Why Ebola Isn't Going to "Go Airborne"
And stop sounding so excited about it
We have now reached the stage of the Bundibugyo ebolavirus outbreak where the “what if it goes airborne” discussion really starts to rev up. I have been asked by numerous worried friends and family members on a daily basis if they need to worry about an Ebola pandemic as they see suspected case counts and mortality continue to grow. How could this outbreak spread so quickly to so many people over such a vast region if it weren’t transmitted like COVID or seasonal flu? Can’t viruses mutate and become more transmissible? IT HAPPENED IN OUTBREAK!
Outbreak depicts a fictional Ebola response that is entirely divorced from reality. This movie features 100% more capuchin-chasing, magical serum-making, and CDC epidemiologists dogfighting Morgan Freeman in attack helicopters to prevent him from violating the Biological Weapons Convention (BWC) than have ever occurred in any real-life Ebola outbreak to date. So when you watch this infamous scene—in which Dustin Hoffman discovers that the virus has gone airborne using the tried-and-true method of identifying mutations by looking around the room and thinking real hard—keep in mind that “IT’S AIRBORNE” is just one example of a thing in this movie that is completely implausible.
Viruses are full of surprises and I am always open to their capacity to do new things that catch us off guard. But I have studied Ebola virus pathogenesis (process by which infection causes disease) since 2012. I am very confident that a scene like this will never occur, because I spent the last 15 years studying how ebolaviruses cause disease.
Ebola viruses can infect you and kill you if you inhale them. We’ve known that since before Outbreak came out. But a person infected with Ebola will not transmit virus to others via the respiratory route. You can get Ebola from breathing it in, but you can’t give Ebola from breathing it out.
For this reason, in my opinion, we will thankfully not have to deal with an airborne variant of Ebola, because this virus will not emerge. There are a number of scientifically established reasons why not and I am going to shamelessly support some of them with my own Ebola pathogenesis research.
1. Ebola pathogenesis does not directly involve the respiratory tract
We used to call the disease that ebolaviruses cause “Ebola hemorrhagic fever.” The name changed to Ebola virus disease (EVD) after the 2014 West African epidemic, in which more than 28,000 people were infected. In diverse hosts—like humans—you will see many diverse disease outcomes. After so many people got Ebola, we learned that people don’t always get hemorrhagic disease. Some people with Ebola have severe gastrointestinal disease, where they can lose liters of fluid through vomiting or diarrhea. Some people can have neurological, sensory, or cognitive problems. Some people develop sequelae that sound an awful lot like “long Ebola.” Ebola can persist in survivors and be sexually transmitted years later for reasons we don’t fully understand. But one thing Ebola is not is a primary cause of severe respiratory pathology (damage/injury). I could only find a single case report of viral pneumonia seemingly caused by Ebola, in an Italian physician who was evacuated from Sierra Leone.
Although Ebola causes some conditions associated with respiratory disease ranging from mild (nasal congestion, sore throat, cough) to severe (pulmonary edema), this is not because the virus is directly infecting the cells lining the airway. It is because, in the earlier stages of the disease, the mild symptoms also suggest activation of antiviral and inflammatory host response pathways. When these pathways are activated, a variety of different cell types will make cytokines and chemokines, which are basically protein messengers that alert other cells about an infection or injury. When immune cells in the bloodstream detect cytokines and chemokines, they follow the trail of chemical messages to the site of the injury.
Because they can regulate powerful immune responses, inflammatory cytokines can themselves cause injury if they are uncontrolled. They cause hyperinflammation of any cell that is in contact with the bloodstream or lymphatic system. They activate immune effector cells nonspecifically, causing extensive tissue injury. They kill immune cells capable of clearing the infection and regulating the immune response. Ebola’s primary mechanism of injury is the cytokine storm: systemic, uncontrolled circulation of potent inflammatory cytokines that is as destructive and chaotic as it sounds.
The Ebola cytokine storm does very specific things to the vascular system, including messing with its most important function: keeping blood in. Blood vessels have to allow immune cells to leave circulation when they respond to infections and injuries throughout the body without causing bleeding. Inflammatory cytokines normally allow the vascular endothelial cells that line the capillaries to open up enough to let immune cells get to the combat zone so they can unleash Th1 polarized hell on a burgeoning viral infection. Cytokines can also activate the blood clotting system, to prevent bleeding as part of the inflammatory response to injury. This is especially important in capillaries, where the vascular barrier is only as thick as a single endothelial cell.
