Longtime readers know of my fascination with Ebola. Much of it is fueled not by the fact that it’s a major killer of humanity, because it’s not: in 30 years, it’s been responsible for a bit less than 2,000 human infections, and ~1,200 deaths. Bats have long been suspected to be a reservoir of the virus, and recent studies have confirmed that they can carry the virus.

With at least one strain of Ebola (Ebola Reston), we know that our primate cousins are more severely affected than we are. This strain has been found to infect captured primates brought into the United States from the Philippines, proving highly lethal to the affected ape species but causing only sub-clinical infections in humans. Ebola in wild African apes was first documented in 1994, when an outbreak occurred in chimpanzees in Ivory Coast. Since that time, reports of deaths from Ebola in wild apes have circulated during several human outbreaks of the disease. A recent paper again highlights the horrible effects Ebola has wreaked upon our native primate species, and suggests that living in groups may have made them even more vulnerable.

It’s been known for several years that Ebola is decimating great apes in Africa. Many populations of gorillas and chimpanzees that have been under surveillance by primatologists for years have all but disappeared. Previous studies of this phenomenon have focused on numbers of apes pre- and post-outbreak, but the current study is the first to try and figure out just what is going on within the gorilla populations during the outbreak. To do this, the authors used two different models of viral transmission, investigating which was more important in maintenance of the epidemic: transmission to apes from the reservoir species, or transmission of the virus from ape to ape.

The investigators use variations on a SEIR model, which stands for Susceptible, Exposed, Infectious, and Removed. This is a pretty typical mathematical model, which breaks the population up depending on their status with regard to the microbe in question. When a new infection enters a population, all of the population will be susceptible. As individuals are exposed to the infectious agent, they may then become infectious, spreading the microbe to others in the population. If they recover from the infection, immunity will generally result; if they don’t recover, then obviously they’ve succumbed to the infection. Either way, this results in their removal from the model, as they’re unable to further contribute to the maintenance or spread of infection. Of course, this is a highly simplified version of reality (and I’m even simplyfing the explanation of the model; if you look at figure 1 of the paper for the model schematic, you see arrows all over the place), but it’s a common starting point in the creation of a mathematical model of disease. The two models they used were SEIR2 (which assumed significant ape-to-ape transmission of the virus), and a second model called Spillover2 (using the assumption of frequent contact of apes with the Ebola reservoir, and less emphasis on ape-to-ape spread).

When they examined the fit of the different models to the data, they found that they couldn’t rule out either model. This was somewhat novel, as previous research had suggested multiple introductions of Ebola from the reservoir, rather than sustained ape-to-ape spread.

They also found that the epidemic hit hard and quickly. Deaths began in December of 2003, peaked in May of 2004, and the epidemic finally ended at the end of that year. However, 95% of the affected gorillas had already disappeared by 6 months into the epidemic, in June 2004. And, as the title of the paper suggests, the central finding of their study was that living in groups put apes at a higher risk of death from Ebola during this outbreak than those who were solitary (95% vs. 77% for solitary animals). Additionally, they mention that almost all the gorilla groups disappeared as a unit, while only one was partially affected, suggesting rapid and efficient spread within a group.

From this, they suggest that infection pressures similar to those demonstrated in this paper may have also affected early hominid social groups. I think this is an interesting area, but a bit too sweeping of a conclusion to take. One thing that makes Ebola so fascinating is that it’s fairly unique among pathogens, so to extrapolate back to our early ancestors the conclusions of this singular study of infection with one pathogen in one area of the world in one population of apes is an over-reach, in my opinion. Still, certainly the interplay of microbes and host on the foundation and function of a society is an area that’s ripe for further investigation.

References

Cailaud et al. 2006. Gorilla susceptibility to Ebola virus: the cost of sociality. Current Biology. R489-R491.

Rouquet et al. 2005. Wild Animal Mortality Monitoring and Human Ebola Outbreaks, Gabon and Republic of Congo, 2001-2003. EID. 11:283-90. Link.

