I just noticed that in the new issue of the New Yorker Michael Specter has written an article on the viruses in our genome. I wrote about this research in the New York Times a year ago. I haven't had a chance to read the article through yet, but I was mortified to come across this line...
Until recently, the earliest available information about the history and the course of human diseases, like smallpox and typhus, came from mummies no more than four thousand years old. Evolution cannot be measured in a time span that short.
What happened to the New Yorker's legendary fact-checking staff? Scientists can make important observations of virus evolution in their labs in a matter of weeks. HIV evolved from a chimpanzee disease to a human one over the past few decades. Perhaps Specter meant something more specific than "evolution," like the evolution of human beings and their viruses over the past few million years. But that's a charitable interpretation.
Anyway--let me know what you think of the piece.
Update: Wed. 11/28 4:20--Having read the piece, I must say it's very good. It gets into a lot of cool experiments and the even cooler implications about how viruses may have shaped us. Some of the wording could have been made more precise, like the sentence I cited above, but having struggled to convey this sort of material myself, I shouldn't be casting too many stones. I am also a bit confused by the ending, in which a scientists claim that HIV is driving the evolution of resistance mutations in humans and that resistant humans will acquire viruses in their genomes that will mark the creation of an entirely new species. I can't tell if he's saying that a reproductive barrier will emerge between the resistant humans and other humans, or if the resistance genes are supposed to simply take over the world population through selection. No matter which he means, speciation doesn't work that way.
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I guess it depends on what you mean by "evolution." I think it's safe to say that HIV mutated. But "evolution" implies larger-scale, more significant changes over time in response to external pressures. In particular, the term "evolution" when used casually implies speciation, which doesn't really happen to viruses at all in any meaningful sense.
It's undeniably true to say that you can't describe human evolution over a span of 4,000 years. The signal large-scale adaptations to external pressures gets lost in the noise.
For instance, is the presence of CCR5-delta 32 in some people of European extraction evolution of the human species? Or is it just an example of genetic diversity within our species? I tend to go with the latter.
Carl,
I read that article last night, and choked on the same sentence that you noticed. The rest of the article is pretty good, though. Unfortunately, there are a couple of little disconnects that could be confusing to some readers, and that indicate that Specter does not have a complete grasp of the subject.
BTW, "evolution" just means "genetic change." The term does not imply anything about the extent or nature of the change. It is a common misconception. If a new gene shows up, that's evolution ... even if the new gene does not do anything that we can discern.
The full paragraph reads:
In that context, I think Specter probably meant that evolution of humans and [other] apes from a common ancestor cannot be measured in that time span. Note that his next paragraph discusses how conserved retroviral sequences in humans and chimpanzees provide powerful support for evolution.
@Jeff Harrell:
In principle, the evolution of any population can be described over any span of time. The relative abundance of all human alleles and heritable traits will be different tomorrow, much less 4000 years from now.
The differences may be miniscule over short times, and we may be technically limited in our ability to detect them, but they happen and they're part of evolution.
The mere presence of an allele like CCR5-delta 32 can't be evolution, by definition. It's only evolution when the frequency of that allele in the population changes over time.
It's also imprecise to say that HIV mutated. Populations don't mutate, they evolve.
HIV researchers can trace the evolution of the virus within a single infected host over time. I haven't kept up with the HIV literature very well in recent years, but presumably the virus is evolving in response to avoid assaults from the immune system, a living case of natural selection.
One by one, though, after molecular battles that raged for thousands of generations, they have been defeated by evolution.
There are a lot of statements in there like this one that makes me cringe. Defeated by evolution? Isn't that like being defeated by football? Evolution is the game. The winners defeat the losers, but defeated by evolution?
Ack.
I guess I used too much shorthand when I mentioned CCR5-delta 32. What I was referring to was the apparent increased occurrence of that particular mutation in people of European extraction. It's an oft-repeated hypothesis that this is a consequence of the Black Death which drastically culled European populations in the 1300s. Or maybe it was smallpox. I don't think anybody knows, but the prevalence of this mutation in people of European extraction is often linked to one of the various cullings of that population in past centuries. I'm not educated enough to know whether this hypothesis holds water. But if it does, then that's clearly a measurable change within a species over time in response to outside pressures.
I think there's always going to be a conflict between the casual use of terms like "evolution" and the strict use. If you walked up to a random person on the street and asked for a definition of "evolution," you'd get something that approximates the strict definition of speciation. Organisms changing over time, and in particular the emergence of new species of organisms out of older species.
Given the choice between using a word in its strictest scientific sense and confusing most readers, or using it in the commonly accepted sense and irritating a few readers, I think any decent writer would go with option A. That might be because I'm a writer and not a scientist; if I weren't, I might have a different opinion.
