Relay-Version: version B 2.10 5/3/83; site utzoo.UUCP Path: utzoo!mnetor!seismo!ll-xn!husc6!hao!boulder!eddy From: eddy@boulder.Colorado.EDU (Sean Eddy) Newsgroups: sci.bio Subject: Re: AIDS a Pentagon accident? Message-ID: <1421@sigi.Colorado.EDU> Date: Mon, 22-Jun-87 12:53:06 EDT Article-I.D.: sigi.1421 Posted: Mon Jun 22 12:53:06 1987 Date-Received: Tue, 23-Jun-87 04:29:31 EDT References: <1418@sigi.Colorado.EDU> Sender: news@sigi.Colorado.EDU Reply-To: eddy@boulder.Colorado.EDU (Sean Eddy) Distribution: world Organization: University of Colorado, Boulder Lines: 117 In article <1418@sigi.Colorado.EDU> tmb@PREP.AI.MIT.EDU writes: > During the evolution of HIV's ancestors, two important >steps must have taken place: (1) creation of a human viral >pathogen with novel properties and (2) transfer of this virus >into human beings. > > Both of these events are unlikely, but they did occur, as >the existence of HIV demonstrates. You seem to have a problem imagining that viruses can evolve on their own to become human pathogens, without the help of Fort Detrick. The very fact that viral pathogens exist is proof that new human pathogens can indeed arise without the intervention of science. In recent history, there are, in fact, several cases of highly virulent viruses that have appeared out of nowhere. Rocio virus appeared in 1975 to cause an encephalitis epidemic in Brazil. Marburg virus suddenly appeared in 1967, killing several people in Germany. O'nyong nyong virus (what a name!) spread as in epidemic proportions through East Africa in 1959 -- and virtually disappeared three years later. > Any work involving recombinant DNA research with mammalian >viruses and subsequent packaging and culturing of these >viruses greatly increases the likelihood of (1). The reasons >for this are technical: > > o DNA/RNA preparations are always contaminated to a > considerable degree with sequences derived from the > host genome; recombinant DNA experiments therefore > generate a small but significant fraction of 'clones' > with unexpected and unpredictable constitution HIV has no sequences that seem to be derived from the host genome. > o mammalian genomes contain a large number of > inactive, altered, or dormant integrated viruses > that could recombine with the virus under study > or use it as a helper virus HIV is not an endogenous human retrovirus. No homologous sequences have been found in the human genome by hybridization studies. > o mammalian genomes contain a large number of genes > that could become integrated into a viral genome > and enhance the pathogenicity of the virus, alter > its effects, or alter its host range (proto-oncogenes > being the most well-known example; the recent > discoveries about the causes of neuro-pathogenicity > of HIV suggest that HIV has indeed acquired some > mammalian intercellular signal protein) The HIV genome does not have room for the 'intracellular signal protein' you suggest. It is more likely that the 'neurovirulence' is coded by natural variants of the HIV CD4-specific antireceptor. (There is some recent evidence that only some, not all, strains of HIV can infect cells in the CNS.) >None of these events are, of course, events that could not >also occur in nature. However, the point is that certain >kinds of work greatly increase the likelihood of generating >pathogens with novel properties and may also greatly speed up >the evolution of such pathogens. No, I disagree. Considering Nature is trying out all these things every second of the day, in every living thing in the planet, I think there is little a researcher can do to speed up the course of evolution by accident. And we've covered the 'speed up evolution deliberately' argument for HIV already. > Personally, I do not feel at risk working with >invertebrates and invertebrate cell lines. Spilling a >Schneider line tissue culture is a nuisance because I have to >redo the experiment, but any virus that might be in there is >very unlikely to infect mammals, and I do not culture viruses >anyhow. Any kind of molecular biology involving organisms or >pathogens of organisms that distant from humans is unlikely >indeed to result in the creation of a human pathogen (I don't >think there are known pathogens that are dangerous to both an >invertebrate species and humans). Speaking of knowing the risks one is dealing with -- what kind of invertebrate cells are you working with? Drosophila (Sindbis virus can infect Drosophila cells; 1 lab-related fatality)? Mosquito, tick, or mite (many laboratory fatalities from arboviruses)? While these accidents all occurred in virus labs, not just from handling cell lines, don't be so sure invertebrates don't carry human pathogens. > It does not matter how HIV arose, accidentally in >biological weapons work, accidentally in the development of >some vaccine using recombinant DNA techniques, or in some >monkey in the middle of Africa. We should all the same >abandon biological weapons research since the risks don't >outweigh the benefits; we should always remind ourselves as >researchers in basic and medical research of the possible >dangers and not-understood areas of our fields; and we should >stop eating half-cooked monkey brains. > > Thomas. In fact, it matters a hell of a lot how HIV arose. Scientifically, because the origins of the virus could tell us a lot about the mechanisms of its pathogenicity, and could indicate the proper model systems to study to learn more. Socially, it matters a hell of a lot too. Wild rumors about the origins of HIV in a virus research lab, or as a result of the smallpox vaccine, or God knows what else people will think of, cannot in any way further the progress of AIDS research. There is plenty of distrust of science in this field ("they're not telling us everything") already. - Sean Eddy - MCD Biology; U. of Colorado at Boulder; Boulder CO 80309 - eddy@boulder.colorado.EDU !{hao,nbires}!boulder!eddy - - "You see, we're on a mission from God." - -Elwood Blues