Bats and ebola
Ebola is a nasty disease. Sufferers endure a high fever and severe internal bleeding from every mucus membrane in the body. Depending on the strain, it can kill as many as 90% of its victims. A 2007 outbreak in the Congo killed 186 of 264 people who contracted the ebola virus (71%). The puzzle is how something so virulent manages to survive.
Think about it: Any disease-causing organism (called a pathogen) is completing some kind of life cycle in its host. That means that the pathogen is using the host as an environment to produce offspring (or for some pathogens to mature to a form that can produce offspring somewhere else). In some cases the host is actually required for the pathogen to complete its life cycle. So it's actually in the pathogen's best interest not to kill its host. Do that, and there won't be any baby pathogens. For pathogens that kill their hosts quickly, there must be some other place that the pathogen hides out when not causing disease. For example, the anthrax bacterium, which can efficiently kill people in about 24 hours, normally lives in the soil. What about the ebola virus?
Bats have long been considered the "reservoir" of the ebola viruses, and a 2005 paper from Leroy et al. found indirect evidence of ebola virus infections in fruit bats. More recently, a research group from SUNY Buffalo found actual ebola-like genes in the genomes of certain bats, rodents, and insectivores, which implies that ebola's been hiding out in more than just bats. I commented on this research last year.
Now the same group is back with a paper that indicates that these virus genes might in some way be functional to the mammals that have them. Their research was done using evolutionary and comparative methods, but I think the basic message is probably the same for creationists: The virus genes in Myotis bat species still have "open reading frames," even though they appear to have been integrated into the host genome before Myotis diversified into multiple species. Usually when extra DNA is integrated into a host genome, it tends to break down due to mutations that build up randomly in the DNA sequence. In this case, there seems to be a mysterious lack of mutations that would disable a gene, which is what we might expect from DNA sequences of no use to the host.
When discussing this research last year, I wondered,
Longtime readers will recall Liu and Soper's exogenation hypothesis for the origin of viruses. They proposed that endogenous retroviruses were originally part of mammalian genomes that escaped and caused trouble. Could we now add ebola viruses to that list as well?
Something to think about.
Taylor et al. 2011. Evolutionary maintenance of filovirus-like genes in bat genomes. BMC Evolutionary Biology 11:336.
Feedback? Email me at toddcharleswood [at] gmail [dot] com.
Think about it: Any disease-causing organism (called a pathogen) is completing some kind of life cycle in its host. That means that the pathogen is using the host as an environment to produce offspring (or for some pathogens to mature to a form that can produce offspring somewhere else). In some cases the host is actually required for the pathogen to complete its life cycle. So it's actually in the pathogen's best interest not to kill its host. Do that, and there won't be any baby pathogens. For pathogens that kill their hosts quickly, there must be some other place that the pathogen hides out when not causing disease. For example, the anthrax bacterium, which can efficiently kill people in about 24 hours, normally lives in the soil. What about the ebola virus?
Bats have long been considered the "reservoir" of the ebola viruses, and a 2005 paper from Leroy et al. found indirect evidence of ebola virus infections in fruit bats. More recently, a research group from SUNY Buffalo found actual ebola-like genes in the genomes of certain bats, rodents, and insectivores, which implies that ebola's been hiding out in more than just bats. I commented on this research last year.
Now the same group is back with a paper that indicates that these virus genes might in some way be functional to the mammals that have them. Their research was done using evolutionary and comparative methods, but I think the basic message is probably the same for creationists: The virus genes in Myotis bat species still have "open reading frames," even though they appear to have been integrated into the host genome before Myotis diversified into multiple species. Usually when extra DNA is integrated into a host genome, it tends to break down due to mutations that build up randomly in the DNA sequence. In this case, there seems to be a mysterious lack of mutations that would disable a gene, which is what we might expect from DNA sequences of no use to the host.
When discussing this research last year, I wondered,
What we would really like to know is whether any of these putative insertions exist at homologous chromosomal sites in mammals that are likely to be of different baramins. That would suggest that they were created there rather than inserted.This new report confirms that the inserts in some rodents are "positionally homologous," which would imply that they were created at that spot. So bats and some rodents were created with ebola genes? Fascinating!
Longtime readers will recall Liu and Soper's exogenation hypothesis for the origin of viruses. They proposed that endogenous retroviruses were originally part of mammalian genomes that escaped and caused trouble. Could we now add ebola viruses to that list as well?
Something to think about.
Taylor et al. 2011. Evolutionary maintenance of filovirus-like genes in bat genomes. BMC Evolutionary Biology 11:336.
Feedback? Email me at toddcharleswood [at] gmail [dot] com.