There's a pretty interesting article on National Geographic's site about zoonotic diseases and the difficulty in detecting them:
http://magma.nationalgeographic.com/ngm/2007-10/infectious-animals/quam…
You beat me to it. I just finished ranting on the same thing (and a couple of other lines that also bugged me), and then I see you've already pointed it out.
factician (#6) quotes from the article:
... then responds:
I actually kind of like it. Sure -- at one level its poetry -- a case of reification. But it is the evolution of the viral population within the host that defeats the host's immune system. Same thing with cancer -- once the cancerous cells revert to what is essentially a bacterial lifestyle. The host is largely fixed in how it can adapt.
Interestingly, however, it would appear that there is a close relationship between retroviruses and the RAG1/RAG2 complexes responsible for lymphocyte somatic rearrangements that form the basis for the adaptive immune system. The spacer between RAG1 and RAG2 in mammals consists of a defective L1 and SINE. (1, 2) L1s are retroposons, essentially degenerate indogenous retroviruses - which were acquired exogenously.
SINEs are evidentally created through L1 replication through a process of during error-prone L1 replication, but when the pol promoters are preserved can replicate as the result of proteins with which their corresponding L1s initiate their own replication. (3, 4, 5, 6, 7). However, the relatively rapid evolution of the repeat sequence poly-tail in L1s and SINEs tends to result in the inability of SINEs to replicate as the poly-tails diverge. (6)
Proteins found in both RAG genes have "suggestive homologies" with integrases found in both bacterial and retroviruses. (1, 2) Likewise, the error-prone replication of SINEs would appear to be what is responsible for the origin all but the shorter tandem repeat sequences.
It is commonly accepted that spliceosomal introns descended from bacterial/archaeal type-II introns (8), that alternate splicing relies upon complementary repeats which exist in high numbers within introns subject to alternate splicing (9), and likewise, that the catalytic core of the spliceosomal complex is a reverse transcirptase (9).
Given the fact that type-II introns are mobile, employing reverse transcription, this would make them a form of retroelement, and thus our spliceosomal introns would also be retroelements, albeit far removed from retroviruses. (8, 10) In fact, since exogenous retroviruses are specific to multicellular life, they too would appear to have descended from type-II introns with which they have shared motifs with respect to their reverse transcriptase. (11)
So at a certain level, it is the descendants of a common ancestor which are battling things out when the adaptive immune system and retroviruses battle each other. Or to put it another way, it's all in the family.
1. Marchalonis et al, Rapid Evolutionary Emergence of the Combinatorial Recognition Repertoire, Integrative and Comparative Biology 2003 43(2):347-359.
icb.oxfordjournals.org/cgi/content/full/43/2/347
2. Laird, et al., 50 million years of chordate evolution: Seeking the origins of adaptive immunity, PNAS | June 20, 2000 | vol. 97 | no. 13 | 6924-6926
www.pnas.org/cgi/content/full/97/13/6924
3. Sachiko Matsutani, Links Between Repeated Sequences, J Biomed Biotechnol. 2006; 2006: 13569.
www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1510936
4. Ogiwara, et al, Retropositional parasitism of SINEs on LINEs: identification of SINEs and LINEs in elasmobranchs, Molecular Biology and Evolution 1999, Vol 16, 1238-1250
mbe.oxfordjournals.org/cgi/content/abstract/16/9/1238
5. Nishihara, et al., Functional noncoding sequences derived from SINEs in the mammalian genome, Genome Res. 2006 July; 16(7): 864-874
www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1484453
6. Szafranski, et al., Template jumping by a LINE reverse transcriptase has created a SINE-like 5S rRNA retropseudogene in Dictyostelium, Mol Gen Genomics (2004) 271: 98-102
genome.imb-jena.de/publications/download/free/Szafranski_2004.pdf
7. Lavie, et al., The human L1 promoter: Variable transcription initiation sites and a major impact of upstream flanking sequence on promoter activity, Genome Res. 14:2253-2260, 2004
www.genome.org/cgi/content/full/14/11/2253
8. Toro, Bacteria and Archaea Group II introns: additional mobile genetic elements in the environment, Environmental Microbiology (2003) 5(3), 143-151
9. Zhang, et al., Structural Insights into Group II Intron Catalysis and Branch-Site Selection, Science. 2002 Mar 15;295(5562):2084-8
www.sciencemag.org/cgi/content/abstract/1069268v1
10. Toor, et al., Coevolution of group II intron RNA structures with their intron-encoded reverse transcriptases, RNA 2001 7: 1142-1152
www.rnajournal.org/cgi/reprint/7/8/1142.pdf?ck=nck
11. Belcour, et al., Mobile group II introns, DNA circles, reverse transcriptase and senescence, Genetica 1994, Volume 93, Numbers 1-3, 225-228