The Ebola cytokine storm tells every endothelial cell lining every blood vessel to open wide. It activates the blood clotting system throughout the entire circulatory system, resulting in disseminated intravascular coagulation. That is a clinical way of saying tiny blood clots throughout all of the peripheral blood that use up all the clotting factors in the blood. Those clotting factors aren’t coming back anytime soon, because the hepatocytes in the liver that would normally make them are busy getting killed in the process of being turned into ebolavirus factories. Ultimately, EVD kills people with hypovolemic shock: dehydration and the body’s inability to manage fluids. This is probably why pulmonary edema occurs in EVD patients: because the host cannot regulate fluids throughout the body, not because the lungs are directly infected.
2. Ebolaviruses don’t infect cells that stay in the respiratory tract
Ebolaviruses can cause an infection any time they get access to the bloodstream or manage to cross a mucosal barrier (eyes, mouth, nose, vagina, urethra, and rectum). Whatever the route of exposure, the first targets of Ebola virus infection are the macrophages and dendritic cells (DCs). These are two types of white blood cell that begin their developed life as a monocyte circulating in the bloodstream, but eventually move to organs and stay there, becoming specialized “residents.”
There are resident macrophages and DCs in every tissue and in every organ that are adapted to handling various types of organ-specific immune business. In the liver, hepatic stellate cells are specialized macrophages that store vitamin A. In the skin, Langerhans cells are specialized DCs that detect infection due to a puncture or cut. In the brain, microglia are resident macrophages that are critical for maintaining the blood-brain barrier. In the lungs, pulmonary macrophages are specialized to deal with all the crap people are inhaling constantly: pollutants, bacteria, fungi, viruses, pollen, and whatever other particulate matter is floating around in the air. These cells are in every tissue, and they are all susceptible to Ebola virus infection. Therefore, a person can be infected by any route that introduces the virus to one of these cell types. That includes the respiratory route.
Macrophages and DCs are phagocytes, which means they engulf (or “eat”) things they come across as they move around the interstitial spaces of the tissue where they reside like terrifying insatiable little amoebas. If they happen to eat a virus, or a molecule that looks like it came from a virus, they respond. If they happen to eat an infectious ebolavirus particle, it will productively infect them.
Macrophages and DCs are both antigen-presenting cells, which means they take whatever they ate (the antigen) and “present” it to T cells to activate them in an virus-specific manner. CD4 “helper” T cells then orchestrate the adaptive (virus-specific) immune response: inducing B cells to make antibodies, sending CD8+ “killer” T cells to kill infected cells, and inducing immune memory.
T cells are found in the spleen and lymph nodes, so when macrophages and DCs “eat” an Ebola virus, they take it to the nearest secondary lymphoid organ. Unfortunately, they are also infected, so when they get there, they infect all the other macrophages and DCs that are also there in large numbers. Ebola doesn’t infect the B or T cells, but infected DCs cause them to commit cellular suicide by apoptosis. The infected DCs do the immune equivalent of antibody-making B cells and the specialized antiviral T cells in that lymph node kill themselves. Bye bye, adaptive (virus-specific) immune response. And it just gets worse from there.
3. Infectious ebolaviruses are mostly in the bloodstream
After the macrophages and DCs get into the lymph nodes and spleen, all those newly infected DCs and macrophages start cranking out new progeny ebolaviruses along with inflammatory cytokines and the host develops very high viremia (virus in the blood). This is amplified as blood filters through the liver, resulting in infection of both resident macrophages and DCs and the hepatocytes. Cells in many types of tissues become infected late in disease, but not the epithelial cells that line the airway. The targets of Ebola infection are primarily cells in the blood or the lympthatic system or in the visceral organs.
The vast majority of infectious ebolaviruses produced by an infected host are internal. That’s why it’s primarily transmitted in the context of caring for the sick and preparing bodies for burial. People can be exposed to blood and any number of other bodily fluids via many different routes (including by inhaling aerosols) while treating patients or handling bodies. But they are not being infected by Ebola virus in exhaled breath, because there just isn’t very much virus around in the upper respiratory tract.
4. Infectious ebolaviruses are not shed into the airway
Ebolaviruses are in the family Filoviridae, which means “thread viruses,” because the virions (virus particles) are filamentous and look like threads. Newly made progeny virions bud from an infected cell into the space around it. A virus will only be able to transmit from person to person via the respiratory route if these virions are budding out of an infected cell in the airway.
Respiratory viruses like H1N1 or H3N2 influenza, SARS-CoV-2, and rhinoviruses also infect the epithelial cells that line the airway. They are adapted to infect the epithelium of the upper respiratory tract. Some of the common cold viruses are temperature sensitive, because the nose is cooler than the rest of the body. Most rhinoviruses grow optimally at 33°C rather than 37°C (body temperature). Respiratory viruses’ preference for infecting cells in the upper airway makes them very good at spreading from person to person, since virus is shed directly into the terminal exit point of the respiratory tract and is exhaled. If they don’t replicate in the lower tract, they are very transmissible, but not very pathogenic. Viruses that replicate primarily in the lower tract are more pathogenic because they can cause viral pneumonia, but if they don’t also shed into the upper airway, they won’t be as transmissible.
