Shortsighted Evolution? In Section 1.2, we covered evidence that HIV populations

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Shortsighted Evolution? In Section 1.2, we covered evidence that HIV populations within individual hosts evolve resistance to AZT and other antiretroviral drugs. HIV populations also evolve the ability to evade the host's immune response. The immune system attacks HIV with antibodies and killer T cells (see Figure 1.6). These eliminate many of the virions in the HIV population, but not all. Due to errors during rep- lication, the HIV population is genetically variable. Some of the variants are less susceptible than others to the immune system's assault. Antibodies and killer T cells recognize HIV and HIV-infected cells by binding to epitopes-short pieces of viral protein displayed on the surface of the virion or the infected cell. These epitopes are encoded in HIV's genes. Mutations in the genes change the epitopes and may enable the mutant virion to evade detection by the host's current arsenal of antibodies and killer T cells. By the time a new in- fection enters the chronic phase (see Figure 1.8), the HIV population has already changed. Variants easily targeted by the first wave of the immune attack have dis- appeared; variants less easily detected persist (Price et al. 1997; Allen et al. 2000). Epitope TSTLQEQIAW TSNLQEQIAW 1,600 1,200 Research by A. J. Leslie and colleagues (2004) documents an example of a mutation that helps HIV virions evade the immune response in some patients. The mutation affects an epitope in a protein, called p24, that is a component of the capsule that surrounds the core of the HIV virion. Infected host cells display this epitope on their surface, along with a host protein called a human leucocyte antigen, or HLA. When a killer T-cell recognizes the foreign epitope alongside the self HLA protein, it destroys the infected cell. 800 E 400 10-9 0 10-5 Epitope concentration (M) In a survey of virions from more than 300 patients, Leslie and colleagues found that in most strains of HIV, the third amino acid in the epitope is threo- nine. However, in most HIV strains from patients who carry either of two par- mutation Each letter in the ticular alleles of HLA-B B5801 or B57-the third amino acid is asparagine. epitope represents an amino acid Ex d T for threonine; S for serine; N for periments in test tubes showed why. Leslie and colleagues took white bloo cells from a patient with the B5801 allele and exposed them to different versions of the p24 epitope (Figure 1.28). The patient's cells reacted much more strongly to the version with threonine than to the version with asparagine. White blood nterleukin-gamma. From Leslie cells from patients with the B57 allele showed a similar pattern asparagine, and so on. The units of immune response are number of cells, per million, producing and colleagues (2004)

Explanation / Answer

Statement i is correct, because from the graph for P24 having T at third position immune response has started at low concentration of epitope, as well as immune response, is high compared to that with p24 having N at the third position at any point of time. Statement ii is wrong because in patients having HLA-B5801 or HLA-B57 HIV virions having P24 with asparagine at the third position may be preferred not in other patients with some other alleles. statement iii patients having the HLA-B57 virions with P24 having the asparagine at the third position would be selected against those with Threonine since in such patients immune response to Asparagine is less. Grammer in the third statement is quite confusing. Statement 4 is true in patients having HLA -B5801 and HLA-B57 virions would evolve such that asparagine at the third position of P24 protein. and statement 5 is also correct since patients having some other alleles virions would evolve such that at the third position of P24 Threonine is predominant. so from options A and D are correct

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