I think that all knowledgeable people are fully aware that droplet transmission is possible. I have never said otherwise. What I say, and what all of the published data supports is that Ebola is not airborne. As any PhD trained microbiologist will tell you, there are very important differences between droplet and airborne transmission, (or between droplets and droplet nuclei). And the infection control measures are different for each kind of transmission.
I questioned your claim regarding epithelial infection because the ZMAPP drug began as an effort to transport modified alleles to treat cystic fibrosis. The researcher used Ebola glycoproteins due to the virus' efficient transduction of lung tissue. Your claim doesn't jibe with the ZMAPP work.
Hmm, it looks like you have ZMapp confused with some kind of gene therapy. ZMapp is a cocktail of monoclonal antibodies, and those antibodies are specific for Ebola virus proteins. Those antibodies cannot attach to epithelial cells, or any other cells. They are injected into the blood, where they look for and attach to Ebola viruses. They then act as a signal to the immune system to get to work to destroy the viruses. There is no Ebola protein in the ZMapp.
I notice that you didn't bother putting any kind of reference to your claim that Ebola glycoprotein was investigated for treatment of cystic fibrosis. Despite your garbled description of this work, it did not take long for me to find some references in PubMed. The first thing I notice is that there are few references to this work, none of them recent. The second thing I notice is that this work involved a modified Ebola glycoprotein inserted into an FIV-type virus. By modifying it, they changed its behavior. This means that whatever biological properties either Ebola virus or FIV virus have in their native forms are not applicable. The fact that a modified Ebola glycoprotein can bind with some affinity to epithelial cells says nothing about the binding affinities of the native protein. (Perhaps your failure to include a reference was not an oversight?)
Intracellular Events and Cell Fate in Filovirus Infection Viruses 2011 (PDF pg 4)
Indeed, MARV or ZEBOV can be isolated from any organ or tissue. Besides the typical target cells for ZEBOV and MARV infection in non-human primates, additional target cells were occasionally found in individual animals. These cells included alveolar epithelial cells, bronchial epithelial cells and the cells of endocardial layer.
In other words, finding virus in these non-target cells was a sporadic event--it did not happen in every animal observed, and was rare even when it was observed. That review only had one reference for these observations of virus in non-target cells, meaning that there is little corroboration for this observation. I will also point out that during the course of Ebola infection, the viremia can be extremely high, 10 million virions/milliliter of blood. All cell types undergo a process called "endocytosis", where they engulf molecules from outside of the cell and bring them inside the cell in a tiny vacuole. Although viruses use cell-surface receptor mediated endocytosis to gain entry into the cell, when the viremia is that high, it is quite possible for the cell to randomly endocytose a viral particle or two when it undergoes non-specific endocytosis. So, it is not surprising that an occasional non-target cell might contain some virus. That does not mean, however, that the non-target tissue is teeming with virus, or that the virus can replicate in or bud from the non-target cell.
I should also point out that monkeys are not people; the virus can and does have different tropisms in different animal species.
Ebola haemorrhagic fever Lancet March 2011
You mislabeled this link; it was not a Lancet article, but was the International Journal of Experimental Pathology.
I notice that, although you make a big deal of the researchers finding virus near epithelial cells in Rhesis monkeys--which are not humans, and which show a different pathology--you failed to quote the following from the same article: "Epidemiology studies of human disease out-breaks in sub-Saharan Africa did not suggest that aerosol transmission of filoviruses was likely in that setting. Virus did not spread easily from person to person during the Ebola virus epidemics in Africa, and attack rates were highest in individuals who were in direct physical contact with a primary case (Bres 1978). The rates were 3.5 times higher in people who provided nursing care than in those who were in casual contact with a primary case; no cases occurred in children whose only known exposure to the virus was sleeping in the huts occupied by their fatally ill parents. Although coughing was common among the human Ebola haemorrhagic fever cases in Africa, there was no direct evidence for aerogenic spread of Ebola virus in human populations. (Emphasis mine.) So, back in 1995, Ebola researchers noted what Ebola researchers said previously and what they continue to say now: Ebola is not an airborne disease.
Your problem is that you want desperately to believe that it is transmissible by aerosols, and you are looking for straws to support that belief. You have no independent evidence of aerosol transmission, and (unfortunately for you) no Ebola researcher has ever experimentally or epidemiologically established an aerosol route of transmission.
agreed that it's unlikely that Ebola will mutate into the epidemiological definition of an airborne disease. Nor must it undergo such mutation. Fomite, contact, droplet and aerosol are more than sufficient to spread it far and wide, as we're seeing now in West Africa.
Airborne transmission = aerosol transmission (unless you are speaking of artificially created aerosols)
Droplets can be propelled through the air, but are not airborne.
