An example

The way we always teach about sickle-cell anemia isn't entirely accurate. We talk as if there is a wild-type allele and the sickle-cell allele. In fact, there are at least three alleles at this locus in many populations where there is a high frequency of sickle-cell allele. In the wild-type, $A$, allele there is a glutamic acid at position six of the $\beta$ chain of hemoglobin. In the most common sickle-cell allele, $S$, there is a valine in this position. In a rarer sickle-cell allele, $C$, there is a lysine in this position. The fitness matrix looks like this:

$$\begin{array}{cccc} & A & S & C \\ A & 0.976 & 1.138 & 1.103 \\ S & & 0.192 & 0.407 \\ C & & & 0.550 \end{array}$$

There is a stable, complete polymorphism with these viabilities:

$$\begin{eqnarray*} p_A &=& 0.83 \\ p_S &=& 0.07 \\ p_C &=& 0.10 \quad . \end{eqnarray*}$$

If allele $C$ were absent, $A$ and $S$ would remain in a stable polymorphism:

$$\begin{eqnarray*} p_A &=& 0.85 \\ p_S &=& 0.15 \end{eqnarray*}$$

If allele $A$ were absent, however, the population would fix on allele $C$.⁵

The existence of a stable, complete polymorphism does not imply that all subsets of alleles could exist in stable polymorphisms. Loss of one allele as a result of random chance could result in a cascading loss of diversity.⁶

If the fitness of $AS$ were 1.6 rather than 1.103, $C$ would be lost from the population, although the $A-S$ polymorphism would remain.

Increasing the selection in favor of a heterozygous genotype may cause selection to eliminate one or more of the alleles not in that heterozygous genotype. This also means that if a genotype with a very high fitness in heterozygous form is introduced into a population, the resulting selection may eliminate one or more of the alleles already present.