Is It Worth Imagining Airborne Ebola?

Back in September, when the West African Ebola outbreak was getting worse with every passing week, a lot of people began to worry that the virus could spread by air. And even if it couldn’t spread by air yet, they worried that it might be on the verge of mutating into an airborne form.

When I talked to virus experts, they saw little ground for either concern. The epidemiology of the outbreak, like previous ones, had the sort of pattern you’d expect from a virus that spreads mainly through contact with body fluids. A look at the evolutionary history of viruses indicates that a fluid-adapted virus would be unlikely to switch to going airborne with just a couple mutations. (I wrote in the New York Times about these conversations here and here.)

The anxiety over airborne Ebola has faded. The outbreak itself has dwindled down dramatically, although driving it down to zero may prove hard. But a new “Opinion/Hypothesis” piece published in the journal mBio, called “Transmission of Ebola Viruses: What We Know and Do Not Know,” has breathed some new life into the old worry.

The piece was written by Michael Osterholm of the University of Minnesota and a number of other researchers. Back in September, Osterholm wrote a controversial op-ed in the New York Times, declaring, “If certain mutations occurred, it would mean that just breathing would put one at risk of contracting Ebola.”

In the new mBio piece, Osterholm and his colleagues survey a number of past studies on how Ebola spreads. These studies don’t tell us as much as we’d like. We know less about Ebola than we do about, say, influenza, because it’s a lot rarer and a lot deadlier. Scientists thus have fewer opportunities to study it, and when they do, they have to take enormous precautions. But the evidence we do have offers a pretty clear picture, Osterholm and his colleagues write: “Available data indicate that direct physical contact and exposure to infected body fluids are the primary modes of Ebola virus transmission.”

Those fluids may be the blood of a sick patient, or diarrhea, vomit, or sweat. People can get infected by touching those fluids, but it’s also conceivable that the virus can reach a new victim in a spray of fluid. The droplets in these fluids don’t travel far, so they don’t create airborne transmission in the same sense that a virus like measles is airborne–with tiny aerosols drifting on air currents. Some animal studies have shown that Ebola can spread without direct contact, but they don’t demonstrate clear evidence that aerosols delivered the virus. Still, Osterholm and his colleagues note that when Ebola victims are autopsied, the viruses sometimes turn out to be present in their lungs. A cough or a sneeze could conceivably deliver virus-laden aerosols.

While that’s theoretically possible, Osterholm and his colleagues acknowledge that this route has never been documented in humans. “This could be because such transmission does not occur or because such transmission has not been recognized, since the number of studies that have carefully examined transmission patterns is small,” they write.

There are other factors in Ebola outbreaks that we still don’t understand well. Some evidence suggests that certain people may become “superspreaders,” transmitting Ebola to many more people than usual, but we don’t know what’s responsible for these differences. It’s also possible that different strains of Ebola have genetic differences that cause some to spread faster than others. Some preliminary studies suggest that people who got sick in the West African outbreak build up more viruses in their bodies than people in earlier outbreaks.

After surveying what we do and don’t know about Ebola transmission, the authors offer what they call a hypothesis: Ebola might indeed be able to become airborne. Infected people might cough up virus-laden droplets, which other people might then breathe into their lungs, setting off an infection. Mutations could make this route easier for the virus to take. “We agree this is an improbable (although not impossible) scenario,” Osterholm and his colleagues acknowledge, but they point out that Ebola has sprung many surprises on us in the past. “We should not assume that Ebola viruses are not capable of surprising us again at some point in the future,” they conclude.

I got in touch with some other experts to see what they thought about this new piece. The most positive of them was Pardis Sabeti, a Harvard scientist who has been analyzing the genes of Ebola viruses to track their evolution. “I think that overall it is a really nice and thorough review,” she told me. She agreed it was important to figure out whether different Ebola lineages spread differently. As for airborne Ebola, she considered it unlikely although not impossible. “We should continually monitor its properties as it continues to evolve,” she said.

But other researchers were less enthusiastic. “I don’t see any new data that really sheds any new light on things in terms of the outbreak,” said Thomas Giesbert of the University of Texas. Most of the scientists I reached out to found the hypothesis of airborne Ebola even less impressive. “I guess you can make hypothesis about anything, and a ‘hypothesis’ about ‘potential’ isn’t very strong,” said Edward Holmes of the University of Sydney. “It fails to deliver,” said Vincent Munster of the National Institutes of Health.

