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Recently, CIDRAP at the University of Minnesota announced that Ebola may be more transmissible through aerosols than previously thought.

I lack the familiarity with the field to critically evaluate this release. They also seem to more interested in making the point that there is a risk of aerosol transmission, not to settle whether it does transmit by air or not.

  • What is the simple answer? Can Ebola really be transmitted by aerosols?
  • If so, how come nobody realized this before? Is this a general phenomenon allowing any pathogen to become airborne? I don't see why you couldn't aerosolize a great many pathogenic objects, not just Ebola virus.
  • How does the number of virions necessary for successful infection compare to what you could get from aerosols?
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Interesting question and hard to answer definitively. First of all: It seems still pretty clear that the major (and by far most important) infection route comes from direct contact with infected people or their body fluids and that aerosol transmission is of far less significance. Ebola is infecting cells of the immune system (mostly macrophages and dendritic cells) which are located in the skin which makes the route through the respiratory organs pretty uneffecient, but it is possible.

However, there are reports for Ebola transmissions (or at least unclear cases in which a direct contact could be excluded), which suggest that the aerosl transmission is possible. There are reports of Ebola infections which spread among experimental animals between infected and non-infected (and without direct contact) control groups. This has been observed between rhesus monkeys and pigs. It was also possible for the pigs to infect non-human primates (see references 1-4 for details).

This results should be seen with some caution: At least for pigs an Ebola infection seems to be pretty much different than one in humans. There it looks more like a respiratory disease with all what comes along with it: Extended sneezing and coughing - which makes a lot of aerosol droplets. See reference 3 for the original paper and 5 and 6 for a summary and a classification. I think it is also possible that anatomical differences to the humans make such an infection route easier or harder.

Finally there are some reports of infected people which had no direct contact to people (see reference 7). However, this is rare and mostly restricted to people which where involved in health care for infected persons. These people come in close contact to the infected people which raises their chance of getting infected by aerosols. This underlines the importance for health care workers to get the right protective equipment.

References:

  1. Transmission of Ebola virus (Zaire strain) to uninfected control monkeys in a biocontainment laboratory.
  2. Replication, Pathogenicity, Shedding, and Transmission of Zaire ebolavirus in Pigs
  3. Transmission of Ebola virus from pigs to non-human primates
  4. Aerosol exposure to Zaire ebolavirus in three nonhuman primate species: differences in disease course and clinical pathology
  5. Pig-to-monkey Ebola: is there something in the air?
  6. New paper on Ebola–no primate-to-primate transmission seen
  7. Ebola Hemorrhagic Fever, Kikwit, Democratic Republic of the Congo, 1995: Risk Factors for Patients without a Reported Exposure
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    $\begingroup$ Nice answer but I think "spreaded" isn't a word and should be just "spread". $\endgroup$ – Kenshin Oct 24 '14 at 10:06
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    $\begingroup$ @Mew You're right. It's an irregular verb. BTW: If you spot errors like these, click on the edit function below an answer or question and correct it. Your edit will undergo a review until you have a certain number of credit points. This is a perfectly accepted way of improving answers. $\endgroup$ – Chris Oct 24 '14 at 11:36
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It is not airborne, because if it had be we would have a really big problem.

Normal immunocompetent mice are not susceptible to non-adapted filoviruses. There are therefore two strategies available to establish a murine model of filovirus infection: adaptation of the virus to the host or the use of genetically modified mice that are susceptible to the virus. A number of knockout (KO) strains of mice with defects in either their adaptive or innate immunity are susceptible to non-adapted filoviruses. In this study, A129 α/β −/− interferon receptor-deficient KO mice, strain A129 IFN-α/β −/−, were used to determine the lethality of a range of filoviruses, including Lake Victoria marburgvirus (MARV), Zaire ebolavirus (ZEBOV), Sudan ebolavirus (SEBOV), Reston ebolavirus (REBOV) and Côte d’Ivoire ebolavirus (CIEBOV), administered by using intraperitoneal (IP) or aerosol routes of infection. One hundred percent mortality was observed in all groups of KO mice that were administered with a range of challenge doses of MARV and ZEBOV by either IP or aerosol routes.

Ebola virus disease is not an airborne infection. Airborne spread among humans implies inhalation of an infectious dose of virus from a suspended cloud of small dried droplets.

This mode of transmission has not been observed during extensive studies of the Ebola virus over several decades.

