Two Reported Antidotes from the University of Wisconsin

‘Failed’ experiment yields a biocontrol agent that doesn’t trigger antibiotic resistance

New drug blocks influenza, including bird flu virus

The two press releases linked above report work with broad claims for the control of disease.

The first discusses the production of a bacterial plasmid that undergoes lethal runaway self-replication. The researcher also has developed a bacterial host organism for the plasmid, such that the benign host is able to suppress the runaway self-replication. Bacteria with which it conjugates and transfers the new plasmid to do not receive the suppression property, and thus are killed by the new plasmid. It sounds to me like this technology will likely require specific targetting of disease agents, since the generality of each host will be limited by how picky the actual disease agent is in recognizing other bacteria for conjugation. The press release doesn’t give details about how the suppression of the plasmid is accomplished, so it isn’t clear that this property would always remain safely behind in the host organism. Nor is it clear that the obvious optimism of the researchers that the suppression property is unevolvable in disease organisms is well-founded. Another thing to consider is whether in conjugation, the host organism could be made virulent by what it receives from a disease agent. It is possible that answers to these concerns have already been made, but were not communicated in the press release.

The second discusses a broad treatment antiviral agent against influenza viruses, one that blocks the virus from entering cells in its host. The agent in this case is a peptide. The researchers noted 100% protection against infection with various influenza, including the H5N1 viruses (aka “bird flu”). As an “entry blocker”, the new agent differs from vaccines, which prepare the immune system to mount an effective response on infection with a pathogen. A note at the end of the article speculates that it might be possible to generate vaccine-like action with this entry blocker, if the entry blocker could be tuned to block only most instead of all viruses from entry to cells. The idea here is that the patient would get enough viral load to trigger an immune response, but not so much as to make them more than mildly sick. Vaccine production currently requires quite a lot of work to produce a specific vaccine, and given the rapid evolution observed in influenza, by the time a vaccine is produced, the disease agent in the wild may be considerably different, reducing the effectiveness of the vaccine. Being able to produce vaccine-like action on a short time scale and with a cheaper process could help considerably with response to emerging viral disease agents.

Wesley R. Elsberry

Falconer. Interdisciplinary researcher: biology and computer science. Photographer. Husband. Christian. Activist.