A sickle cell heterozygote has many copies of both the mutant and the normal form of hemoglobin. At very low oxygen some of the sickle-inducing fibers can form since there are so many copies of the defective protein, but not nearly as many as in a homozygote, making the symptoms much less severe in a heterozygote.
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Fig. 14.17 shows this, and you can see there that the heterozygote has some unpolymerized non-mutant protein resulting in some, but not all, red blood cells having a sickle shape under very low oxygen conditions. This is because both copies of the hemoglobin gene are expressed strongly in a heterozygote.