Monkey AIDS and Man
Connections can be made between animal and human disease. The fact that a pathogen can be transmitted from animals to humans demonstrates that there is a human version to the animal disease. Non-human primate AIDS, and SIV, was identified during the early 1980’s, several years AFTER the recognition of AIDS in humans in 1981. Researchers say that simian AIDS could have been identified long before, and had it been recognized, it may have hastened the discovery of HIV and the treatment/prevention of AIDS in humans.
Retrospective research showed that documented outbreaks of “rare” and “unusual conditions” in monkeys were actually opportunistic infections of AIDS caused by SIV. During the 1960’s and 1970’s primate centers and laboratories, particularly the New England Regional Primate Center and The National Center for Primate Biology at the University of California, Davis, reported lymphoma in monkeys. The lymphomas were initially associated with being caused by herpesvirus.
Additional rare conditions were often attributed to other infectious agents or environmental toxins. Several cases of Yersinia pseudotuberculosis were found in macaques and attributed to gastrointestinal disease. Another disease, Avian tuberculosis was associated with infection by SIV. Monkeys were also found to have Mycobacterium Avium-Intracellulare (MAI), herpesvirus simiae, and oral candidiasis. Morever, another disease, Progressive Multifocal Leukoencephalopathy (PML) was found in macaques, several of which also had shigellosis, avian tuberculosis, chronic anemia, and lymphoma.
Many viruses were suspected at the time to cause these disease in monkeys, such as, herpes viruses, simian sarcoma virus, gibbon ape leukemia virus, and Mason-Pfizer virus. This presented several problems for researchers to discern the root cause. The “rare” and “unusual conditions” seen in monkeys were illnesses that could be linked to other viruses. Later, it came to be understood that these were secondary infections. At times, two viruses or diseases were present within the animal at once, making it difficult to decipher which was the cause and which was the effect. When clusters of a single disease were present, there was no reason to suspect immunosuppression.
Connecting The Dots….Or Not
Numerous cases presented opportunities for scientists to make the correlation that they were dealing with an infectious agent. For example, Inoculum in the form of lymphoma cells were transferred from sick to healthy rhesus monkeys. Within three weeks the healthy monkeys would develop lymphoma. PML had already been associated with immune deficiency, caused by treatment with immunosuppressive agents, and possibly by viral infections. The fact that some monkeys infected with Simian Virus 40 (SV-40) also developed PML, but others did not, should have suggested that SV-40 was not the cause of PML, and that immunosuppression was prerequisite for PML. Mason-Pfizer virus was even found in macaques with severe immunosuppresion, but this virus is unrelated to SIV and HIV.
Other missed clues include; vertical transmission of disease from mother to offspring, that disease spread from cross-transfusion of blood, and that prior infection with herpes virus hominis was common; all of which are shared characteristics of human HIV/AIDS. The conditions were even associated with c-type retroviruses. The follow-up studies necessary to prove a correlation between an infectious agent that caused immunosuppression, and subsequent opportunistic disease were never done, and Simian AIDS went undiscovered.
Even given all these instances, It is arguable whether the recognition of simian AIDS would have hastened the discovery of HIV/AIDS in humans. RNA tumor viruses were known in animals for decades. However, during the mid twenties century, at the time of the outbreaks in monkeys, there was little interest in infectious disease research. Additionally, it was believed that no cancer-causing human retroviruses existed. AIDS in monkeys primarily presented with lymphoma and leukemia, however, the same is not true of AIDS in humans, where lymphoma is not a common opportunistic disease. In humans the primary conditions indicative of AIDS are lymphadenopathy and Pneumocystis Carinii pneumonia; an opportunistic infection caused by fungi. However, a major complication of human AIDS is Kaposi’s Sarcoma; a rare cancer not associated with lymphoma. A few years after AIDS was recognized in humans, the virus known as HIV was identified as its cause.
Hindsight, What We’ve Learned As Scientists
In summary, antiquated sociopolitical beliefs concerning science coupled with a lack of cooperation between laboratories, hindered valuable and necessary research that could have predicted HIV/AIDS. Clusters of outbreaks of “rare” and “unusual conditions” in monkeys, were a warning sign of what was arising in humans. This missed opportunity of discovery, led undoubtedly to the stigmatization of people diagnosed with AIDS and their untimely deaths; as it was not believed that the disease was caused by a virus. This “public health tragedy” should serve as a cautionary tale for researchers. The lesson to be learned is that knowledge should be managed in an efficient and responsible way, that offers interdisciplinary collaboration and exchange of data. Surveillance (literature review), communication, creative thinking, and continued vigilance are essential for scientific advancement, and should not be outweighed by popular opinion and dogma.
Theodore M. Hammett and Roderick T Bronson, 2016. Unrecognized “AIDS” in Monkeys, 1969-1980: Explanations and Implications. American Journal of Public Health 106.6 pg 1015-1022.