There was a lot wrong with Micheal ‘Lilo‘ Behes description of HIV-1 in last years book, ‘Edge of Evolution‘. There is a lot of discussion in the Evilutionist community as to what constitutes a Creationist, but there are a few mistakes Creationists continually make when trying to argue against evilution, especially regarding ‘mutations’.
Despite Lilos acceptance of common descent and educational training as a biochemist, he made the same childish mistakes Creationists make when they are wrestling with ‘mutation’:
Because of the difference in mutation rates HIV has actually experienced about ten thousand times as many mutations as would a comparable number of malarial cells. The very many copies of HIV in the world would be expected to contain almost every imaginable kind of mutation. As one study put it, “Each and every possible single-point mutation occurs between 104 and 105 times per day in an HIV-infected individual.”
Behes focus in ‘Edge’ with HIV-1 was just that– a generic Creationist obsession with point mutations, and how they are all bad or unremarkable (except the ones that are good– those were inserted by Jesus, personally).
Yes, a great source of diversity in HIV-1 is caused by mistakes in reverse transcription.
Another source of HIV-1 mutation is APOBEC3G– a part of your innate immune system that tries to screw up retroviruses by plopping in uracil where there is supposed to be a cytidine. More point mutations.
But those arent the only sources of genetic variation in HIV-1. Retroviruses have sex. Kinda.
If Lilo had spent 30 seconds researching HIV-1 before he wrote ‘Edge’, he might have decided to put less of an emphasis on point mutations, and more than one sentence on that ‘other sorts of mutation’ (or maybe he would have realized how stupid it was to put HIV-1 in ‘Edge’ at all).:
In addition to all those point mutations, enormous numbers of insertions, deletions, duplications, and other sorts of mutations would occur as well.
That one sentence downplays how vital recombination is for HIV-1s genetic diversity. HIV-1 could actually be described as a diploid organism. Every virus contains two copies of the HIV-1 genome, even though it technically only needs one. Reverse Transcriptase can hop back and forth between the two genomes, creating chimeric viruses– just like you are a chimera of your mom and your dad.
Sometimes these hopping events are very subtle:
If both of the genomes packaged within a virus are the same, hopping back and forth wont make ‘drastic’ changes. A lot of hopping occurs within my gene of interest, env, and we see lots of inserted/deleted chunks of genome, which changes the size and structure of the envelope gene– the target for neutralizing antibodies. Not only do these ‘tiny’ changes add to the diversity of an already moving target for your immune system, some labs have found that the shorter envelope genes are actually the ones transmitted better (we didnt find it with our patients, but that doesnt mean its not so).
So these insertions/deletions might be subtle, but theyre still a big deal.
But just because the two packaged genomes are the same, doesnt mean there cant be HUGE genomic changes:
Unequal crossovers can lead to gene duplications (or deletions!). That is exactly what happened with Vpr and Vpx in HIV-2– Vpx is just a copy of Vpr. Gene duplication and divergence is a classic route of evolution (look at the different kinds of antibodies we can make because of gene duplication and divergence!). Its also possible that Vpu in HIV-1 is the result of a same kind of event, but it has diverged so far from its parent sequence, we have no idea where it came from
Here is where retroviral sex becomes a huge problem– When HIV-1 infects a cell, it normally down-regulates the receptor HIV-1 needs to infect cells. That means its basically peeing on the fire hydrant. THIS CELL IS MINE!!! It doesnt want to share with another virus, but that doesnt always work out. If an individual is infected with two kinds of HIV-1– say, Subtype B and Subtype C– its possible that both a B and a C virus infect the same cell. A B and C viral genome can be packaged into a progeny virus:
What if Virus 1 has already developed resistance to multiple reverse transcriptase inhibitors, and Virus 2 has already developed resistance to multiple entry inhibitors? Virus 3 is now resistant to both kinds of drugs. Statistically-impossible-totally-not-gonna-happen-through-point-mutation events are just a hop/skip/jump away. Literally.
Once again– be very, very glad Mr. Lilo is not an HIV-1 researcher.