Parker A. Small Jr.: When scientists create a bird flu virus


Published: Sunday, January 15, 2012 at 6:01 a.m.
Last Modified: Wednesday, January 11, 2012 at 11:12 p.m.

By Parker Small Jr., MD

Special to The Sun

There is a controversy, as discussed in The Sun (Jan. 6), over whether to publish the method that was used to make a bird flu virus (H5N1) that can spread to humans. One needs some background information to understand this issue.

Why does bird flu kill more than half of its victims, but not spread to other people? To infect a cell, a virus must first attach to that cell.

Picture the virus as having a socket wrench on its surface that can fit and “grab” a nut on the cell’s surface. The virus’ wrench must turn the nut to open the cell, so it can get inside and take over the cell’s machinery to make more virus.

The “wrench” on the surface of the influenza virus is a protein, called hemagglutinin (the H in H5N1). The “nut” on the cell surface is called a receptor. Most human cells lining the respiratory tract have different shaped “nuts” (e.g. square vs hexagonal nuts) than do those on bird cells.

Because the receptor for the human flu virus is present throughout the human respiratory track, human flu virus sometimes infects only the nose, the nose and wind pipe or the nose, wind pipe and lung. It is easy to cough particles of secretions containing flu virus from infected noses or wind pipes, and spread flu. Rarely do such infections begin by infecting the lung, and therefore are lethal in only a small percent of flu cases.

Bird flu is the exception. The bird flu receptor is found deep in the air sacs of the human lung. If a person inhales a fine mist containing bird flu virus that gets to the air sac, the bird virus will infect those cells and cause pneumonia, but not infect the wind pipe or nose.

Viral pneumonia, due to flu that starts by infecting the air sacs, has a high mortality rate, greater than 50 percent with H5N1. People with bird flu pneumonia do not infect others because, unlike infections of the nose or wind pipe, it is very difficult to cough out the air and virus that is in their air sacs.

There is no secret about at least some of what the scientists did when they made a bird flu virus that could spread from ferret to ferret and, therefore, human to human. They changed the flu surface protein (the socket wrench), so that it could bind to the human flu virus receptor (nut). Now, the new bird flu virus can infect any part, or all of the human respiratory tract. Nasal and windpipe infections will induce sneezes and coughs that will spread the virus.

Since the details of the controversial experiment have not been revealed publicly, I cannot be sure how difficult it was to change the shape of the “socket,” or whether other changes had to be made. However, the gene that controls for the “wrench” protein, and even the order of the building blocks that determine the shape of the socket, are well known for both bird and human flu virus. This knowledge of what changes need to be made is public information, and the techniques for doing so are widely available.

But, experiments often don’t go as expected, and, as suggested by requiring five mutations, it might have been more difficult than anticipated. If so, I do not favor publishing the “extra steps.” If not, there is little to be withheld.

I believe Mother Nature, with her ongoing experiments, is more apt than terrorists to repeat the controversial experiment and release the deadly virus that will spread around the world. For a terrorist to release the virus, it would be mass suicide, potentially killing the terrorist, his family and those who support his cause ... not just innocent victims.

This new bird flu virus should now be used, in strict isolation of course, to develop seed virus to speed the subsequent production of both flu vaccines, the shot and nasal spray. We must be prepared for either terrorists or Mother Nature.

Parker A. Small Jr., MD, is a professor emeritus in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida and a member of the Emerging Pathogens Institute.

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