Immunodeficiency viruses and prion disease
Two threatening human diseases have emerged during the past 35 years. Human immunodeficiency virus (HIV) was transmitted from non-human primates – e.g., the chimpanzee to humans – and then spread into populations all over the world. To date, around 35 million people are infected and no vaccine is available because the virus undergoes rapid mutation, resulting in a swarm of virus strains. At best, therapeutical intervention is possible with antiviral drugs; however because of its capacity to rapidly mutate, resistant virus strains develop. Since non-human primates (NHPs) carry simian immunodeficiency virus (SIV), we could assess infection and immunity by SIV/HIV in rhesus monkeys (
M. mulatta) as a model for acquired immunodeficiency syndrome (AIDS).
Transmissible spongiform encephalopathy (TSE) emerged in ruminants in the 1980s and shortly thereafter appeared in humans, leading to variant Creutzfeldt–Jakob disease (vCJD). The vCJD is a terminal neurological disorder since it heavily and irreversibly damages the brain. No cure is at hand. The causative agents for TSE are prions. They are unusual pathogens and enigmatic since they lack nucleic acid as inheritable information. On the other hand, prions were suspected as infectious agents for years and suspected to be the etiological agent of scrapie in sheep. Molecular biology and medicine have clearly identified prions in recent years as the responsible agent for bovine spongiform encephalopathy in ruminants (BSE). BSE has been transmitted to humans, resulting in around 225 vCJD cases. Similar to the SIV/HIV model for Acquired Immunodeficiency Syndrome (AIDS), we could establish a prion infection model in rhesus monkeys.
HIV/AIDS and vCJD are zoonoses since their original pathogens can be transmitted from animals to humans. Our experimental efforts to understand these intriguing pathogens and their corresponding diseases in rhesus monkeys as a valid model for both human diseases are summarized in this review.