scientists now believe that AIDS appears to have started in Africa. The fact that several monkey and chimpanzee species found in Africa are infected with retroviruses that are closely related to HIV has led to the speculation that HIV arose from a simian (monkey or chimpanzee) derived retrovirus. Several hypotheses have been put forward as possible mechanisms by which the simian-derived strain of the retrovirus, SIV (Simian Immunodeficiency Virus), may have been introduced into humans. SIV seems to cause no illness in chimpanzees, even though humans and chimpanzees are 98% genetically similar (Altman). Mutation of the simian-derived SIV strain may then have yielded a strain not only capable of replication in human cells but also far more pathogenic in humans.

There are several ways by which humans may have become infected by a simian retrovirus. One hypothesis believes its emergence came from human use of monkeys. HIV-2 is very closely related to a strain of SIV found in sooty mangabees and the location of sooty mangabees in West Africa coincides with the incidence of HIV-2. There is evidence that sooty mangabees are occasionally killed and eaten in this region. A hypothesis suggested by F. Noireau in 1987 suggested cross-species transfer of SIV to humans might have occurred when monkey blood was applied to human genitals after pubertal circumcision. Such practices could have eventually led to the emergence of a new strain of SIV capable of infecting humans and causing AIDS. Based on the DNA sequences of SIV and HIV-1 and HIV-2, it appears that SIV may have given rise to HIV-2. The origin of HIV-1 is unknown but it is presumed to have arisen from another monkey virus. It is thought that HIV may have begun to spread in Africa after the Second World War when medical personnel began to administer antibiotics by syringe. Syringes were often limited in supply and were generally reused. HIV could then easily be transmitted from an infected individual to an uninfected individual. The virus then might be carried from a rural population into an urban population where it would continue to spread by sexual contact, transfusions etc. It is possible that individuals would have died of some opportunistic infection like Pneumocystis Carinii pneumoma, and no one would have known it was AIDS.

Another hypothesis suggests HIV introduction by early malaria research. According to Charles Gilles, a British tropical disease expert, the early malaria research took blood from chimpanzees, sooty mangabees and macaques to vaccinate human volunteers against malaria; if this blood was infected with strains of SIV it might have infected the human volunteers and slowly mutated to give rise to HIV-1 or HIV-2.

Or, the entrance of HIV in humans may have occurred via a polio vaccine. Early polio vaccines may have been contaminated with SIV. Introduction of the polio vaccine into humans may then have provided a vehicle for massive cross-species transfer of SIV into humans. Dr. Jonas Salk developed the first widely used polio vaccine in 1954. His vaccine used ultraviolet light and formaldehyde fixation to inactivate (kill) the polio virus. A live, attenuated polio vaccine was developed by Dr. Albert Sabin, and human vaccination trials with that vaccine began in 1956. The attenuated vaccine was acquired by repeated growth of the virus in monkeys, of monkey kidney cells, until a weakened, but living virus was isolated. A weakened virus had certain advantages over the inactivated vaccine. Because the virus was alive, it could grow in human cells for a limited time, inducing a more pronounced immune response. During the same period an oral, attenuated, vaccine was also developed by Dr. Hillary Koprowski. His vaccine was the first vaccine given to a large population; in 1957 the vaccine was administered via an oral spray to over a quarter of a million individuals in the Belgian Congo (known as Zaire and more recently as The Republic of The Congo). In 1958, vaccination continued with 75,000 children in Leopoldville (now Kinshasa, Zaire) receiving the vaccine (Hooper).

Each of the early polio vaccines were derived from the poliovirus grown in monkeys and monkey kidney cells, unfortunately, additional monkey viruses were also harvested. In the Salk vaccine the progress of inactivation of the polio virus by formaldehyde fixation generally inactivated many contaminating viruses. However, one contaminant virus that was not inactivated was the retrovirus simian virus 40 (SV40; named because it was the fortieth simian virus found contaminating the early polio vaccine). In the Sabin and Kaprowaki vaccines, the polio virus was not inactivated and even more live contaminating viruses were harvested along with the polio virus. Koprowski's vaccine was developed in minced rhesus macaque monkey kidneys to weaken the virus. Later, the rhesus macaque monkey was shown to be the natural host for SV40. Koprowski then switched to the African green monkey to grow the vaccine. Although the African green monkey was free of SV 40, it may have been the source of an even more serious contaminating virus, SIV or another precursor to HIV.

If SIV was introduced into humans by means of the oral polio vaccine, there are still several questions about the polio vaccine being the source of HIV-1 infection. SIV is more closely related to HIV-2 than HIV-1, but it is HIV-infection that is widespread in Zaire, not HIV-2 infection. The earliest recorded case of AIDS was the Bantu man in 1959. If he became infected from someone in Africa in 1957 or 1958, then the man must have died very soon after infection. HIV is far more pathogenic than SIV. How did the virus become so pathogenic in humans? There are numerous examples of viruses of low pathogenicity having increased pathogenicity when introduced into another species. For example, canine papovavirus, a virus that causes damage to the heart and intestinal tissues in dogs, is thought to have arisen from an attenuated cat vaccine. Although the vaccine is a weakened virus for cats, its introduction into dogs appears to greatly increase in pathogenicity to them. Another example of increased viral pathogenicity across species lines was observed during the development of the polio vaccine. In 1932, a polio researcher was bitten by a monkey, contracted monkey B virus and died (Hooper). In monkeys this herpes family virus causes mild fever blisters, but in humans the virus results in paralysis and death.

References:
Altman, Lawrence. "Scientists Say Chimp Virus Is African Chimpanzee Species Has Similar, Nonfatal Virus." 1 February 1999.
Hooper, Edward, THE RIVER, New York: Little, Brown And Company, 1999.
Kuby, Jan and Susanne Leb, Biology 330 Lecture Guide: AIDS: The Biology of A Modern Epidemic. California San Francisco State University, 1999.

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