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.
