You misunderstand. A
given beneficial substitution will "reach fixation" faster than a
given neutral substitution. But that's not the issue in Haldane's Dilemma. The issue is the
average substitution rate -- how many generations per substitution, averaged over time.
Neutral evolution is faster than beneficial evolution, and is a universally accepted result among evolutionary geneticists. See Motoo Kimura, for example.
ReMine's peer-reviewed paper explains why.
I see. Even considering that, why should we think that the Haldane Limit poses any kind of problem for human-chimp ancestry? In order for there to be a problem, we would have to know that there are indeed more than 1,667 beneficial substitutions in the human genome that are absent in the chimpanzee genome and vice-versa. Or, more correctly, we would need to know that humans and/or chimps have more than 1,667 beneficial substitutions than their common ancestor had. Although we know the nucleotide similarity between chimpanzees and humans, we don't know how many of those nucleotides represent mutations which are beneficial/neutral/deleterious (especially since a single mutation can alter many nucleotides at once). We haven't done an exhaustive investigation of the function of all our alleles yet.
EDIT: Perhaps I spoke too soon.
This source (which gets its information from
this study) says that only about 238 beneficial genes have become fixed in our genome since the last common ancestor of humans and chimps. That's well below the Haldane Limit of 1,667 beneficial genes by more than 7-fold. I'd say Haldane's Limit is not a problem whatsoever here.
Virus genomes are tiny, and have little room for mutations that are neutral or harmful. Mammal genomes are large, and have lots of room for mutations that are neutral or harmful. This difference allows a mammal genome to 'carry' a much higher amount of mutation that is neutral or harmful, and achieve higher substitution rates (again, neutral or harmful).
Put another way. Motoo Kimura's derivation of the rate of neutral evolution assumes an "infinite sites" model of the genome. In effect, he assumed the genome is infinitely large, with an effectively infinite number of nucleotide sites that can be neutral. That assumption is suited to mammals, but not to a virus (which has a tiny genome). As a consequence, a tiny genome (such as a virus) cannot achieve as fast a substitution rate (neutral or harmful) as a mammal.
Let's do some more math.
According to
"Analysis of Genetic Inheritance in a Family Quartet by Whole-Genome Sequencing", the genomic mutation rate in humans is ~1.1 x 10^-8 per site per generation. Multiply this by number of nucleotides in the human genome (~3 billion) and you get ~33 mutations per generation.
According to
"Retrovirology", the genomic point mutation rate for HIV ranges between ~2.2-5.4 10^-5 per site per generation. Multiply this by the number of nucleotides in the HIV genome (9,749) and you get somewhere between ~0.2 and ~0.5 mutations per generation.
Seems that moderately-sized mammals do indeed acquire more mutations per generation than viruses do. However, the important difference becomes clear once you compare generation times between the two. Putting in human generation time (15-20 years), we can calculate an average of 1.65-2.2 mutations per year.
Now we look at the generation time for HIV.
This website puts it at around 11 hours, this website says 10 hours,
this one says 2.6 days. We will assume a "worst-case scenario" and use the 2.6 day number. Taking this number means there are about 140 generations of HIV per year, putting the mutation rate between 28 and 70 mutations per year.
So we see that, despite there being more mutations per generation for humans than HIV, HIV still has significantly more mutations per unit time than humans do (between 12 and 42 times higher). Since the generation time for HIV is also more than 2,000 times faster than for humans, mutations should reach fixation at a significantly more rapid pace for HIV as well.
Even if you take the 175 mutation figure mentioned earlier in the thread, HIV still mutates faster (8.75-11.7 mut/yr vs. 28-70 mut/yr).
I would also like to point out that the rate of substitution fixation in a population is equal to its mutation rate when genetic drift alone is at work (which works for neutral mutations). To quote my textbook:
Evolutionary Analysis said:
Here we show a calculation establishing that when genetic drift is the only mechanism of evolution at work, the rate of evolutionary substitution is equal to the mutation rate (Kimura 1968).
Imagine a diploid population of size N. Within this population are 2N alleles of the locus of interest, where by "alleles" we mean copies of the gene, regardless of whether they are identical or not. Let v be the rate of selectively neutral mutations per allele per generation, and assume that each mutation creates an allele that has not previously existed in the population. Then every generation, there will be
2Nv
new alleles created by mutation. Because by assumption all new alleles are selectively neutral, genetic drift is the only force at work. Each new allele has the same chance of drifting to fixation as any other allele in the population. That chance, equal to the frequency of the new allele, is
1/2N
Therefore, each generation the number of new alleles that are created by mutation and are destined to drift to fixation is
2Nv x (1/2N) = v
The same argument applies to every generation. Therefore, the rate of evolution at the locus of interest is v substitutions per generation.