Although they can replicate in cells that are in the upper respiratory tract (macrophages and DCs) and airway (capillaries in the lung), these cells either don’t stay in the airway or don’t shed enough virus into the airway to create a risk of onward transmission through exhaled breath. Ebolaviruses replicate better at 37°C, so infection of the upper tract is less likely to result in high titer virus production. If infected host cells are not dumping enough infectious virus into the airway to breathe out, then Ebola cannot become a respiratory pathogen. People will not be able to transmit it to others by the respiratory route.
5. Transmission route is dependent on disease characteristics
Ebola virus disease is caused by ebolavirus infection, but it is also caused by how the host responds. The host response to infection is equally if not more critical than the virus for determining how severe the disease actually is. The symptoms of EVD are dependent on the type of cells it infects, because of the type of injury they can inflict. The damage in EVD is primarily caused by inflammatory cytokines that are produced by the host, not the virus. If ebolaviruses didn’t infect macrophages and DCs capable of producing these cytokines, it wouldn’t be able to induce a cytokine storm. If ebolaviruses didn’t infect hepatocytes, the host would still be able to make blood clotting factors. If ebolaviruses didn’t trick DCs into inducing T and B cells to kill themselves, the host would have a more robust adaptive immune response. Every infection is a battleground between the host and the virus, and the host response is what determines who wins.
Don’t believe me? Here’s the paper where my colleagues and I showed this using a mouse model of EVD we developed back in 2014!
We still called it Ebola hemorrhagic fever because the West African epidemic was occurring at the same time that we published it. The focus was stopping the epidemic, not naming the disease. Ebola was spreading in major cities and containment was the necessary focus, just as it is now. Ultimately, more than 11,000 people died. But they didn’t die of whatever the hell the makeup crew at Outbreak came up with:
The West African epidemic showed the full range of disease outcomes when thousands of diverse, complex, variable people get infected with Ebola. Just as in our pathogenesis model, not every patient develops hemorrhagic disease. Fewer than half of them do. And actual hemorrhagic pathology in EVD does not involve blood gushing out of your ears.
The most common clinical feature of hemorrhagic disease in EVD is a macropapular petechial rash. This is caused by the loss of vascular barrier function in the capillaries due to the systemic inflammatory cytokine storm. You are effectively bleeding out of your capillaries, which causes a red, raised rash. Rarely, these appear like bigger blood blisters, but most often they just look like a rash. Sometimes people will have bleeding gums, bruising, or blood in their urine, vomit, or diarrhea. Nobody is spouting blood out of every orifice.
In the West African epidemic, the majority of patients did not have any clinical evidence of hemorrhagic disease. Most of the physicians evacuated from West Africa to wealthy countries generally did not develop coagulopathy or bleeding. One exception was Ian Crozier, who developed a raging petechial rash on day 3 after symptom onset and was so severely ill with EVD that he would have died if not for the heroic efforts of the experienced medical team at the biocontainment unit at Emory Medical Center. However, case reports from the other evacuated patients showed more GI involvement than hemorrhage.
Ebola virus is a rock star among emerging viruses in part because the concept of a “viral hemorrhagic fever” evokes a gory spectacle that is as engaging as it is terrifying. It is a sexier vision of horror than “viral 10 liters of watery diarrhea a day disease” or “viral puking your guts out fever.” But death by dehydration through vomiting and/or diarrhea is no less horrific.
The cytokine storm that causes increased vascular permeability also has that effect on other organs that have barrier function. For example, the gastrointestinal tract. When GI barrier function decreases (and when the kidneys don’t work normally, as often occurs during EVD), it completely screws up your body’s ability to absorb and regulate water. Widespread GI inflammation also causes nausea and diarrhea, as does hepatitis (inflammation of the liver caused by the fact that the entire thing is infected). Ebola really screws up the liver. My co-author who did these experiments at the BSL-4 lab at the National Institutes of Allergy and Infectious Diseases (NIAID) described the hemorrhagic liver shown in D below as being the texture of “soft tofu.” The reason this liver is so pale compared to the liver from the mouse with non-lethal Ebola is that it is covered with tiny, oozing blood spots. The entire organ is riddled with Ebola virus and infiltrating inflammatory cells and every blood vessel is leaking.
