One by one, though, after molecular battles that raged for thousands of generations, they have been defeated by evolution.

… then responds:

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?

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
http://www.pnas.org/cgi/content/full/97/13/6924

3. Sachiko Matsutani, Links Between Repeated Sequences, J Biomed Biotechnol. 2006; 2006: 13569.
http://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
http://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
http://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
http://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
http://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

http://magma.nationalgeographic.com/ngm/2007-10/infectious-animals/quammen-text.html

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 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.

Darwin’s surprise almost certainly would be mixed with delight: when he suggested, in “The Descent of Man” (1871), that humans and apes shared a common ancestor, it was a revolutionary idea, and it remains one today. Yet nothing provides more convincing evidence for the “theory” of evolution than the viruses contained within our DNA. 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. Endogenous retroviruses provide a trail of molecular bread crumbs leading millions of years into the past.

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.

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.

It’s undeniably true to say that you can’t describe human evolution over a span of 4,000 years. The signal