Ronald R. Cherry
Un-scientific American
By Ronald R. Cherry
A misleading assertion regarding the Ebola virus was published recently in an online essay at Scientific American.
"[T]he [Ebola] virus would have to develop attachments that would allow it to easily attach receptors in the upper respiratory pathway – something that neither it (nor any of its viral cousins) has been known to do in the wild... The delicate lock-and-key protein – virus fit required for the virus to successfully latch onto and replicate in the airway has not developed because there is no evolutionary pressure for it to do so..."
This is simply not true. It is readily apparent from actual scientific literature that the Ebola virus quickly attaches to and replicates in the respiratory tract of non-human primates. No doubt the cellular biology of the Ebola virus – respiratory receptor interaction needs further investigation, but Ebola must be able to easily attach to receptors in the upper and lower respiratory system – a lock-and-key protein-virus fit has already developed – otherwise the Ebola virus would not have such an affinity for the nose, oropharynx, airway epithelium and lung parenchyma of non-human primates, and presumably also for human primates.
"The potential of aerogenic infection by Ebola virus was established by using a head-only exposure aerosol system. Virus-containing droplets of 0.8-1.2 microns were generated and administered into the respiratory tract of rhesus monkeys via inhalation. Inhalation of viral doses as low as 400 plaque-forming units of virus caused a rapidly fatal disease in 4-5 days... Immunocytochemistry revealed cell-associated Ebola virus antigens present in airway epithelium, alveolar pneumocytes, and macrophages in the lung and pulmonary lymph nodes; extracellular antigen was present on mucosal surfaces of the nose, oropharynx and airways. Aggregates of characteristic filamentous virus were present within type I pneumocytes, macrophages, and air spaces of the lung by electron microscopy. Demonstration of fatal aerosol transmission of this virus in monkeys reinforces the importance of taking appropriate precautions to prevent its potential aerosol transmission to humans."
Int J Exp Pathol. 1995 Aug;76(4):227-36
Viral-receptor interaction is a fixed biological mechanism whether it occurs "in the wild" or in the experimental lab. Since Ebola viral affinity for the nose and lungs of non-human primates has been demonstrated in the lab, we must make allowance for it occurring in the wilds of human society. Since Ebola quickly kills non-human primates via the respiratory tract, it behooves us to take precautions in preventing the same from happening to humans – via immunization, ZMapp or similar therapy, and through a higher level of respiratory protection than is currently recommended by the CDC.
"Being at first skeptical that Ebola virus could be an aerosol-transmissible disease, we are now persuaded by a review of experimental and epidemiologic data that this might be an important feature of disease transmission, particularly in healthcare settings... We believe there is scientific and epidemiologic evidence that Ebola virus has the potential to be transmitted via infectious aerosol particles both near and at a distance from infected patients, which means that healthcare workers should be wearing respirators, not facemasks... Facemasks...do not offer protection against inhalation of small infectious aerosols, because they lack adequate filters and do not fit tightly against the face. Therefore, a higher level of protection is necessary." Center for Infectious Disease Research and Policy
In their rush to quell legitimate questions regarding the Airborne Transmission of Ebola, Scientific American joins with the Public Health Agency of Canada in the propagation of politically correct pseudo-science.
© Ronald R. Cherry
September 19, 2014
A misleading assertion regarding the Ebola virus was published recently in an online essay at Scientific American.
"[T]he [Ebola] virus would have to develop attachments that would allow it to easily attach receptors in the upper respiratory pathway – something that neither it (nor any of its viral cousins) has been known to do in the wild... The delicate lock-and-key protein – virus fit required for the virus to successfully latch onto and replicate in the airway has not developed because there is no evolutionary pressure for it to do so..."
This is simply not true. It is readily apparent from actual scientific literature that the Ebola virus quickly attaches to and replicates in the respiratory tract of non-human primates. No doubt the cellular biology of the Ebola virus – respiratory receptor interaction needs further investigation, but Ebola must be able to easily attach to receptors in the upper and lower respiratory system – a lock-and-key protein-virus fit has already developed – otherwise the Ebola virus would not have such an affinity for the nose, oropharynx, airway epithelium and lung parenchyma of non-human primates, and presumably also for human primates.
"The potential of aerogenic infection by Ebola virus was established by using a head-only exposure aerosol system. Virus-containing droplets of 0.8-1.2 microns were generated and administered into the respiratory tract of rhesus monkeys via inhalation. Inhalation of viral doses as low as 400 plaque-forming units of virus caused a rapidly fatal disease in 4-5 days... Immunocytochemistry revealed cell-associated Ebola virus antigens present in airway epithelium, alveolar pneumocytes, and macrophages in the lung and pulmonary lymph nodes; extracellular antigen was present on mucosal surfaces of the nose, oropharynx and airways. Aggregates of characteristic filamentous virus were present within type I pneumocytes, macrophages, and air spaces of the lung by electron microscopy. Demonstration of fatal aerosol transmission of this virus in monkeys reinforces the importance of taking appropriate precautions to prevent its potential aerosol transmission to humans."
Int J Exp Pathol. 1995 Aug;76(4):227-36
Viral-receptor interaction is a fixed biological mechanism whether it occurs "in the wild" or in the experimental lab. Since Ebola viral affinity for the nose and lungs of non-human primates has been demonstrated in the lab, we must make allowance for it occurring in the wilds of human society. Since Ebola quickly kills non-human primates via the respiratory tract, it behooves us to take precautions in preventing the same from happening to humans – via immunization, ZMapp or similar therapy, and through a higher level of respiratory protection than is currently recommended by the CDC.
"Being at first skeptical that Ebola virus could be an aerosol-transmissible disease, we are now persuaded by a review of experimental and epidemiologic data that this might be an important feature of disease transmission, particularly in healthcare settings... We believe there is scientific and epidemiologic evidence that Ebola virus has the potential to be transmitted via infectious aerosol particles both near and at a distance from infected patients, which means that healthcare workers should be wearing respirators, not facemasks... Facemasks...do not offer protection against inhalation of small infectious aerosols, because they lack adequate filters and do not fit tightly against the face. Therefore, a higher level of protection is necessary." Center for Infectious Disease Research and Policy
In their rush to quell legitimate questions regarding the Airborne Transmission of Ebola, Scientific American joins with the Public Health Agency of Canada in the propagation of politically correct pseudo-science.
© Ronald R. Cherry
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