My lab has gone on to use this mouse model to show that the timing and nature of the inflammatory response is so intrinsic to EVD pathogenesis that inflammatory gene expression actually predicts disease outcome. We used machine learning classification on gene expression data from mice with different Ebola outcomes and found that we could accurately predict outcome in human patients. The genes we used to predict outcome were all related to the timing and magnitude of the inflammatory response, which determines whether the host fights off the infection or dies after the onset of a cytokine storm.
Because the symptoms of EVD are so linked to the types of cells that are infected and the routes of transmission, it is very relevant to consider what kind of symptoms those are. They are primarily not respiratory. There is no selection pressure on EVD to “go airborne” since it transmits very effectively by other routes. It’s very unlikely that we will ever see the emergence of airborne ebolaviruses.
Why Does This Matter?
Although vomiting and diarrhea can create infectious aerosols that put health care workers and caregivers at risk of infection, they aren’t driving the majority of the spread during ebolavirus epidemics. The vast majority of ebolavirus spread during outbreaks occurs in the context of caring for sick people or contact with dead bodies.
Wasting time speculating about unlikely scenarios wastes time and resources that are desperately needed NOW to contain what is looking like the worst ebolavirus outbreak in history. There are nearly 1000 suspected cases and more than 220 deaths. This outbreak started at most two months ago. More healthcare workers are getting infected in DRC and Uganda. Safe burial practices are not always followed. Violence and distrust are fueling anger and resentment toward public health workers. But speculation and false claims about “airborne transmission” from supposed global health experts is not helping the situation.
Respiratory protection is an essential component of Ebola personal protective equipment (PPE) because of the risk of exposure to infectious aerosols, but it is not the only essential protection. Protective suits, gloves, face and eye protection, and burial supplies are also critically important to reduce all potential sources of transmission for health care workers and safe burial teams. Reliable testing is needed to ensure patients are isolated and treated appropriately (EVD can be clinically similar to malaria, gastroenteritis, and other viral hemorrhagic fevers, so molecular diagnostics is critical), and health care workers can take appropriate precautions themselves.
The people currently facing the BDBV outbreak are dealing with extremely limited resources since Elon Musk fed USAID “to the woodchipper” during the DOGE destruction spree in early 2025 and the US completed its withdrawal from the WHO in January 2026. Health care worker infections are increasing because the courageous people in DRC and Uganda who are responding to the outbreak do not have access to adequate PPE at all.
Making unsupported claims that actual experts are so intent on minimizing or dismissing attention-seeking armchair ebolavirologist “IT’S AIRBORNE” concerns further diverts public focus from the real problem: the US withdrawal from WHO and devastation of foreign aid has severely hindered outbreak containment. It also misplaces blame, shifting it to people who are risking their lives and safety to try and contain an exploding epidemic from those who are truly responsible: President Donald Trump and everyone in his administration. They intentionally chose to cause even more profound suffering in a part of the world where the bar for profound suffering is already exceptionally high through negligence, solely for personal and political gain. This Bundibugyo virus outbreak is on track to exceed the body count of the West African epidemic. The death toll from slashing USAID and PEPFAR funding and withdrawing from WHO will be measured on the scale of tens of millions.
This outbreak is the result of what is, in my opinion, a crime against humanity. Baseless fearmongering diverts time and resources from where they are needed, undermines expertise, and cultivates public distrust. People who knowingly frame what should be a serious discussion focused on saving lives and preventing infections are not only scientifically incompetent, lying quacks who like to be on TV. They are further hindering outbreak response and putting more people at risk. They are complicit with the regime that annihilated global response capacity in the first place.
“IT’S AIRBORNE” is not likely to ever be a biological reality, but people should understand that further undermining scientific expertise and global health security via sensationalist lies is a political reality borne by the suffering of others. There are many virological reasons that we won’t see airborne Ebola emerge. Let’s address the political reasons that Ebola is spreading and killing a lot of people now.
 | A guest post by
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Thank you very much for a brilliant science based presentation of facts presented in a readily understandable manner. Something the drug-addled mind of RFK, Jr. will never fathom…maybe if we put it in a coloring book format and stuffed it the carcass of a whale and put in creek of sewage next to a dirty toilet seat, he’d take notice.
Before encountering your thorough explanation, I had just read: https://pmc.ncbi.nlm.nih.gov/articles/PMC4298250/ by Dick Wenzel, suggesting we still mask/take precautions d/t potential aerosolization of infectious secretions. Ditto re https://www.cidrap.umn.edu/ebola/experts-suspect-ebola-virus-sometimes-spreads-air
These are older articles, so thinking has evolved? Or are they just using different terminology, since they are referring to aerosolization of infectious material? Thx.