Image from http://www.raydoan.com/images/6308.jpg

Comments

  1. #1 natural cynic
    July 11, 2006

    There might be one saving grace with this information. It should be broadcast heavily to bush meat hunters that the chances of getting Ebola are very high is they kill one of the great apes.

  2. #2 Kevin C
    July 11, 2006

    Good point NC. Getting that info out could also help prevent the viris from spreading to us.

  3. #3 Tim
    July 11, 2006

    A Few Questions

    Note: The earlier part of this will deal with the fruit bats and their possible role as natural hosts for Ebola, then the great apes and human infection, then some broader questions regarding viruses.

    *

    Fruit Bats as a Reservoir…

    I am fascinated by Ebola and Marburg as well, although retroviruses – and in particular prophages – are of even greater interest to me. As I understand it, the good majority of viruses have what are called a “natural host.” This is a species that they have infected for perhaps ten or a hundred thousand years and with which they have entered a coevolutionary relationship. In the case of the natural host, the infection is chronic and oftentimes asymptomatic.

    Looking back on your post regarding the possibility that fruit bats are a reservoir, does it appear that a species of fruit bat is the natural host for ebola? Do we know, for example, whether ebola is asymptomatic in this species of fruit bat? Alternatively, is it possible that different strains of ebola have different species as natural hosts, or would we expect different strains to belong to have the same species of natural host, but belong to different populations?

    *

    Regarding Apes and Humans…

    I know that Ebola Reston was transmitted via an airborne vector among chimps. Does this appear to be the case with the great apes? Currently Ebola Reston is unable to achieve anything more via an airborne vector in humans other than what is essentially a case of the flu — essentially because it is unable to breach the barrier between the lungs and the bloodstream. Is there any reason to think that this might change? What of Marburg? Do we know whether it has airborne vectors among any primate species?

    As I understand it, both filoviruses become infectious only once the victim becomes too sick to travel. How does this compare to other primates? I have also heard that the rate of mutation among filoviruses is especially high. How does it compare with HIV-1?

    *

    Broader Questions Regarding Viruses…

    Additionally, I understand that at least one “species” of virus has made the leap before from plants to humans. Are you aware of several instances of this, and if so, how many? Are you aware of any instances where there were significant symptoms?

    Finally, as I understand it, the view that in deep evolutionary time, close to the origins of life itself all viruses shared much the same origins (in an RNA world) appears to be becoming increasingly mainstream. Do you see this happening, and do you share this view?

  4. #4 Tim
    July 11, 2006

    PS

    I realize the above post was more than a few questions. Please feel free to address only those questions you find interesting. I won’t mind.

  5. #5 Tara C. Smith
    July 12, 2006

    Hi Tim,

    Looking back on your post regarding the possibility that fruit bats are a reservoir, does it appear that a species of fruit bat is the natural host for ebola? Do we know, for example, whether ebola is asymptomatic in this species of fruit bat? Alternatively, is it possible that different strains of ebola have different species as natural hosts, or would we expect different strains to belong to have the same species of natural host, but belong to different populations?

    We’re still very much in the dark with regard to Ebola’s natural host. As I mentioned in the prior post, bats have been linked to infection for a number of reasons, including their presence in areas where an index case of Ebola or Marburg was known to have spent time. Lab studies have confirmed that some bats can be experimentally infected and show no symptoms, and in the field studies I discussed, they found bats that were antibody or PCR-positive and healthy, so asymptomatic carriage seems likely. (And it was actually a few different species of fruit bat).

    As far as different species, sure, it’s possible, especially since that study found it in several already, and we don’t know whether any of them are actually a significant reservoir species or not.

    I know that Ebola Reston was transmitted via an airborne vector among chimps. Does this appear to be the case with the great apes?

    You mean in the current study with the gorillas? The way it’s designed, they can’t really tell whether gorilla-to-gorilla spread would be via the air, close contact, or contact with blood or other secretions (or even tell for certain if it’s g-t-g spread or multiple introductions from a reservoir). To even begin to address that question, you’d need to closely observe a large number of infected gorillas, and note every time they touched each other, or came into contact with the feces, or urine, or blood, etc. of another animal. Not exactly easy to do in a field study.