The virulence (ID50, LD50) is unkown for humans, but ebola is considered a highly virulent disease with low LD50 based on the studies with animals.

INFECTIOUS DOSE: Viral hemorrhagic fevers have an infectious dose of 1 - 10 organisms by aerosol in non-human primates Footnote 41.

Although outbreaks of Ebola virus have largely been confined to endemic regions, their high fatality rate, ability to transmit person-to-person, and low lethal infectious dose make Ebola virus a dangerous threat to public health and pose a great risk for researchers working with these viruses as well as health care personnel treating patients during outbreaks. Furthermore, their potential to be developed into aerosolized biological weapons also causes grave concern for their use as a bioterrorism agent ( Bray, 2003).

Ebola virus is a highly virulent pathogen capable of inducing a frequently lethal hemorrhagic fever syndrome. Accumulating evidence indicates that the virus actively subverts both innate and adaptive immune responses and triggers harmful inflammatory responses as it inflicts direct tissue damage. The host immune system is ultimately overwhelmed by a combination of inflammatory factors and virus-induced cell damage, particularly in the liver and vasculature, often leading to death from septic shock. We summarize the mechanisms of immune dysregulation and virus-mediated cell damage in Ebola virus–infected patients. Future approaches to prevention and treatment of infection will be guided by answers to unresolved questions about interspecies transmission, molecular mechanisms of pathogenesis, and protective adaptive and innate immune responses to Ebola virus.

The LD50 of mouse-adapted EBO-Z virus inoculated into the peritoneal cavity was ~1 virion. Mice were resistant to large doses of the same virus inoculated subcutaneously, intradermally, or intramuscularly. Mice injected peripherally with mouse-adapted or intraperitoneally with non-adapted EBO-Z virus resisted subsequent challenge with mouse-adapted virus.

The high virulency is compensated by low transmissibility, that's why it is not a real threat currently for western countries (it is easy to quarantine). The current strain seems to be special, because it has about 100 times higher mutation rate than the old ones. It may mutate into a more transmissable strain, but I think there is not enough data and knowledge available to calculate the risk of such an event.

Sequencing of 99 different Ebola isolates from patients in the 2014 West African outbreak of Ebola showed the virus to be rapidly mutating,[15] with a mutation rate of 2.0 x 10-3 substitutions per site per year making it as fast changing as seasonal influenza.[16] This is likely to represent rapid adaptation to human hosts as the virus is repeatedly passed from human to human (as opposed to usually being passed between fruit bats and only occasionally crossing over into humans), and may pose challenges for the development of a vaccine to the virus.[17][18]

Molecular evolutionary analyses for Ebola and Marburg viruses were conducted with the aim of elucidating evolutionary features of these viruses. In particular, the rate of nonsynonymous substitutions for the glycoprotein gene of Ebola virus was estimated to be, on the average, 3.6 x 10(-5) per site per year. Marburg virus was also suggested to be evolving at a similar rate. Those rates were a hundred times slower than those of retroviruses and human influenza A virus, but were of the same order of magnitude as that of the hepatitis B virus. When these rates were applied to the degree of sequence divergence, the divergence time between Ebola and Marburg viruses was estimated to be more than several thousand years ago.

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  • $\begingroup$ Thinking that ebola can evolve to become airborne is kind of like thinking horses can evolve to fly. It's not that kind of virus. What it can do, though, is very dangerous, akin to a horse learning to run faster. $\endgroup$ – anongoodnurse Oct 26 '14 at 4:14
  • $\begingroup$ @anongoodnurse I don't know whether airborne ebola is possible, but it certainly can become a more transmissible disease, e.g. it can become more stable in vitro, more resistant to UV light, heat, etc... $\endgroup$ – inf3rno Oct 26 '14 at 4:16
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    $\begingroup$ But it won't learn to float on dust particles. Probably the most dangerous mutations would involve a decreased virulence, such that people will not feel as sick early on (while maintaining transmissibility) so that quarantines are rendered less effective. But it's all speculative. $\endgroup$ – anongoodnurse Oct 26 '14 at 4:21
  • $\begingroup$ @anongoodnurse Then why are we talking about it? "I think there is not enough data to calculate the risk or say something about it is possible or not." $\endgroup$ – inf3rno Oct 26 '14 at 4:51
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    $\begingroup$ Just trying to counter a common but unfounded fear. Is there a reason we should not? $\endgroup$ – anongoodnurse Oct 26 '14 at 4:59

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