Again, the blog (website) whyevolutionistrue brought a topic to my attention, where Matthew Cobb (of the University of Manchester) asked if there is any justification for trying to recreate a deadly virus. I left a comment on the post with my own thoughts on the matter, and thought I’d also post them here, for the record.
The question asked by Professor Cobb was inspired by a recent paper by Watanabe et al. (2014) [PDF] in Cell Host & Microbe, where a group of US and Japanese scientists report that they “generated and characterized a virus composed of avian influenza viral segments with high homology” to the flu virus which was responsible for the 1918 flu pandemic. To do this the authors identified genetic sequences in contemporary strains of flu whose protein products were structurally similar to those of the 1918 virus, and then using these sequences to re-engineer a virus similar to the original 1918 virus, with the aim of assessing its pathogenic potential. They argue that this is necessary in order to understand what made the 1918 virus so deadly, which will help to prevent and mitigate future pandemics caused by similar viruses in the future. This is logically justified as there is a plethora of flu viruses in circulation, some of which contain sequences similar to those of more pathogenic viruses. As different flu viruses are capable of exchanging genetic information upon co-infection of a host cell, this means that there exists a possibility of new and ‘improved’ viruses emerging, that combine the infectious properties of both parent strains.
Schematic depiction of an influenza virus particle, where a protein shell protects a cargo of coiled RNA, which contains the genetic information for producing more virus particles upon invasion and infection of a host cell. Image from the Centre for Disease Control (http://www.cdc.gov/flu/images.htm).
As a (trainee) geneticist, I see the merit of this work, as it is by understanding the structure of the preoteins that compose a flu virus that allows us to understand its biology and function: how it evades the host immune system, how it infects host cells, how it replicates therein, and how it is transmitted to new hosts. This is possible as a flu virus is little more than a macromolecular ribonucleic-protein structure. To understand how its different components function is essential to understanding how the virus particle itself functions, and how its infectious properties emerge, and this is the focus of much research on the structure of infectious viruses. Therefore, the study of a highly infectious virus, such as the 1918 virus, or a re-constituted strain, allows us to understand what set these viruses apart from more benign strains and inform us of critical structural changes that underlie the increased pathogenic potential of some viral strains over others. This is classical genetics, where knowledge and understanding is derived from the comparison of structural differences, and the functional differences that result. Ideally, such research will inform us of critical structures that govern and modify the infectivity of viruses, to help us identify promising targets for new drugs. The ultimate aim of such research is, of course, to prevent and treat infection in the future.
As a (wannabe) philosopher of science, I find it harder to justify this kind of work, as virologists have been studying the structure of flu viruses for decades, with very few breakthrough discoveries (such as the design and/or discovery of effective drugs) having resulted. In science this is often the case, as it progresses incrementally by accumulating information about detailed specifics, but without resulting in a higher-level understanding of how these specifics influence general mechanisms. When it comes to flu virology, the field is still awaiting its ‘eureka’ moment where all the pieces fall into place and the biology of a flu virus becomes easily characterised just by looking at its component parts. As the matter stands, we’re not there just yet: whilst we understand the flu virus in detail, it’s not sufficiently to be of any practical use to us. Without virologists understanding the biology of the average flu virus sufficiently to treat and prevent infection and epidemics by annual, benign strains, how can we expect them to gain any constructive understanding of more pathogenic strains? Considering the risks involved with working with highly pathogenic virus strains with pandemic potential, it seems ill-advised to generate these in the laboratory when there is no real benefit to be derived from such work to justify it being carried out in the first place.
As with everything in life and science, it is important to understand the basics before you move on to more complicated tasks. Failure to do so seems, to me, more like mis-guided and self-serving sensationalism without a genuine purpose, rather than well-guided science for the common good. So to answer the original question: is there any justification for trying to recreate a deadly virus?, no, there isn’t. Not yet.