Ebola can be spread by droplets, but not through aerosols.
You seem to think that no one should be the least bit concerned about the spread of Ebola to the western hemisphere. That is your right, of course, but your continued insistence that you know all possible epidemiological factors is odd given that the researchers engaged with this virus will not say the same. Every statement I've heard and read regarding vectors is predicated with a statement that much is unknown regarding transmission and pathogenesis.
When did I ever say that the potential of Ebola disease introduction into the US is not a concern? I don't recall saying that at all. What I have done is point out that it is extremely unlikely for Ebola to cause an outbreak like that in Africa. It is certainly quite appropriate to alert clinicians to the potential of such a disease so that they can recognize it if a case *does* come into their facility. I have certainly implied, if not said, that Ebola won't be a problem as long as we are prepared for it and stay vigilant--that is not at all the same thing as saying that there is nothing to worry about, and we can be complacent. I was pretty much the same way before Y2K--I figured that people were busy remediating the potential problems ahead of time, so that Y2K would not end up being the end of civilization--and I was right. No reason to get all worked up when proper preparations are in place.
Marburg, another filovirus disease that is almost identical to Ebola, *has* entered the US. No one even knew about it; our normal infection control measures were sufficient to prevent any secondary cases.
I have pointed out many times that there is a LOT of unknown surrounding Ebola. I think that you mistake my confidence in the things that I know are true as somehow my being convinced that I know everything. Go back and reread some of my previous posts. You will see that I am actually very clear about where knowledge is limited. I have said that Ebola spreads through direct contact with infected liquids or sick patients--this is well-established. I have also said that Ebola could spread through fomites--this has not been definitely established or ruled out. I have also said that there is no evidence that Ebola spreads through a natural aerosol route--a study to address this matter has not, to my knowledge, been carried out, but there is enough epi evidence and some collateral experimental animal evidence to be able to discount this mode of transmission.
I suspect continued efforts to communicate with you will not prove fruitful.
That's because you haven't really been communicating. You've been trying to make a claim that simply is not true, and I have taken a considerable amount of time to explain to you why it is not true, and to try to get you to understand the nuances of the issue. You do not have to respond to this post, but I will continue to try to educate people on the various aspects of this disease.
Except for the terrorism aspects of it, I will not talk about that.
As for ZMAPP I never said ZMAPP contains EBO glycoproteins (that was an actual facepalm moment.) But since you asked, here is one of the studies that started the researchers' move from CF gene therapy research to Ebola post-exposure treatment research.
Journal of Virology May 2003: Lentivirus Vectors Pseudotyped with Filoviral Envelope Glycoproteins Transduce Airway Epithelia from the Apical Surface Independently of Folate Receptor AlphaAbstract
The practical application of gene therapy as a treatment for cystic fibrosis is limited by poor gene transfer efficiency with vectors applied to the apical surface of airway epithelia. Recently, folate receptor alpha (FRα), a glycosylphosphatidylinositol-linked surface protein, was reported to be a cellular receptor for the filoviruses. We found that polarized human airway epithelia expressed abundant FRα on their apical surface. In an attempt to target these apical receptors, we pseudotyped feline immunodeficiency virus (FIV)-based vectors by using envelope glycoproteins (GPs) from the filoviruses Marburg virus and Ebola virus. Importantly, primary cultures of well-differentiated human airway epithelia were transduced when filovirus GP-pseudotyped FIV was applied to the apical surface. Furthermore, by deleting a heavily O-glycosylated extracellular domain of the Ebola GP, we improved the titer of concentrated vector severalfold. To investigate the folate receptor dependence of gene transfer with the filovirus pseudotypes, we compared gene transfer efficiency in immortalized airway epithelium cell lines and primary cultures. By utilizing phosphatidylinositol-specific phospholipase C (PI-PLC) treatment and FRα-blocking antibodies, we demonstrated FRα-dependent and -independent entry by filovirus glycoprotein-pseudotyped FIV-based vectors in airway epithelia. Of particular interest, entry independent of FRα was observed in primary cultures of human airway epithelia. Understanding viral vector binding and entry pathways is fundamental for developing cystic fibrosis gene therapy applications.
I first heard about the CF to Ebola to ZMAPP link during a BBC Horizons episode regarding this outbreak. The relevant portion begins at around the 37:00 mark. I'm sure you'll forgive my propensity for giving Dr. Kosinger far more credence than an anonymous stranger on the internet. He says Ebola glycoprotein spikes effectively adhere to airway epithelial cells and I have no reason to doubt him given his CV and the results of his work.
As I've written earlier, we will have much more data on transmission in a year. At that time those of us looking at that topic can revisit the current dogma surrounding the issue and determine how much of what is claimed to be known is accurate given new data. My bet is that much current dogma will be upended.