Question: Human immunodeficiency virus (HIV) is known to infect T cells and macrophages possessing the CD4 receptor. In addition to the CD4 receptor, there are a variety of coreceptors that are also needed for certain strains of HIV to infect cells. One of these coreceptors is called CCR5 and is needed for the most common strains of HIV (called R5) to infect their host cells. The more CCR5 receptors a cell has, the greater the rate of infection for the cell. Some individuals have the delta-32 allele of CCR5 that leads to a decreased risk of HIV infection.
Women are at a much higher risk for contracting HIV from a male partner than a male is for contracting HIV from a female partner. Some of the increased risk for women is dependent on sex hormones. It has been hypothesized that women have different risks of contracting HIV at different points in their reproductive cycles. For example, women may be at a greater risk of contracting HIV following ovulation during the last 2 weeks of their cycle as opposed to the first 2 weeks of their cycle prior to ovulation. The difference between risk of infection before and after ovulation relates to sex hormones produced at various points in the reproductive cycle. It seems that the estrogen that is produced prior to ovulation provides a somewhat protective, although certainly not absolute, role against HIV infection. For women who do become infected with HIV, studies have shown that women in the first 3 to 5 years after HIV infection carry lower HIV viral loads than men, perhaps due to the influence of estrogen. This suggests a major role for sex hormones in the infection and progression of HIV.
Some populations with the delta-32 CCR5 mutation seem to have close to $100 \%$ protection against HIV, while other populations with the delta-32 CCR5 mutation seem to have only partial protection. What could account for this difference?

Options:
A. There is an environmental influence on expression of the delta-32 CCR5 phenotype.
B. The delta-32 CCR5 allele exhibits incomplete dominance. Homozygotes have complete protection while heterozygotes have only partial protection.
C. The expression of the delta-32 CCR5 allele can be masked by epistasis.
D. Those that have only partial protection against HIV infection have been exposed to larger doses of HIV.
Answer: To answer this question, you need to rely on your knowledge of genetics. The passage states that the delta-32 CCR5 mutation is protective against HIV infection. The question indicated that there are two different phenotypes noted within the delta-32 CCR5 mutation-one that offers near 100 percent protection against HIV infection and one that offers only partial protection. The best explanation for why two phenotypes (complete protection and partial protection) are observed would be that the delta-32 allele exhibits incomplete dominance. An individual that is homozygous for the allele (meaning he or she inherited two copies of the delta-32 allele) would have full protection, while an individual who is heterozygous (meaning he or she has one normal copy of the allele and one copy of the delta-32 allele) would have an intermediate phenotype (being partial protection). This is indicated by choice B. Since the question indicates that the differences in phenotype (protection) are related to the delta32 mutation, choices A and D can be eliminated as they suppose that something other than the allele is providing protection. Choice C suggests that epistasis is involved in masking the delta-32 allele. While this might sound remotely plausible, choice B is a much more likely explanation. The correct answer is B.