Vincent Racaniello of Columbia was even harsher: “It can be viewed as a scare tactic, although to what ends I do not know,” he said.

Racaniello and the other critics note that there’s no evidence of that the Ebola virus has evolved in any significant way during the latest outbreak. And the fact that no one has found compelling evidence of aerosol transmission since the virus was discovered in 1976 suggests that shifting to that route is a major challenge, not an easy evolutionary maneuver.

In fact, viruses in general don’t show the massive evolutionary potential that Osterholm and his colleagues see in Ebola. Smallpox and influenza have infected billions of people by airborne transmission for thousands of years, and there’s no evidence that they have evolved a new route. Poliovirus and norovirus take the oral route, as they always have.

“No human virus has ever changed the way it is transmitted – at least in the 100 years or so we have been studying them,” said Racaniello. “There is no reason to believe that Ebolaviruses will become respiratory pathogens.”

(For more, see this blog post Racaniello published this weekend. For more on viruses generally, see my book A Planet of Viruses.)

9 thoughts on “Is It Worth Imagining Airborne Ebola?

  1. aerosolization is what every breath dor abs ebola is shed by breath. Period and not in dispute. It is the vapor pressure differential that creates viable virus for transport and study of most any virus. The engineered process of viable preservation is called lyaphilization aka freeze drying. The freezing is unimportant to the process but the speed of dessication is. Speaking of evolution, the high speed dessication overcomes the natural brining that the Cl in NaCl does in slower evaporation. What is so surprising from all the virology experts here is fundamentally, influenza only aerosolizes for shorperiods at 100%RH but increasingly at increasingly lowered RHs of 48% 20F. Ebola is lower but I estimate 35% RH. The key to Viable aerosolization events are viable virus (100F at 100% RH) breathed into low vapor pressures (70F at say 35%). The dessication of ~1 micron droplets which are the ones that go deep into our lungs, takes about ~1 microsecond. The resulting micron particle material is reduced in weight by 95%, the NaCl has been shown by VPI to crystallize and be ejected. Now the particle is less dense than a feather and warmer than the air it is in. It is now subject to room air thermoclines, drafts and hard to argue inviable.

    The problem with all this expert falderal about aerosolization is that for Dallas, Tx, this event only occurred in a private lab in Maryland. I know the parameters of both spread events and hence my RH speculaion. The day was Oct 4th in Dallas, indoor RH was ~ 30%. The conditions in Nebraska’s containment room, indoor RH are controlled for higher humidity, ask them. The trick in all this disease dias with measles, SARs, MERs, influenza and probably ebola is vapor pressure differential from sick breath info dry room air. The effect is some viable pathogenic material that does nor obey gravity.

    More importantly is how susceptible people become on the indoor environment air change from moist to low RH air. that’s what I think occurred here in dallas from our extensive national measurement systems and database. We are welloinc. com and our worldwide app is free WelloWatch on both iPhone and Android. Itll tell you your indoor RH right now. Go figure. Its a phenomena and its real. 🙂

  2. It makes sense that there would be nothing to worry about considering that human viruses have a track record for maintaining their transmission pathways (HIV entering the body through white blood cells, etc.). However, have we considered the fact that Ebola is from a very small family of viruses (Filoviridae) that includes other viruses such as Marburg which does exhibit airborne transmission (i.e. via aerosolized organisms) in non-human primates? Have we discussed Ebola Reston, let alone the implications of how closely related these viruses are in spite of their very-different transmission methods (i.e. human vs. primate, how they enter and begin affecting the body and then spread from there). I would also like to know what the experts think about the fatality rates in the more current outbreaks. Let’s face it; the quicker a virus kills, the less chance it gives it’s host to spread it (which is why ebola is so rare). If ebola kills all of the people in a remote village in the Congo before anyone has a chance to spread it to a populated area, the world does not really care. However, if the virus evolves to be less deadly or to have a longer incubation time, it has a far higher likelihood of reaching a populated area. Are the lower fatality rates due to genetic or phenotypic changes in the virus or simply a matter of improved access to medical treatment? How close are the genes responsible for methods of transmission to genes responsible for toxicity (for lack of a better term) on the virus’ RNA? Would a mutation be likely to affect both factors simultaneously do to their relative locations in the sequence (Yes, we all know that multiple genes affect each characteristic in an organism in most cases, nonetheless….)? Do we even know? Have we mapped the Filoviridae genomes at all? It just seems silly with only 100 or so years of history studying and understanding viruses that the experts would be so unwilling to engage in a conversation about such an important thing as this. The true danger is not from Ebola. I believe it is from scientists and public health officials who are more concerned about saving face than educating the public and working hard to understand the biology of outbreaks such as this.

