Experts at the Centers for Disease Control and Prevention have shown that a molecular change in the 1918 pandemic influenza virus stops its transmission in ferrets that were in close proximity, shedding light on the properties that allowed the 1918 pandemic virus to spread so quickly and potentially providing important clues that could help scientists assess emerging influenza viruses, such as H5N1.
The study, which is published in the Feb. 5 issue of Science, showed that a modest change of two amino acids in the main protein found on the surface of the 1918 virus did not change the virus's ability to cause disease, but stopped respiratory droplet transmission of the virus between ferrets placed in close proximity. The experiments were conducted with ferrets because their reaction to influenza viruses closely mimics how the disease affects humans.
The 1918 influenza strain killed tens of millons of people. The interest in studying the 1918 strain is driven in part by fear that the avian flu H5N1 might mutate to cause a similar big killer human pandemic.
But do not panic. This result does not mean that H5N1 bird flu is only 2 mutations away from causing a massive human pandemic. Bird flu probably has additional mutations that make it more suited to spead in birds than in humans.
To spread and cause illness, the influenza virus must first bind to host cells found in humans and animals. The Science study suggests that the hemagglutinin (HA), a type of protein found on the surface of influenza viruses, plays an important role in the 1918 virus's ability to transmit from one host to another efficiently. This research suggests that, for an influenza virus to spread efficiently, the virus's HA must prefer attaching to cells that are found predominately in the human upper airway instead of cells found predominately in the gastrointestinal tracts of birds. Other changes may be necessary as well. Current H5N1 viruses prefer attaching to avian cells, suggesting the virus would need to make genetic changes before it could pass easily between humans.
What I want to know: Will increased knowledge of what makes influenza strains more lethal get used more to reduce the spread of influenza than it will get used by crazies to make lethal strains? Initially I expect this knowledge to be more useful on the side of good. But in the longer run biotechnologies will make the creation of custom virus strains easy for amateurs.
Advances in microfluidics will enable the development of beneficial treatments including full body rejuvenation therapies. But as microfluidic chips become cheaper and the software for controlling these devices becomes more powerful and easier to use individuals in personal labs in their own bedrooms or cellars will be able to develop customized lethal pathogens.
Reasons for optimism? First off, most people do not want to die. The internet enables large numbers of people to contribute solutions to problem. If malicious biological script kiddies start tossing out killer pathogens into the world's population the number of people who will organize to develop defenses will far exceed the number generating killer pathogens. Also, those fighting for the defense will probably be much smarter than those who are malicious. I am expecting people who feel they have low status to tend toward malicious acts.
But will sheer numbers of smart brains be sufficient to defeat malicious makers of dangerous pathogens? Or will defense against designer pathogens run into difficult problems similar to the relative difficulties of stopping versus delivering nuclear bombs? My fear is that the defensive side will be the more difficult.
When it comes to natural pathogens I expect human brains controlling computer simulations and automated equipment to near totally defeat them. Biological evolution won't be able to keep up with computers and microfluidic devices. So we'll reach a point where most of the remaining big killer pathogens cease to rack up big death tolls..
|Share |||Randall Parker, 2007 February 03 11:51 AM Dangers Natural Bio|