The inter-species transmission of viruses and other pathogens (see data below) poses a serious threat to public health, the global economy as well our environment and biodiversity. Just look at Ebola; SARS and Hendra viruses. With the numbers of emerging viruses increasing year on year, how best are we to deal with this incoming threat? As they say, the most effective bioterrorist is nature herself; so how can we stop her?
|Increasing numbers of emerging infectious diseases. Jones et al (2008)|
First of all, we can identify a number of possible routes that may be followed if we are to successfully combat or at least limit human infection with other animal viruses. These would include:
- Identifying what viruses may make (or are in the process of making) the jump into humans, i.e. what viruses are out there?
- What are the molecular mechanisms behind inter-species transmission and adaptation?
- Can we identify temporal and geographical (or cultural) 'hotspots' that correlate with increased risk of virus emergence?
- How can we develop potential vaccines/antivirals to further protect vulnerable local/global populations?
And, perhaps most importantly - and the most difficult aspect:
- How are we going to fund this and what are the most cost-effective measures of doing this, i.e can we identify the best places to protect ourselves and place our resources there?
|Hantavirus - a deadly group of re-emerging viruses. http://virology-online.com/|
Orrock et al, publishing recently in the journal American Naturalist, give their contribution to this complex virus protection scheme by identifying key ecological regulators of the potential emergence of a fatal human virus from its rodent species reservoir. Knowledge of this may allow us to pin-point potential danger areas in terms of countries/regions or seasons (by applying their principles to other viruses and ecosystems), which would increase the risk of human infection. By placing emphasis on these areas we could develop a safer, more cost effective strategy to protect at-risk populations.
The model system the group used was that of the rodent-borne hantvirus, Sin Nombre virus (SNV) infecting its host, the deer mouse, Peromyscus maniculatus on the Californian Channel islands. This virus was only relatively recently found to be present among Channel islands deer mice. Hantaviruses are a group of trisegmented negative sense RNA viruses that naturally infect rodent species around the world. Two groups are recognised: one found throughout the new world and the other, throughout the old. When a human is infected by one of the new world viruses (Sin nombre virus, for example), they may develop what is known as hantavirus cardiopulmonary syndrome (HCPS), a life-threatening disease (with up to 50% mortality) caused by leakage of fluids into the lungs. Humans get infected through coming into contact with infected rodents through their aerosolised urine, feces or saliva. In the U.S, the deer mouse (Peromyscus maniculatus) is the primary reservoir of this viruses. Environmental determinants of rodent density are thought to play a significant role in the risk of rodent-human disease through increasing the chances of human/deer mouse contact.
Specifically, they obtained SNV-specific antibody data relating to infected mice across all islands, giving them an accurate estimate as to the prevalence of SNV in these mouse populations. The group also compiled data corresponding to a number of environmental factors of these islands, including: area, perimeter, elevation, annual precipitation ( a good correlate with island productivity) and finally the number of deer mouse predators found across the islands. These numbers allowed Orrock et al to determine which ecological factor correlated well with SNV prevalence individually or in combination with others; data that would allow for the prediction of at-risk areas across the islands.
A number of factors were identified, for example: SNV prevalence correlated well with annual precipitation on the islands as well as island area, which I guess may be expected given that these factors influence the food sources that the mice eat as well as potential space to leave and breed.
Predator richness negatively correlates with SNV prevalence, suggesting that if we were to artificially remove top predator species from this ecosystem, rodent population density would increase, leading to more and more SNV-infected mice with a greater chance of infecting both themselves and humans. The authors state that the protection of both biodiversity and individual predators within ecosystems would serve to protect human populations from rodent-human virus transmission through the better regulation of host density. Also, environmental increases in primary productivity within the isalnd may also increase the risk of emergence.
So, Orrock et al have demonstrated the key role of a number of ecological regulators of virus prevalence using a unique island-rodent virus model system. They specifically focused on a potentially fatal virus that can infect humans and hence their work has medical significance within the island system. They have also identified possible situations (bigger islands/more rainfall/low predator richness) that favor an increase in SNV prevalence although, they have not determined exactly why each occurs. This adds to the debate on the relevance of biodiversity to general protection from zoonotic disease.
This work supplies important evidence for the potential prediction of 'at-risk' regions - not just within the Californian Channel islands - that pose a threat of virus emergence. Seasons with increased rainfall that increase primary production and hence possibly increase rodent densitie. Predictions such as these have recently been used within China and South Korea to identify areas for targeted control of hantavirus infections.
Orrock, J., Allan, B., & Drost, C. (2011). Biogeographic and Ecological Regulation of Disease: Prevalence of Sin Nombre Virus in Island Mice Is Related to Island Area, Precipitation, and Predator Richness The American Naturalist, 177 (5), 691-697 DOI: 10.1086/659632