  3. Racaniello is simply wrong, and people should stop citing his fallacious reasoning. First, in its native host, influenza A is a gastrointestinal virus. It acquires the ability to be transmitted by a respiratory route. It mutates from a virus that prefers the terminal sugars of bird glycoproteins to one that prefers the different terminal sugars of mammalian glycoproteins with very few substitutions required. Second, a virus need not “change” its mode of transmission. It could have multiple modes of transmission that differ in efficiency. When HIV was discovered to be able to be transmitted from mother to infant was that a “new” mode of transmission or merely a previously unrecognized mode of transmission?

  4. Third, is the argument being made that there is something special about humans and human viruses? Are human viruses a special creation? Actually influenza A is a human virus, and it does change its mode of transmission, although not in humans per se. Finally, since when is precedent a valid scientific argument? Until there were prions there were no infectious proteins. Until there were human retroviruses discovered, there were no human retroviruses. The “no precedent” argument should be retired.

  5. @ David Sanders

    > Finally, since when is precedent a valid scientific
    > argument? Until there were prions there were no
    > infectious proteins. Until there were human
    > retroviruses discovered, there were no human
    > retroviruses. The “no precedent” argument should be
    > retired.

    You are confusing probability (which is not binary), and existence (which is). Public policy decisions need to be made based on probability, and the whole post is discussing the probability of the mode of transmission changeover.

    In this context, what you call “precedent” (which it isn’t, its merely a compendium of observations, which is different, especially since “precedent” has a connotation of being used in the legal arena where decision is largely “by fiat”) is useful.

  6. Ebola + flying insects = airborne transmission.
    In all the coverage of Ebola for the last 6 months, I have never seen anyone connect flies with efficient and rapid transmission, even though, if you look up transmission of disease by fly, there many details about how they do spread many serious diseases, particularly in the tropics.

    Having seen how flies will swarm around blood and manure and dead animals in barnyards, and how they will also land on animals faces near eyes and mouths, it amazes me that no one has connected them to transmission in any of the articles I’ve read so far.

  7. stop citing Racaniello ?
    you’ll have to cite it when you discuss it. You yourself are doing it.
    I think it’s sad that there is no (more) real discussion in internet about such
    controversy issues, it’s not being encouraged by the “system”, authors
    probably don’t want it. I’d like to see the discussion thread on the
    vbulletin/phpbb/… forum on Racaniello or Osterholm or Sanders
    webpage or an easy-to-find host for these.
    Instead we find these snippets on blogs and articles like this.
    Typing some keyphrase into google.
    Once upon a time there was USENET…
    Some journals and blogs allow comments after registering
    and reading pages of terms.

    One of the main topics on Racaniello’s blog over the years is how
    to mutate H5N1 so to make it better transmissable in ferrets
    (but “humans are not ferrets”) They discuss this in audios
    on TWiV (no transcript, no writte/searchable internet discussion,
    replies by audio-email-letters)
    So I don’t really know how he meant that citation and would
    like to see his reply.
    What mutations and how many might be needed to make ebola
    better transmit by airosole in humans ?
    How may generations of passaging [plus adding mutations or recombinations
    by researchers] in -whatever- might achieve this ?
    One day we might be able to add whole genes or segments from
    influenza to ebola ….

  8. What Rik Heller says about vapor pressure and dessication makes some sense. The ability of a virus or bacteria to survive in a low humidity environment, not necessarily general air humidity but surface humidity, would determine the period in which it can re-infect. A spray of droplets from a sneeze (could also include blood from an ebola victim?) may linger on a surface, the face of another person or a wet towell, until touched and spread further. An aerosol is something else: the drying period would be very short in a low humidity environment so as far as ebola is concerned, would not be an ideal medien for transmission.

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