Deadly, virulent viruses have jumped species from nonhuman primates such as chimpanzees to the human species three times in history: the SIV virus that almost certainly led to the worldwide AIDS pandemic, the SV-40 "cancer" virus that was accidentally included in polio vaccines in the 1950s, and the deadly Ebola virus.
Now, in a scenario that sounds more like science fiction than reality, biodefense researchers are quietly looking at the remote possibility some day of a fourth instance of species jump: simian hemorrhagic fever virus, which is either more deadly and untreatable than Ebola, or the key to unlocking cures for such species-jumping viruses.
Research on SHFV could either put the lid back on Pandora's box, or open it even wider.
This sort of research is one of the reasons that regulatory agencies monitor scientific advances in the transfer of human genetic materials from nonhuman species to human beings. This sort of work could, some believe, lead to instances where a deadly, untreatable virus "jumps species" before we're able to understand the ramifications.
The truth is that mankind is on the cusp of a new genetic era. We've mapped the human genome, as well as the genome of the bonobo, our closest relative. Xenotransplantation, the ability to replace an organ such as a kidney in a human with one from an animal, is just over the horizon.
Gene expression is leading to revolutionary theories about DNA changes that can be passed from one generation to the next. And, yet, we know very little about unintended consequences in this new world of genetic manipulation.
Is it ethical or safe to "drop out" a gene in a chimp that causes organ rejection in humans, grow a kidney from human DNA, and use it in xenotransplantation to replace a sickly human kidney? Will we introduce untreatable viruses, such as Ebola or SHFV, to the human species through such experimentation?
Science, though, marches forward in the race toward the endless frontier. Some believe, it may simply be a matter of time before someone decides to push that boundary and perhaps unwittingly introduces genetic complications that no one foresaw.
The simian hemorrhagic fever virus — a close cousin to the Ebola virus — could potentially jump species. Thankfully, to the best of anyone's knowledge, it hasn't. And that makes it valuable for researchers.
The first identification of SHFV in a wild, nonhuman primate was published in an open-source, research journal (PLOS One) in 2011.
While SHFV has caused lethal outbreaks of hemorrhagic disease in captive primates, no one knew whether it could be found in primates in the wild. The PLOS One study last year, however, described the discovery of two novel, divergent SHFV variants that had co-infected a single, male, red colobus monkey from Kibale National Park in Uganda.
The viruses were detected directly from blood plasma using pyrosequencing, a process that takes a single strand of actual DNA and essentially compares it to synthetic, complementary DNA strands.
The two new SHFV variants found in the wild, colobus monkey were highly divergent from each other, which helped researchers document that this was the first known instance of SHFV in a wild primate.
The SHFV virus is uncharacterized — which means that we know virtually nothing about its origin, virulence, treatability, path of transmission, or whether it will kill us like Ebola should it jump species.
What is known about SHFV is that it's an acutely fatal disease of Asian macaques.
Researchers have been able to identify sporadic outbreaks of SHFV in macaques at primate research facilities. Because none of the outbreaks was linked to human disease, researchers have speculated that SHFV could be used as a model for hemorrhagic fever viruses such as Ebola, Marburg, and Lassa viruses. A recent study identified ways in which SHFV might help map out the progression of a virus such as Ebola in humans.