    Currently Ebola Reston is unable to achieve anything more via an airborne vector in humans other than what is essentially a case of the flu — essentially because it is unable to breach the barrier between the lungs and the bloodstream. Is there any reason to think that this might change? What of Marburg? Do we know whether it has airborne vectors among any primate species?

    As an RNA virus, change is always a possibility. I’m not aware of any research that’s given a reason at the genetic level why Reston is more easily transmissible than other strains–if we knew this, we could more easily predict if other strains (or related viruses, such as Marburg) could acquire this or not. As far as Marburg being airborne, I don’t know of any studies that support that, but there has been some anecdotal evidence where exposures beside causal contact weren’t found. This doesn’t necessarily mean it was spread via the air, but it’s one hypothesis. Either way, it doesn’t seem to be spread efficiently this way.

    As I understand it, both filoviruses become infectious only once the victim becomes too sick to travel. How does this compare to other primates?

    That one I’m not sure of–I don’t know when chimps or gorillas become infectious, or how long they shed virus. Not sure if anyone knows in wild apes.

    I have also heard that the rate of mutation among filoviruses is especially high. How does it compare with HIV-1?

    According to this, Ebola is about 100x slower than HIV, at least when looking at the glycoprotein gene. Not sure if that holds over the entire viral sequence or not (obviously I’d expect some variation, but I don’t know if the glycoprotein gene is representative of the rest of the genome or not).

    Additionally, I understand that at least one “species” of virus has made the leap before from plants to humans. Are you aware of several instances of this, and if so, how many? Are you aware of any instances where there were significant symptoms?

    I’m only aware of the one, and no symptoms. I won’t be too surprised if we find more in the future, though; some are probably being missed just because we’re not looking, and/or tools were applied that couldn’t find them.

  6. #6 Tim
    July 12, 2006

    Thank you for the lengthy and in depth response!

    It is a really neat way to start my birthday.

  7. #7 Tim
    July 12, 2006

    PS

    I should probably try and get some sleep soon…

  8. #8 Tara C. Smith
    July 12, 2006

    Happy birthday! I should probably get some sleep myself. :)

  9. #9 Stephen Uitti
    July 12, 2006

    If a scientist says that 2,000 gorilla deaths is devestating, but 2,000 human deaths is insignificant, they will almost certainly be pounded down for being insensitive. Too bad there aren’t 6,000,000,000+ gorillas so that it could be just as insignificant for them too.

  10. #10 Chris Noble
    July 12, 2006

    Tara, the paper you referenced estimated the evolution rate for Ebola (via the rate of non-synonymous substitutions) not mutation rate.

    The mutation rate for Ebola is probably similar to HIV. The paper even hints at this by looking at the rate of synonymous substitutions. These were comparable to estimates for HIV and influenza suggesting that the underlying mutation rates are similar.

    Mutation rates refer to number of substitutions per replication. This primarily reflects the fidelity of the replication. Evolution rates refer to the number of substitutions per year seen in a population. The evolution rate is a factor of the mutation rate, the replication rate and natural selection. All RNA viruses have high mutation rates but not all RNA viruses have high evolution rates.

    I just wanted to point this out because the two terms are often conflated and some notable and some not so notable HIV “rethinkers” appear be incapable of understanding the difference.

    From Tim’s original comment it appears that he might have been interested in the evolution rate but it is not completely clear.

  11. #11 Tara C. Smith
    July 13, 2006

    Ah, hadn’t noticed that, thanks—that’s what I get for looking for papers at 3AM. :)

  12. #12 fnxtr
    July 19, 2006

    seek:sought::wreak:wrought.

    You are now nit-free. :-)

  13. #13 perde
    February 13, 2009

    I just wanted to point this out because the two terms are often conflated and some notable and some not so notable HIV “rethinkers” appear be incapable of understanding the difference.

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