I have now been asked a perfectly reasonable question that arises from our recent paper on chimpanzee “AIDS” several times (see previous entry). The question is, should we reinvigorate biomedical testing of SIV infection in chimpanzees as a model for HIV? The simple answer is no. There are several compelling reasons for this.
First, there are the ethical considerations. Given the genetic and phylogenetic closeness of chimpanzees to humans and their complex psychology and social behavior, the use of chimpanzees in experimental medical studies is not an ethically viable practice. Second, there is the legal fact that chimpanzees are an endangered species and therefore protected from such uses by international law. Third, is the simple economic argument. Chimpanzees are too expensive to maintain for the types of insights biomedical research on them is likely to yield. Fourth, they are impractical as an animal model. Chimpanzees live for 40 years or more in captivity and the time course of SIV pathology — while still not entirely understood — is certainly slow (remember the lenti– in lentivirus means slow). Remember, the surprising thing about our paper is that no one noticed AIDS-like pathology either in the wild or in experimentally infected chimps in captivity. Finally, we have much better animal models. SIVmac infection of rhesus monkeys provides an excellent model of infection and pathogenesis. Rhesus macaques are much less long-lived, are not endangered, have a much shorter time-course of pathogenesis, and their social systems make them far easier to manage in captivity. Of course, parallel ethical arguments can be used against biomedical research on any primate species as those for chimpanzees, but I’m going to duck that for the time being since this is a post on chimpanzees.
That’s the take on invasive, laboratory-based, biomedical research. Naturalistic studies of SIVcpz are another story altogether. We strongly believe that field studies of naturally infected ape populations (western lowland gorillas also have naturally acquired SIV infection) should be expanded. These studies would help us understand HIV pathogenesis by providing fecal, urine, and post-mortem samples for virological and immunological analysis. With regard to post-mortem samples, it is particularly important to have a constant field presence. Even when the mortality hazard is 16 times the baseline, death is a relatively rare event and bodies disappear amazingly fast in tropical forests (perhaps I’ll post some day about the maddening difficulty of trying to collect feces in a rainforest).
Our results open up an opportunity to compare pathogenesis in two closely related species. We hope that this will accelerate the identification of both viral and host factors responsible for disease progression. This, in turn, could lead to the development of novel therapeutic or preventative measures that have the potential to benefit both chimpanzees and humans. I am particularly sanguine about the possibilities of finding host factors that are protective against infection. With my former post-doc and current NCEAS scholar, Sadie Ryan, I have been doing some analysis of chimpanzee sexual networks. I don’t want to spill the beans here before we submit the paper, but suffice it to say, there is a lot of exposure to SIVcpz in chimpanzee sexual networks. This shouldn’t be surprising to anyone who has even a passing familiarity with chimpanzee mating systems, but the formalization makes it particularly striking.